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1

Lean, M. E. J. "Brown adipose tissue in humans." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333609.

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2

Deiuliis, Jeffrey Alan. "The metabolic and molecular regulation of adipose triglyceride lipase." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1185546165.

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3

Hansen, Ida R. "The secretome of brown adipose tissue." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-102934.

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Brown adipose tissue has long been known for its heat-producing capacity, but less is known about its possible effects as a secretory organ. This thesis summarizes information about presently known factors secreted from brown adipose tissue and about their actions. We were able to add factors to the list by the use of a signal-sequence trap method. Results from the signal-sequence trap generated a list of suggested brown adipocyte secreted proteins; gene expression of these proteins was then further studied with microarray technique. One of the genes further analyzed was the adipokine chemerin. Gene expression of chemerin in brown adipose tissue was decreased in cold acclimation but increased with a high-caloric diet. This indicates that factors other than norepinephrine influence chemerin gene expression. The effects on chemerin gene expression were not be reflected in serum levels; therefore, chemerin secreted from brown adipose tissue is ascribed an autocrine/paracrine role. Signal-sequence trap and microarray studies suggested adrenomedullin, collagen type 3 a1, lipocalin 2 and Niemann Pick type C2 to be highly secreted from brown adipocytes. Gene expression of these factors was examined in vivo and in vitro. Our studies showed that both cold acclimation and high-caloric diet have an effect on gene expression of these factors. However, there was no effect on gene expression of chemerin and collagen type 3 a1 in norepinephrine-treated brown adipocyte cell cultures. This suggests that effects on gene expression of the examined possible brown adipocyte secreted proteins are not solely controlled by norepinephrine.

At the time of doctoral defence the following papers were unpublished and had a status as follows: Paper 1: Manuscript; Paper 3: Manuscript; Paper  4: Manuscript; Paper 5: Manuscript

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4

Mattsson, Charlotte L. "Role of caveolin-1 in brown adipose tissue." Doctoral thesis, Stockholm : The Wenner-Gren Institute, Stockholm University, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-37125.

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Diss. (sammanfattning) Stockholm : Stockholms universitet, 2010.
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript. Paper 3: Manuscript. Paper 4: Manuscript. Härtill 4 uppsatser.
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5

Warncke, Urszula Osinska. "Profiling Fatty Acid Composition of Brown Adipose Tissue, White Adipose Tissue and Bone Marrow Adipose Tissue of Healthy and Diet-Induced Obese Mice." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1440097081.

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6

Robb, Louise. "The effect of exercise on rat brown adipose tissue." Thesis, University of Ottawa (Canada), 1989. http://hdl.handle.net/10393/5739.

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7

Gibbins, J. M. "Hormonal control of carbohydrate metabolism by brown adipose tissue." Thesis, University of Bristol, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375016.

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8

Shaikh, Muhammad Iqbal. "Alpha-2 adrenoreceptors in brown adipose tissue of infant rats." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/27195.

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This thesis consists of five chapters. The first chapter deals with general background and introduction. Each of the subsequent chapters are divided into sections. The first section deals with pharmacological characterization of ∝₂-adrenoceptors using various ligands. The second section pertains to the study of binding characteristics of ∝₂-adrenoceptors following chemical sympathectomy by 6-hydroxydopamine and chronic blockade of ∝₂-adrenoceptors by yohimbine injections. The third section deals with the study of guanylate cyclase system in relation to ∝₂-adrenoceptors stimulation in brown fat fragments of 7-day-old rats. The fourth section is devoted to the study of the physiological response associated with the stimulation of ∝₂-adrenoceptors in isolated adipocytes from brown fat of 7-day-old rats. Finally cyclic GMP production in obese and lean mice in relation to ∝₂-adrenoceptors stimulation was discussed in the fifth section. Binding characteristics of ∝₂-antagonists ([³H]-RX-78- 1094, [³H]-yohimbine, [³H]-rauwolscine) and agonists ([³H]-clon- idine, [³H]-norepinephrine) to ∝₂-adrenoceptors on isolated plasma membrane fragments from brown adipose tissue were studied. The binding of [³H]-yohimbine was rapid,saturable and reversible. Yohimbine, (-)-epinephrine, and clonidine displaced [³H]-yohimbine from its binding sites in that order of potency as would be expected of binding to ∝₂- adrenoceptors. A Scatchard plot of yohimbine binding showed an equilibrium constant (K[sub d]) of 18 nM and total binding capacity (B[sub max] ) of 0.15 pmol/mg protein. Binding of [³H]-RX781094 and [³H]-clonidine showed a similar pattern of rapid, stable, saturable and reversible binding. Studies on the binding of (-)[³H]-norepinephrine indicated the presence of more than one binding site. Scatchard analysis of the (-)[³H]-norepinephrine binding using (-)-epinephrine or yohimbine as the displacing agent, revealed a K[sub d] of .60.4 nM and 65.8 nM respectively, and B[sub max] values of 0.22 and 0.24 pmol/mg protein. Norepinephrine, yohimbine and ∝₂-epinephrine probably shared one common binding site; the other site with of 64.5 nM was present in much lower number (71.3 fmol/mg protein) and was specific for (-)-norepin-ephrine and yohimbine only. In addition, a Hill coefficient of 1.4 further supported the presence of two positively cooperative binding sites. Binding of (-)[³H]-dihydroalpre-nolol was displaceable by practolol and norepinephrine with a K[sub d] of 50 nM and 10 nM respectively (β₁-site) and B[sub max] of 0.19 and 0.5 pmol/mg protein. However, (-)[³H]-dihydroal-prenolol binding could also be displaced by yohimbine suggesting either a relative non-specificity of the ligand or an atypical nature of the β₁-adrenoceptors in brown fat of infant rats. It is suggested that the plasma membranes from actively proliferating brown fat of infant rats possess both β₁-and ∝₂-adrenoceptors. The physiological in vivo agonist (-)-norepinephrine may exert its effects via both or either adrenoceptor sub-type. Binding studies carried out with [³H]-yohimbine on membranes isolated from brown fat of chemically sympath- ectomized infant rats showed smaller number of high affinity yohimbine binding sites when compared to those isolated from control (saline-injected) rats of the same age. The (-)[³H]-norepinephrine binding to identical membrane preparations revealed the presence of both high (K[sub d] = 36 nM) and low (K[sub d] = 200 nM) affinity binding sites; with a Hill coefficient of 1.5. The total number of norepinephrine binding sites more than doubled after sympathectomy; this increase was caused by emergence of low affinity sites. Chronic yohimbine pre- treatment resulted in more than two-fold increase in the number of binding sites for both [³H]-yohimbine and (-)[³H]- norepinephrine. The affinity of ∝₂-adrenoceptors for yohimbine binding sites decreased whereas that for norepinephrine remained unchanged. These results not only confirm the presence of ∝₂-adrenoceptors in brown fat of developing rats but also indicate that the binding characteristics of these receptors can be altered by chemical sympathectomy and by chronic exposure of infant rats to an ∝₂ -receptor blocker. Incubation of brown fat tissue pieces with clonidine (0.2-20μM) showed a dose- and;time-' dependent elevation of tissue cyclic GMP content. The peak response occurred at the concentration of 20μM for one-month-old rats. For brown fat from one-week-old rats, the peak response occurred at 0.5 - 1μMof clonidine and 3 - 5 minutes of incubation. The response could be blocked by prior incubation with yohimbine. When tissue cyclic GMP concentration, elevated in response to clonidine incubation, was separated into releaseable and receptor-protein bound fraction, a similar trend was seen. The data supported the hypothesis that ∝₂-receptor stimulation of brown fat is linked (directly or indirectly perhaps via Ca²⁺) to guanylate cyclase activation. Earlier in vivo experiments had shown a defective response of brown fat cyclic GMP production in obese mice upon acute cold exposure and catecholamine injections as compared to control litter mates which showed a dose- and time- dependent increase. Preliminary in vitro experiments where where fragments from obese and lean mice were stimulated with clonidine, showed two-fold increase in the cyclic GMP concentration compared to non-stimulated controls. This suggested that tissue capability to respond by an increase in cyclic GMP production in obese mice is the same as that in the lean mice. Forskolin and Isobutylmethylxanthine stimulated glycerol release in isolated adipocytes from brown fat of one-week-old rats. Clonidine, prostaglandin E₂ and nicotinic acid showed inhibitory effects on glycerol release. Inhibition of glycerol release by clonidine was concentration-dependent and was antagonized by yohimbine. Inactivation of inhibitory regulatory protein (Ni) by pertussis toxin abolished the inhibitory effect of clonidine. This indicated that the inhibitory effect of clonidine on glycerol release is mediated via inhibitory protein (Ni). It was suggested that, perhaps, the anti-lipolytic effect of ∝₂-adrenoceptors may have a role in controlling the state of activity of fat cells.
Graduate and Postdoctoral Studies
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9

Park, Ian R. A. "Studies of the growth and regulation of brown adipose tissue." Thesis, University of Ottawa (Canada), 1989. http://hdl.handle.net/10393/5700.

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10

Harper, Mary Ellen. "Ion transport and brown adipose tissue activity in energy balance." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7486.

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The objective of this work was to study the activity of the Na$\sp+$,K$\sp+$ pump and the thermogenic activity and capacity of brown adipose tissue (BAT) under conditions of dietary energy deficit and surfeit in both human subjects and laboratory animals. While controversial, it had earlier been hypothesized that Na$\sp+$,K$\sp+$ pump activity (1) acts as a "metabolic pacemaker" in the control of cellular energy expenditure, and (2) "adapts" during undernutrition so that overall energy expenditure is decreased. That BAT thermogenic activity increases during overfeeding and decreases during undernutrition is well recognised; BAT thermogenesis has hence been proposed as an "energy buffer" mechanism. However, at the outset of this work the effectiveness of dietary saturated fat in the induction of BAT thermogenesis was controversial. The first sections of this thesis describe the effects of undernutrition and nutritional rehabilitation upon Na$\sp+$,K$\sp+$ pump activity in erythrocytes of children with cerebral palsy (CP). The results show that, unlike results from developing world undernourished children, erythrocyte Na$\sp+$,K$\sp+$ pump activity was not lower in cells from the undernourished children with CP. The later sections describe the simultaneous study of both Na$\sp+$,K$\sp+$ pump and BAT activities during diet-induced obesity (DIO) and dietary restriction (DR) in rats. I hypothesized that both mechanisms might act as "energy buffers" and contribute to metabolic adaptation during DIO and DR. The effects of lard- and tallow-based diets were studied. The extent of DIO was assessed using total body electrical conductivity (TOBEC), carcass analysis and fat pad weights; it was concluded that presently available TOBEC equipment is unsuitable for serial determinations of rat adiposity, and that fat pad weights are good estimates of adiposity. Na$\sp+$,K$\sp+$ pump activity increased in thymocytes of rats fed the high saturated fat diets; activity decreased in erythrocytes and hepatocytes in some groups following DR. BAT activity and thermogenic capacity were enhanced by high saturated fat diet-feeding; activity decreased following DR. Lard- and tallow-based diets had differing effects upon the extent and the timing of changes in the activities of the two mechanisms. Despite increases in Na$\sp+$,K$\sp+$ pump and BAT activities, basal metabolic rate (BMR) was not increased in the obese rats; decreases did however occur following DR. Diet-induced alterations in both mechanisms could occur through common pathways such as sympathetic neural activity and/or thyroid hormones. Increases in plasma T$\sb3$ concentrations were associated with high saturated fat diet feeding as were decreases with DR. It is concluded that the alterations in both mechanisms are compatible with the hypothesis that these mechanisms function as energy buffer mechanisms during dietary energy surfeit and deficit.
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11

Oguri, Yasuo. "Tetrahydrobiopterin activates brown adipose tissue and regulates systemic energy metabolism." Kyoto University, 2018. http://hdl.handle.net/2433/232086.

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12

von, Essen Gabriella. "Energy flow and metabolic efficiency attributed to brown adipose tissue." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-140190.

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The large capacity of brown adipose tissue (BAT) to expend energy as heat makes it an interesting potential player in weight regulation and other metabolic conditions. This is of particular interest as it has been recognized that adult humans possess BAT. The protein responsible for the heat production is uncoupling protein 1 (UCP1), which, as the name implies, uncouples the respiratory chain from ATP production; instead heat is produced. Cold is the strongest recruiter and activator of BAT. However, also obesogenic food has a low but nonetheless significant effect on the recruitment and activation of UCP1, although the significance of this has been discussed. In the present thesis, I have studied the effect of diet on BAT and the possibilities for it to be obesity-protective. This can be done by comparing responses in wild-type mice and in UCP1-ablated mice. Since the effect of diet on BAT is low, it is of importance to control the temperature and maintain thermoneutrality. Other confounding factors to keep in mind are differences in actual energy and composition of food and also cohort differences. When controlling all the parameters mentioned and giving the mice the same obesogenic diet, the mice possessing UCP1 compared to UCP1-ablated mice had higher energy expenditure, and lower weight gain, despite eating more. This confirms the presence of a UCP1-dependent diet-induced thermogenesis. Thus, the conclusion must be that possessing UCP1 does result in obesity protection at thermoneutrality. However, the relevance for human energy balance is still not established.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript. Paper 2: Manuscript. Paper 3: Manuscript.

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13

Thomas, Joanna. "Brown adipose tissue a potential early biomarker of metabolic syndrome /." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3356437.

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Thesis (Ph. D.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed July 9, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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14

Clark, Lynne. "Manipulation and control of thermoregulation in the newborn lamb." Thesis, University of Reading, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239505.

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15

Melnyk, Anna. "Brown adipose tissue atrophy, effects on energy expenditure and body composition." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ28359.pdf.

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16

Mercer, S. W. "Studies on lipogenesis and thermogenesis in brown adipose tissue of rodents." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332436.

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17

Reddy, Narendra Lakshmana. "Novel insights in imaging and function of human brown adipose tissue." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/69397/.

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Phenomenal rise in prevalence of obesity and its complications has made it imperative to tackle the issue on a war footing, especially given the failure of current life style and medical approaches. Clearly, alternate means of treating obesity need to be explored. In contrast to white adipose tissue (WAT), which stores excess energy, brown adipose tissue (BAT) dissipates chemical energy in the form of heat by uncoupling oxidative phosphorylation from electron transport chain, to maintain body temperature homeostasis. Recent revelation of functionality of BAT in adult humans provides an excellent opportunity of stimulating it to increase energy expenditure, in turn causing weight loss alongside improving lipid and glucose homeostasis. This thesis sought to investigate the physiological nature of brown fat, by exploring the environmental, biophysical and behavioural factors that can activate BAT. ¹⁸Fluoro-labelled-2-deoxyglucose Positron Emission Tomography (18F-FDG PET) is currently the gold standard and the most sensitive method to study BAT and its function. These studies concluded that younger-age, lower body mass index, female sex and cooler outdoor temperatures are strong determinant factors of BAT prevalence, activity and mass. Interestingly, modest elevation of thyroid hormones in a sustained iatrogenically created thyrotoxic state did not influence any of the BAT indices, contrary to conventional wisdom of strong stimulation, thus highlighting the complexity of BAT metabolism. Arguably, BAT has a role in diet-induced thermogenesis. Manipulation of diet-induced thermogenesis by prolonging meal duration to 40 minutes resulted in excess postprandial energy expenditure loss than shorter meal duration of 10 minutes. However, prolonged meal duration had weakly positive effect on metabolic biochemical markers and no influence on pancreatic and gut hormones relevant to appetite. These studies advocate life style and behavioural public health messages of lowering thermostat in living spaces and chewing the food adequately in order to obtain potential metabolic benefits. As a follow-up of exploring BAT's physiology, a successful attempt at characterising BAT's anatomy was made through novel imaging technique of Iterative Decomposition of Echo Asymmetry and Least Squares Estimation (IDEAL) Magnetic Resonance Imaging. The first ever non-PET imaging demonstration of adult human BAT using IDEAL MRI was achieved with immunohistochemical confirmation, and provided proof of concept for developing MR as a safe, non-radiation exposure imaging biomarker of BAT. In summary, this thesis provided useful insights into environmental, anthropometrical, behavioural, and hormonal factors regulating BAT, whilst also providing a proof of principle of an imaging tool to visualise full extent of both metabolically active and inactive BAT, aiding future pursuits of BAT therapeutics to combat the global obesity epidemic.
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18

Ojha, Shalini. "Pericardial fat is a nutritionally regulated depot of brown adipose tissue." Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/30678/.

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Introduction: Obesity and related cardio-metabolic complications have acquired global epidemic proportions. Suboptimal nutritional environment in early life induces adaptations in energy homeostasis, metabolism and adipose tissue development that may confer short-term survival advantages but are detrimental in later life, particularly if nutrient supply is restored. Brown adipose tissue (BAT) has a unique role in energy homeostasis because it can provide a potential compensatory mechanism against excess weight gain via cold or diet-induced adaptive thermogenesis. Brown adipocytes also have a potential role in lipid and glucose metabolism and BAT activation can increase clearance of lipids and glucose from the circulation. Pericardial fat, particularly epicardial adipose tissue (fat present between the myocardium and the visceral layer of the pericardium), is anatomically and clinically related to cardiac morphology and function and is believed to be a metabolically active organ that affects cardiac function and the evolution of cardiac pathologies. High expression of mRNA for uncoupling protein (UCP) 1 in adult human epicardial adipose tissue suggests that this may be a depot of BAT. Hypotheses: In my thesis, I hypothesised that pericardial adipose tissue is a depot of brown fat in humans and sheep. I also hypothesised that suboptimal nutrition in early life will affect adiposity and development of BAT in this depot. Methods: UCP1 mRNA expression and protein abundance and other BAT and white adipose tissue related genes were studied in pericardial adipose tissue. In the first study, pericardial fat was sampled from newborn and 30 day old sheep born to mothers fed with 100% or 60% of their total metabolisable energy (ME) requirement from 110 day gestation to term. In the second study, pericardial fat was sampled from near-term (140 day gestation) fetuses delivered to mothers fed 100% or 60% of total ME requirement from 28 to 80 days and then fed ad libitum. Gene expression was measured by reverse transcription-polymerase chain reaction and protein abundance by Western blotting and immunohistochemistry. To confirm the presence of BAT in the human epicardial fat depot, relative abundance of UCP1 was measured by Western Blotting in epicardial, paracardial, and subcutaneous fat samples taken from adults. In the final study, epicardial fat samples were collected from 63 children (0-18 years of age) undergoing cardiac surgery and gene expression of UCP1 and other BAT and WAT related genes identified by microarray. The presence of UCP1 was confirmed by immunohistochemistry. Results: Pericardial adipose tissue is a depot of BAT in fetal and newborn sheep. Suboptimal maternal nutrition in late gestation reduces the abundance of UCP1 and downregulates other BAT related genes whilst suboptimal maternal nutrition in early-to-mid gestation followed by ad libitum feeding to term, increases adiposity, enhances UCP1 abundance and upregulates genes involved in brown and white adipogenesis. Epicardial fat from newborn infants, children, adolescents and older adults contains UCP1 confirming that it is a BAT depot in humans. UCP1 gene expression in infancy and early childhood in humans is downregulated in children with poor nutritional states. Conclusions: I have shown that adipose tissue depots present around the heart are a repository of brown fat, at least in humans and sheep. In view of the potential role of BAT in regulation of lipid and glucose metabolism, this may have therapeutic implications for treatment of cardiovascular complications of obesity. Suboptimal nutrition in utero and during early life compromises BAT development. Although the exact mechanism of how these changes affect the propensity towards obesity and metabolic dysregulation remains to be elucidated, a reduction in thermogenesis presents a plausible mechanism for the increased metabolic efficiency associated with nutritional deprivation in early life. BAT persists beyond the neonatal period in to adult life and, therefore, presents a potential target for long lasting nutritional manipulations to promote better health.
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Sarapio, Elaine. "Estudo da ação do hormônio peptídico stanniocalcina sobre o metabolismo de lipídios." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2014. http://hdl.handle.net/10183/101653.

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As stanniocalcinas (STC1 e STC2) são hormônios glicoproteicos identificados primeiramente em peixes ósseos, relacionados com o metabolismo do cálcio e fosfato. Recentes descobertas evidenciaram que as funções das STCs foram mantidas em mamíferos. A descoberta da localização do receptor para STC1 na membrana mitocondrial de roedores e sua ação como desacopladora da respiração celular sinalizam fortemente um importante papel desse hormônio no metabolismo intermediário de mamíferos. A STC estimula a lipogênese no tecido hepático e muscular de ratos, porém, suas ações sobre o metabolismo do tecido adiposo ainda não foram esclarecidas. No presente trabalho, estudamos o efeito, in vitro, da STC1 e da STC2 humanas, nas concentrações (A: 0,01ng/mL; B: 0,1ng/mL; C: 10ng/mL) no tecido adiposo branco (TAB) e no tecido adiposo marrom (TAM) em Rattus norvegicus machos, 300 ± 50g, alimentados ad libitum e submetidos ao jejum de 24 e 48 horas (n=61). Os resultados obtidos demonstram que, no TAB, a STC1 não apresentou efeito. Contudo, a STC2, nas concentrações A e C, diminuiu a formação de 14CO2 em animais em jejum de 24 horas e nas concentrações A e B, aumentou a incorporação de [214C] piruvato em 14C-glicerol, em animais alimentados (controle). No TAM, a STC1 na concentração B, diminuiu a formação de 14CO2 em animais alimentados (controle). Na mesma concentração, aumentou a incorporação de [214C] piruvato em 14C-glicerol em animais em jejum de 24 horas e aumentou a incorporação de 14C-ácido graxo em animais alimentados (controle). A STC2, na concentração B, diminuiu a formação de 14CO2 em animais alimentados (controle) e aumentou a formação de 14CO2 nos animais em jejum de 24 horas. A STC2 não alterou a via gliceroneogênica neste tecido. A dosagem plasmática do hormônio leptina apresentou acentuada diminuição no grupo jejum 48 horas. As STCs 1 e 2, nas concentrações utilizadas, não alteraram a atividade da enzima PEPCKc nos tecidos estudados (TAB e TAM), em animais alimentados (controle). Em quase todos os tratamentos observamos diferenças marcantes entre animais alimentados e jejuados. Este é o primeiro estudo que mostra as diferentes concentrações das STCs no metabolismo de lipídios.
The stanniocalcins (STC1 and STC2) are glycoprotein hormones related to the metabolism of calcium and phosphate first identified in fish bone. Recent findings showed that the functions of STCs were maintained in mammals. The discovery of the location of the receptor for STC1 in the mitochondrial membrane, as well as its uncoupling action of cellular respiration in rodents, strongly indicate an important role of this hormone in the intermediary metabolism of mammals. The STC stimulates lipogenesis in the liver and muscle tissue of rats. However, its action on the metabolism of adipose tissue has not yet been clarified. In this work, we studied the effect in vitro of human STC1 and STC2 concentrations (A: 0,01 ng/ml, B: 0,1 ng/ml, C: 10ng/mL) in white adipose tissue (WAT) and in brown adipose tissue (BAT) in male Rattus norvegicus , 300 ± 50 g , fed ad libitum and fasted for 24 and 48 hours (n= 61). The results show that in the WAT, the STC1 had no effect. However, STC2 at concentrations A and C decreased the formation of 14CO2 in fasted rats for 24 hours and the concentrations A and B increased the incorporation of [214C] into 14C-glycerol pyruvate in fed animals (control). In BAT, STC1 concentration B, decreased the formation of 14CO2 in fed animals (control). At the same concentration, increased the incorporation of [2 14C] pyruvate into 14C-glycerol in fasted rats for 24 hours and increased the incorporation of 14C-fatty acid in fed animals (control). The STC2 concentration B decreased the formation of 14CO2 in fed animals (control) and increased the formation of 14CO2 in animals fasted for 24 hours. The STC2 did not alter the glyceroneogenesis pathway in this tissue. The serum levels of leptin showed marked decrease in the group fasting for 48 hours. The STCs 1 and 2, in the concentrations used, did not alter the PEPCKc enzyme activity in the tissues studied (WAT and BAT) in fed animals (control). In almost all treatments we observed striking differences between fed and fasted animals. This is the first study that shows the effect of different concentrations of STCs in the metabolism of lipids.
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Leite, Juliana Paula 1982. "O efeito do treinamento físico sobre a resistência à insulina em animais tratados com dieta hiperlipídica : modulações de fatores inflamatórios sobre o tecido adiposo branco e marrom de ratos Wistar." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312926.

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Orientadores: Mario José Abdalla Saad, Alexandre Gabarra de Oliveira
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A obesidade representa o maior fator de risco para o desenvolvimento de doenças como diabetes tipo 2, dislipidemia, esteatose hepática, doenças vasculares e alguns tipos de cânceres. Embora o aumento do tecido adiposo seja a principal característica da obesidade, nem todo depósito de gordura é prejudicial. Isso se deve ao fato do tecido adiposo ser subdividido em dois tipos: branco e marrom, os quais apresentam características bem distintas. O tecido adiposo branco estoca energia na forma de triglicerídeos, produz a secreção de vários tipos de citocinas inflamatórias e o seu aumento está associado a um estado inflamatório subclínico do organismo. Já o tecido adiposo marrom é especializado na dissipação da energia em forma de calor, estudos vêm mostrando a sua associação com a melhora da resistência à insulina e menor índice de massa corporal, por isso, o seu aumento pode ser potencial alvo para o tratamento de síndromes metabólicas. Paralelamente, estudos comprovaram que o exercício físico, quando praticado de forma crônica, pode exercer importante efeito anti-inflamatório nos obesos. Este efeito está associado à redução da massa de tecido adiposo branco e estudos comprovaram que o exercício também é capaz de promover o aumento da massa do tecido adiposo marrom. No entanto, ainda não está claro quais os mecanismos envolvidos para tais benefícios. Diante disso, o objetivo do nosso trabalho foi avaliar o efeito profilático do exercício crônico sobre a massa do tecido adiposo (branco e marrom), marcadores inflamatórios e resistência à insulina em ratos alimentados com dieta hiperlipídica. Além de verificar os mecanismos pelos quais o exercício é capaz de aumentar a atividade termogênica do tecido adiposo marrom. Para isso, utilizamos ratos Wistar, divididos em 3 grupos: animais alimentados com dieta padrão para roedores (CTL), animais alimentados com dieta hiperlipídica (HFD) e animais alimentados com dieta hiperlipídica e submetidos ao treinamento de natação (EXE). O protocolo de treinamento utilizado foi de 8 semanas. Nossos resultados mostraram que o exercício crônico de 8 semanas foi capaz de atenuar o desenvolvimento da massa de gordura e a expressão das proteínas de formação do tecido adiposo branco (TAB); apresentou efeito protetor contra a intolerância à glicose e RI. Fora também observado a redução dos circulantes de LPS, TNF-? e AGLs, além da expressão das serinas quinases JNK E IKK. Além disso, os dados demonstram ainda o efeito positivo do exercício na via de sinalização da insulina; aumento da massa do tecido adiposo marrom (TAM) e da expressão de proteínas envolvidas no processo de termogênese. Por último, verificamos que o exercício crônico foi capaz de atenuar a infiltração de macrófagos no TAM e promover maior polarização de macrófagos do tipo M2 no TAM. A partir dessas análises, podemos entender em parte que o exercício físico, quando aplicado antes do estabelecimento da obesidade, é capaz de atenuar o quadro de resistência à insulina e os efeitos deletérios da inflamação causada pela dieta hiperlipídica. Além de contribuir para a maior atividade do TAM através de um mecanismo orquestrado pela ativação alternativa de macrófagos
Abstract: Obesity is a major risk factor for the development of diseases such as type 2 diabetes, dyslipidemia, fatty liver, vascular disease and some cancers. Although the increase in adipose tissue is a hallmark of obesity, not every deposit of fat is harmful. This is because adipose tissue is subdivided into two types: white and brown, which have very different characteristics. White adipose tissue stocks energy in the form of triglycerides, and it is responsible to the secretion of various cytokines and their increase is associated with a proinflammatory state of the organism. As brown adipose tissue is specialized in the dissipation of energy as heat, studies have shown its association with improved insulin resistance and lower body mass index. Therefore, its increase may be a potential target for the treatment of metabolic syndromes. In parallel, studies have shown that chronic exercise may have an important anti-inflammatory effect on obesity due to a reduction mass of white adipose tissue and the capacity to promote the increased mass of brown adipose tissue. However, it remains unclear which mechanisms are involved for such benefits. Therefore, the aim of our study was to evaluate the prophylactic effect of chronic exercise on the mass of adipose tissue (white and brown), inflammatory markers and insulin resistance in high-fat diet rats. Besides, our study verified the mechanisms by which exercise can increase the thermogenic activity of brown adipose tissue. For this, we used 6 weeks male Wistar rats, which were divided into 3 groups as follows: animals fed with standard rodent diet (CTL) animals fed with high fat diet (HFD) and animals fed with high fat diet and submitted to swimming training (EXE). The training protocol used was 8 weeks. Our results showed that 8 weeks of chronic exercise was able to attenuate the development of fat mass and protein expression formation of white adipose tissue (WAT). It was also shown a protective effect against glucose intolerance and insulin and observed a reduction of circulating LPS, TNF-? and FFA, in addition to the expression of serine kinases JNK and IKK. The results also demonstrate the positive effect of exercise on insulin signaling pathway, increasing the mass of brown adipose tissue (BAT) and the expression of proteins involved in the thermogenesis process, which resulted in higher accumulation of fat in the adipocytes of TAM. Finally, we found that chronic exercise was able to attenuate the infiltration of macrophages in the TAM and promote greater polarization of the type M2 macrophages in TAM. From these analyses, we can understand in part that exercise, when applied before the onset of obesity, is able to attenuate the context of insulin resistance and the deleterious effects of inflammation caused by high-fat diet, contributing to the higher activity of TAM through an alternative orchestrated macrophage activation mechanism
Mestrado
Fisiopatologia Médica
Mestra em Ciências
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21

Rodó, Morera Jordi. "Transcriptomic analysis of white and brown adipose tissue during non-shivering thermogenesis." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667915.

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L’obesitat i la diabetis tipus 2 (DT2) són dues malalties estretament relacionades que representen un greu problema de salut, social i econòmic per la seva alta prevalença a tot el món. Ambdues malalties també es relacionen amb altres patologies que presenten una mortalitat elevada. Les teràpies disponibles actualment no són del tot efectives. Per tant, el desenvolupament de noves estratègies terapèutiques per a l'obesitat i la DT2 és crucial. El teixit adipós s'ha definit com un òrgan que té un paper central en el control del balanç energètic. El descobriment de funcions endocrines i termogèniques dels adipòcits han tornat a centrar l’interès en l’estudi d’aquest teixit. La termogènesi no associada a tremolor està descrita per dur-se a terme al teixit adipós marró dels ratolins, però sota certs estímuls, com l'exposició prolongada al fred, cèl·lules amb una morfologia similar als adipòcits marrons (adipòcits beix) apareixen en alguns dipòsits de teixit adipós blanc de rosegadors i humans, un procés conegut com a browning. L’activació a través de l’exposició al fred de la termogènesi no associada a tremolor en humans augmenta el consum energètic en repòs, la sensibilitat a la insulina i millora el metabolisme de la glucosa. No obstant, es necessiten més estudis d'expressió gènica per aprofundir en els mecanismes moleculars subjacents a la millora induïda per fred a través de la termogènesi no associada a tremolor, així com per determinar les diferències entre l'activació del teixit adipós marró (BAT) i el browning del teixit adipós blanc (WAT). En aquesta tesi doctoral, es van examinar els canvis transcriptómica dels dipòsits adiposos blancs epidídimal i inguinal (eWAT i iWAT, respectivament), així com la del dipòsit adipós marró interscapular (iBAT) de ratolins exposats a 22ºC o 4ºC durant 4 dies. L’exposició al fred va augmentar l’activitat metabòlica i termogènica de l’iWAT. En aquest dipòsit, els gens relacionats amb la glucòlisi, el cicle de l'àcid tricarboxílic, la lipòlisi i la degradació d'alguns aminoàcids van presentar una expressió incrementada per mantenir la potència protonmotriu per generar calor. A més, l'expressió de gens relacionats amb la termogènesi també va augmentar molt, demostrant una inducció del browning induïda per fred en el iWAT. S'ha descrit que el dipòsit d’eWAT és resistent al browning. Per tant, l’activació metabòlica observada d’aquest dipòsit va ser suau en comparació amb la d’iWAT, i en aquest dipòsit no es va observar cap millora rellevant de la termogènesi no associada a tremolor. Finalment, l’iBAT ja presentava nivells d’expressió de gens termogènics elevats, ja que els ratolins no estaven estabulats a termo-neutralitat. L’observació que els gens termogènics i metabòlics presentaven un patró d’expressió similar entre les mostres va recolzar l’ús d’eines d’anàlisi de patrons per descriure Atp4b i 1700040L02Rik com a nous gens potencialment implicats en la termogènesi. La sobreexpressió d’Atp4b i 1700040L02Rik en el teixit adipós mitjançant l’ús de vectors AAV va produir una reducció del guany de pes corporal, una disminució del pes de l'eWAT i del fetge, la millora de la hipertròfia dels adipòcits blancs i la reducció de la esteatosi hepàtica. Tots aquests resultats van ser potencialment fruit de la termogènesi millorada detectada en iWAT. En general, aquests resultats indiquen un possible nou paper anti-obesogènic d’aquests gens. Els resultats d’aquesta tesi han contribuit a una millor comprensió de la inducció de la termogènesi no associada a tremolor en els dipòsits de teixit adipós de ratolins. Entre els diferents dipòsits de teixit adipos, l’anàlisi exploratori dels nivells d’expressió gènica va determinar que el iWAT era el dipòsit que va respondre de manera més significativa a l’exposició al fred. A més, tal com es va observar en l’anàlisi de l’enriquiment de vies i d’ontologia gènica, aquesta resposta va ser altament coordinada, presentant un elevat nombre de gens relacionats amb rutes metabòliques que presentaven una expressió altament incrementats. Igualment, l’estudi detallat de les vies metabòliques va destacar una gran inducció de la termogènesi no associada a tremolor, revelar que els mecanismes de producció i de consum d’energia estaven altament sincronitzats. Aquest estudi detallat del teixit adipós també va permetre la identificació de nous gens potencialment implicats en la termogènesi no associada a tremolors.
Obesity and type 2 diabetes (T2D) are two closely related diseases that represent a serious health, social and economic problem due to their high prevalence worldwide. Both diseases are also associated with other pathologies that present high mortality. The currently available therapies are not entirely effective. Thus, the development of new therapeutic strategies for obesity and T2D is crucial. Adipose tissue has been defined as an organ that plays a central role in the control of energy balance. The proved endocrine and thermogenic functions of adipocytes has renewed interest in the study of this tissue. Non-shivering thermogenesis has been described as occurring in brown adipose tissue of mice, but under certain stimuli, such as prolonged cold exposure, brown fat-like cells (beige adipocytes), appear in some white adipose tissue depots of rodents and humans. The activation of non-shivering thermogenesis in humans through cold-exposure increases resting energy expenditure, whole-body glucose disposal, insulin sensitivity, and ameliorates glucose metabolism independently of BMI. However, more gene expression studies to gain insight into the molecular mechanisms underlying the cold-induced enhancement of non-shivering thermogenesis, as well as to determine differences between BAT activation and browning of WAT, are needed. In this study, the transcriptomic response of epididymal and inguinal white adipose depots (eWAT and iWAT, respectively) as well as that of the interscapular brown adipose depot (iBAT) of mice either exposed to 22ºC or 4ºC for the period of 4 days were examined. Cold exposure increased the metabolic and thermogenic activity of iWAT. In this depot, genes related to glycolysis, tricarboxylic acid cycle, lipolysis, and the degradation of some amino acids presented a high upregulation to maintain the protonmotive power to generate heat. Moreover, the expression of thermogenic-related genes was also highly increased, demonstrating a cold-induced browning of iWAT. The eWAT depot has been reported to be resilient to browning. Thus, the observed metabolic activation of this depot was mild in comparison with that of iWAT, and no relevant enhancement of non-shivering thermogenesis was observed in this depot. Finally, iBAT already presented high expression levels of thermogenic genes because mice were not housed at thermoneutrality. The observation that genes related to thermogenesis and metabolism presented a similar expression pattern among samples endorsed the utilization of pattern matching analysis tools to unravel Atp4b and 1700040L02Rik as novel genes potentially involved in thermogenesis. The overexpression of Atp4b and 1700040L02Rik in adipose tissue by means of AAV vectors produced a body weight gain reduction, decreased eWAT, and liver weight, amelioration of white adipocytes hypertrophy, and reduced hepatic steatosis potentially as a result of the detected enhanced thermogenesis in iWAT. Overall, these results indicate a new potential anti-obesogenic role for these genes. The results from this thesis contributed to a better understanding of the induction of non-shivering thermogenesis in adipose tissue depots in mice. Among the different adipose depots, exploratory data analysis of the gene expression levels of mice exposed from 22ºC to 4ºC determined that iWAT was the depot that responded most significantly to cold exposure. Moreover, as observed in the pathway enrichment and gene ontology analysis, this response was highly coordinated, presenting a high number of genes related to metabolic pathways highly affected. The detailed study of the metabolic pathways led to the detection of a high induction of non-shivering thermogenesis, revealing that both energy production and energy consumption mechanisms were highly synchronized. This in detail study of the adipose tissue also allowed the identification of novel genes potentially involved in non-shivering thermogenesis.
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22

Cui, Jingying. "Role of sensory nerves in growth and thermogenesis of brown adipose tissue." Thesis, University of Ottawa (Canada), 1992. http://hdl.handle.net/10393/7655.

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The original objective of work described in this thesis was to study neural control of diet-induced thermogenesis in BAT. The hypothesis was that impairment of central warmth perception by capsaicin-desensitization (CAP-DES) would diminish central suppression of BAT thermogenesis by heat generated as a consequence of food ingestion, and thus enhance sympathetic-mediated diet-induced hypertrophy of BAT. Unexpectedly, CAP-DES caused atrophy of BAT and prevented diet-induced thermogenesis in BAT. This novel finding led to a modification of objectives to find out why CAP-DES induces atrophy of BAT and to study further the consequences for the CAP-DES rat of the atrophied state of its BAT. Atrophy of BAT in the CAP-DES rat involved loss of total protein, loss of mitochondrial proteins and loss of cells. BAT of the CAP-DES rat was unresponsive to stimulation by diet and cold-induced growth was retarded. The most extensive destruction of BAT occurred at 1 day, gradually reversed over the next 28 days, then reappeared at 8 months. A preliminary study in which a neurotransmitter of sensory nerves, calcitonin gene-related peptide (CGRP) was infused for several days suggested that the effect of CAP-DES might be due to removal of a trophic influence of neuropeptides of sensory nerves, known to be depleted in BAT of the CAP-DES rat. The association between atrophied BAT and obesity in several different animal models suggested that CAP-DES rats might become obese. However, CAP-DES rats fed an obesity-inducing diet (high fat) for 10 weeks did not become any more obese than control rats eating the same diet and aging-induced obesity was reduced in the CAP-DES rat. Conclusions. Neuropeptides of sensory nerves play an important role in control of BAT thermogenic capacity, supplementing that of noradrenaline. The relation of atrophied BAT to energy balance in the CAP-DES rat remains to be elucidated.
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23

Chen, Hsiang Yin. "The regulation of brown adipose tissue gene expression in HIB-1B cells." Thesis, University of Nottingham, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.575158.

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The main objective of this thesis is to contribute to our understanding of the regulation of brown adipose gene expression by examining the transcriptional regulation of the two key brown adipogenic genes, UCPl and PGCla during the initial stage of differentiation in a model brown adipocyte cell line. The principal findings were that UCP land PGC 1 a expression was induced by both forskolin and rosiglitazone, and that combination of these drugs produced a synergistic increase which required the full length promoters. These effects on UCPl and PGCla expression were partially suppressed by PKA and PPARy antagonists and results suggested that there is a cross-talk between PKA and PPARy signalling pathways. C~anges in brown adipogenic gene expression similarly provided evidence of cross-talk between PKA and PPARy signalling pathways which may explain the mechanism responsible for the synergistic effects offorskolin and rosiglitazone on UCPl expression. PPARy and CIEBPP, but not PGC 1 a overexpression, increased basal and stimulated UCP 1 mRNA. Similar results were observed with the 3.lkb UCPl-Luc reporter and co-overexpression ofPPARy with PGC 1 a markedly upregulated UCP 1 transcription in response to either forskolin or rosiglitazone. PGCla mRNA was increased in response to C/EBPP, but not PPARy overexpression and these results were confirmed using the 2.6kb PGCla-Luc reporter. PGC 1 a transcription was further up-regulated by co-overexpression of C/EBPP with PPARy in response to either forskolin or rosiglitazone. RIPl40 overexpression inhibited the effect of PG Cl a on rosiglitazone stimulated 3.lkb UCPl-Luc promoter activity. The results suggests that there are differences in transcriptional regulation between UCP 1 and PGCla promoters which indicate that the synergistic effect of cAMP and PPARy ligand stimulation on UCPl expression is a direct results of control of the PPRE and CRE on the UCPl promoter rather than indirect control though the PGCla promoter. vi
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Peachey, Tamsin Jane. "Regulation and organisation of the mitochondrial uncoupling protein from brown adipose tissue." Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278638.

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25

KUO, HSUAN-CHIH. "Apolipoprotein A-IV Enhances Thermogenesis in Brown Adipose Tissue and Energy Expenditure." Ohio University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1628701770248129.

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26

Nnodim, J. O. "Morphological studies on the development and the control mechanisms of brown adipose tissue." Thesis, Bucks New University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356211.

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Carvalho, Aline Penna de. "Efeitos pleiotrópicos da telmisartana nos tecidos adiposos branco e marrom: aumento da expressão gênica e proteica pan-PPAR em camundongos obesos." Universidade do Estado do Rio de Janeiro, 2014. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=7337.

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Receptores ativadores de proliferação perixossomal(PPARs) são fatores de transcrição envolvidos com a oxidação dos ácidos graxos e proliferação celular, mediando diversas vias, o que representa uma estratégia promissora para enfrentar as características da síndrome metabólica. Existem três isoformas de PPARs(PPARalfa, beta/delta e gama), que são diferencialmente expressos em diferentes tecidos.No presente estudo, objetivou-se avaliar os efeitos pleiotrópicos da telmisartana, um anti-hipertensivo, bloqueador do receptor AT1 da angiotensina e agonista parcial PPAR gama, no tecido adiposo branco (TAB) e marrom (TAM) em camundongos obesos induzido por dieta.Camundongos machos, da linhagem C57BL/6 foram alimentados com uma dieta padrão (standard-chow, 10% da energia proveniente de lipídios) ou com uma dieta com alto teor lipídico (high fat, 49% de energia proveniente de lipídios) durante 10 semanas. Em seguida, os animais foram distribuídos aleatoriamente em quatro grupos: SC, SC-T, HF e HF-T (n=10). O fármaco foi administrado (10mg/kg de dieta) durante 4 semanas para os grupos SC-T e HF-T.O grupo HF apresentou sobrepeso, hipertensão arterial sistêmica, perfil de adipocinas pró-inflamatórias, resistência insulínica, diminuição do gasto energético, comprometimento do metabolismo da glicose e distribuição anormal da massa adiposa. Além disso, a obesidade ocasionou diminuição da expressão de PPARalfa, beta/delta e gama noTAB e TAM, resultando na inadequação da captação de glicose e termogênese insuficiente. Por outro lado,a ativação das três isoformas de PPARs, a melhora do perfil inflamatório das adipocinas, o aumento da sensibilidade à insulina e a melhora da captação de glicose, foi vistaapós o tratamento com telmisartana. A ativação dos PPARs no TAB trouxe muitos benefícios. No TAM, resultados surpreendentes foram que a telmisartana provocou o aumento da expressão do recepetor adrenérgico beta 3 (RAβ3), induzido pela ativação de PPARbeta/delta e maior termogênese comaumento da expressão da proteína desacopladora1 (UCP1). Em conclusão, nossos resultados mostram que telmisartanaaumenta a expressão gênica e proteica PAN-PPAR no TAB e TAM em camundongos obesos induzidos por dieta. Nossas observações mostram que, apesar do grupo HF-T ter reduzido a ingestão energética, os efeitossão explicados pela ativação PAN-PPAR da telmisartana, causando a ativação da termogênese e resultando num balanço energético negativo.
Peroxisome proliferator-activated receptor (PPARs) are transcription factors involved in fatty acids oxidation and cell proliferation, mediating different pathways, representing a hopeful strategy to deal with the characteristics of metabolic syndrome. There are three isoforms of PPARs (PPAR alpha, beta / delta and gamma) that are differentially expressed in different tissues. The present study, aimed to evaluate pleiotropic effects of telmisartan, an anti-hypertensive, angiotensin receptor blocker AT1 and PPAR gamma agonist in white adipose tissue (WAT) and brown adipose tissue (BAT) in diet-induced obese mice. Male C57BL/6 mice fed a standard diet (standard-chow, 10% of energy from lipids) or a high fat diet (high fat, 49% of energy from lipids) for 10 weeks. Afterwards, groups were subdivided into: SC, SC-T, HF and HF-T (n=10, each). Treatment with telmisartan (10 mg/Kg BM, in the diet) was maintained for 4 weeks. The HF group showed overweight, hypertension, adipokine pro-inflammatory profile, insulin resistance, decreased in energy expenditure, flawed in glucose metabolism and abnormal distribution of adipose mass. Furthermore, obesity caused reduced expression of PPARalpha, beta/delta and gamma in WAT and BAT, resulting in unproductive glucose uptake and insufficient thermogenesis. On the other hand the activation of the three isoforms of PPARs, the improvement of the inflammatory profile, increased insulin sensitivity and improved glucose uptake was observed after treatment with telmisartan. The activation of PPARs in BAT provided many benefits. In BAT, surprising new findings show that telmisartan caused sympathetic activation with beta-3 adrenergic receptor (RAβ3), induced activation PPARbeta /delta and increased thermogenesis with increased expression of uncoupling protein 1 (UCP1), that it is a target gene of PPARalpha. In conclusion, our results show for the first time telmisartan increases the gene and protein expression PAN-PPAR in WAT and BAT in diet-induced obese mice. Our observations demonstrate that, although the HF-T group have reduced energy intake, the effects are explained by the PPAR-PAN activation of telmisartan, causing the activation of thermogenesis through maintaining sympathetic stimulation and increased expression of UCP1, resulting in a negative energy balance.
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Eley, Judy. "The control of brown adipose tissue function in mice with goldthioglucose-induced obesity." Thesis, University of Ottawa (Canada), 1988. http://hdl.handle.net/10393/5472.

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Sigurdson, S. Lynn. "Control of brown adipose tissue growth and function in normal and myopathic hamsters." Thesis, University of Ottawa (Canada), 1989. http://hdl.handle.net/10393/5567.

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30

Liu, Yang. "Neural Crosstalk Between Sympathetic Nervous System and Sensory Circuits to Brown Adipose Tissue." Digital Archive @ GSU, 2013. http://digitalarchive.gsu.edu/biology_theses/44.

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Brown adipose tissue (BAT) is a critical organ for non-shivering thermogenesis, which is under control of both sympathetic and sensory neural innervation. We utilized both a retrograde sympathetic nerve tract tracer pseudorabies virus and an anterograde sensory tract tracer the H129 strain of herpes simplex virus-1 to locate individual neurons across the neuroaxis that are part of the SNS outflow from brain to interscapular BAT and are part of the sensory input to the brain. We found specific neuronal phenotype of the double-infected neurons distributed from the hindbrain to the forebrain with highest densities in several discrete brain regions: the paraventricular hypothalamus (PVH), lateral hypothalamus (LHA), parabrachial nucleus (PB) and raphe pallidus (RPa). The neuroanatomical reality of the SNS-sensory feedback loops suggests coordinated control of BAT thermogenesis at several sites and indicates plasticity of SNS-sensory crosstalk.
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31

Milner, Rachel Elizabeth. "Studies on the 'activity' of the uncoupling protein in brown adipose tissue mitochondria." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279751.

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32

EFREMOVA, AGRAFENA. "Direct and indirect evidence of brown adipose tissue in adult patients from Yakutia." Doctoral thesis, Università Politecnica delle Marche, 2019. http://hdl.handle.net/11566/263608.

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La scoperta del tessuto adiposo bruno nell’uomo ha destato un grande interesse in quanto la sua induzione potrebbe rappresentare una possibilità per la cura contro l’obesità e i rischi ad essa correlati. L’esposizione al freddo è uno degli stimoli principali che determina la trasformazione degli adipociti bianchi in bruni (fenomeno del browning). Sulla base di studi promettenti svolti sui topi, abbiamo analizzato, anche nell’uomo, la capacità delle cellule mononucleate del sangue periferico di esprimere biomarkers del browning. Infatti, poiché le tecniche di studio del tessuto adiposo bruno sono tutte invasive, l’individuazione nel sangue di opportuni biomarkers sarebbe molto interessante. Abbiamo quindi effettuato studi sul sangue di pazienti Siberiani, abituati a vivere in un clima freddo; da questi studi è emerso che le cellule del sangue esprimono alcuni geni tipici del browning, come Cidea, Hoxc9, Prdm16, Cpt1a e Slc27a1. Questo è un dato molto interessante perché per la prima volta vengono evidenziati questi markers nell’uomo. Tra questi, il dato più significativo è la maggiore espressione del gene Cidea nel gruppo dei pazienti esposti a freddo rispetto al gruppo di controllo. Abbiamo inoltre effettuato studi di immunoistochimica su biopsie autoptiche di tessuto adiposo perirenale e periaortico di pazienti Siberiani, per indagare la presenza di UCP1 (proteina caratteristica degli adipociti bruni) e TH (marker di fibre nordrenergiche). La maggior parte dei depositi studiati contenevano isole brune; inoltre, dividendo i pazienti in due gruppi, uno comprendente i lavoratori in ambienti chiusi ed uno comprendente i lavoratori all’esterno, si è visto che in quest’ultimo gruppo la quantità di tessuto bruno è maggiore e quindi è più alta la positività all’UCP1. C’è anche una correlazione positiva tra il numero di adipociti multiloculari e il numero delle fibre TH-positive. La possibilità di utilizzare un deposito come il sangue, prelevabile così facilmente e in modo non invasivo, per studiare il browning, suggerisce nuove possibilità di approfondire il ruolo del tessuto adiposo bruno nell’omeostasi energetica dell’organismo. Inoltre i nostri studi dimostrano per la prima volta la presenza di una considerevole quantità di tessuto bruno in individui adulti.
After the re-discovery of brown adipose tissue (BAT) in humans, there is increasing interest in the study of induction of this thermogenic tissue as a basis to combat obesity and related complications. Cold exposure is one of the strongest stimuli able to activate BAT and to induce the appearance of brown-like adipocytes in white fat depots (browning process). We analyzed the potential of peripheral blood mononuclear cells (PBMCs) to reflect BAT activity based on previous studies that gave promising results in mice. BAT studies in humans require invasive techniques such as biopsies of adipose tissue or the use of techniques such as positron emission tomography, which implies the use of radioactive isotopes. Thus, it would be of interest to have a readily available source of biomarkers in PBMCs as observed in experimental procedures with mice. Our studies on peripheral blood of Siberian people, have shown that gene expression in PBMCs reflects certain features of brown adipose tissue response to cold exposure. PBMCs are able to express brown markers such as Cidea, Hoxc9, Prdm16, Cpt1a and Slc27a1. To our knowledge, there are no previous reports on the study of browning effects of cold exposure on PBMC gene expression in humans. The most relevant data was the significant increase of Cidea mRNA expression observed in cold-exposed Siberian group. We also performed UCP1 and TH immunohistochemistry on autoptic biopsies from periaortic and perirenal adipose depots of Siberian patients. Our results showed that most of the depots observed, clearly showed UCP1-positive islands both in outdoor and in indoor working patients. Comparing the two groups, we observed that outdoor workers had more BAT and more intensely stained for the functional protein UCP1 than indoor workers. Moreover, there is a positive correlation between the presence of multilocular adipocytes and the density of positive TH fibers. The possibility of using an easily obtainable biological material, such as PBMCs, to perform BAT studies, opens new and interesting possibilities to analyze the relevance of this tissue on energy homeostasis and body weight control in humans, by using non-invasive approaches. Furthermore, our data show for the first time the presence of relevant amount of BAT in adult humans living in Siberia with a positive correlation between multilocular adipocytes and noradrenergic parenchymal nerve fibers.
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33

Tran, Khanh-Van T. "Origin of White and Brown Adipose Cells From Vascular Endothelium: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/591.

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Obesity is associated with insulin resistance, dyslipidemia, and cardiovascular disease. The current obesity epidemic is the result of surplus energy consumption. Excess energy is stored in expanding adipose tissue. Adipose tissue growth entails the enlargement of existing adipocytes, the formation of new fat cells from preexisting progenitors, and the coordinated development of supporting vasculature. Identifying adipocyte progenitors and the mechanism of adipose tissue expansion is crucial for the development of new strategies to combat obesity and its complications. Though important progress has been made towards understanding the developmental origin of adipocytes, the identities of adipocyte progenitors are still not completely known. The main objective of this study is to determine whether endothelial cells of the adipose tissue can give rise to new adipocytes. Our results indicate that murine endothelial cells of adipose tissue are pluripotent and can potentially give rise to preadipocytes. Lineage tracing experiments using the VE-Cadherin-Cre transgenic mouse reveal localization of reporter genes in endothelial cells, preadipocytes and white and brown adipocytes. Moreover, capillary sprouts from human adipose tissue, which have predominantly endothelial cell characteristics, are found to express Zfp423, a preadipocyte determination factor. In response to PPARγ activation, endothelial characteristics of sprouting cells are progressively lost, and cells form structurally and biochemically defined adipocytes. Taken together, our data support an endothelial origin of a population of adipocytes. The ability of the vascular endothelium to give rise to adipocytes may explain how angiogenesis and adipogenesis can be temporally and spatially coordinated. Analysis of BAT and WAT revealed that adipose depots have distinct compositions of adipocyte progenitors. Of the CD45-CD29+Sca1+CD24+ progenitor population, only 17% and 52% express VE-Cadherin in WAT and BAT, respectively. Our data show that the number of these specific progenitors in BAT and WAT are highly variable and suggest that a considerable number of adipocytes progenitors may have a non-endothelial cell origin. Differences in composition and types of adipocyte progenitors may explain the differences in the adipocytes phenotypes that we observe in discrete depots. In brief, we find that the vascular endothelium gives rise to a population of brown and white fat cells, and that the number of endothelial-derived adipocyte progenitors residing in BAT and WAT is highly variable. These results expand our current understanding of adipose tissue growth, and, we hope, will accelerate the development of treatments for obesity-related complications.
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34

Leung, Tsz-mei, and 梁紫微. "Prevalence and factors associated with brown adipose tissue detected by 18F-FDG PET/CT in Hong Kong Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617539.

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Brown adipose tissue (BAT) is a unique organ in existence in mammals. It can induce non-shivering thermogenesis to control body temperature and energy balance through the expression of uncoupling protein 1 (UCP1). In our study, we aimed to evaluate the prevalence of BAT, as detected by fluorine 18-fluorodeoxyglucose (18F-FDG) positron emission tomography combined computer tomography (PET/CT), in a Hong Kong Chinese population. We also assessed the influence of age and sex to BAT in Hong Kong Chinese population. We also determined the factors associated with it, in particular, its relationship with overweight and other metabolic disorders such as diabetes mellitus. We analyzed 1765 consecutive 18F-FDG PET-CT scans of 1442 Chinese for the presence of BAT. Comparison of the variables between positive and negative BAT scans was performed using Student’s t-test. The association between maximum value of standardized uptake value (SUVmax) and variables were explored by Spearman correlation. The predictors of observed BAT were analyzed by multiple logistic regression to determine the significant predictors of positive BAT. The relationship between the monthly numbers of subjects with BAT and the respective mean monthly outdoor temperature was evaluated by Pearson’s correlation co-efficient. P < 0.05 was considered to be statistically significant. Brown adipose tissue was detected in 66 out of 1442 subjects (4.6%). BAT was significantly more commonly found in younger (43.7±13.5 years old vs. 61.4±14.2 years old, P<0.001) and female (59% vs. 46%, P<0.05) subjects. BAT also existed more frequently in subjects with lower body mass index (BMI) (21.2±3.1 kg/m2 vs. 22.4±3.7 kg/m2, P<0.01) and lower blood glucose level (5.9±0.9 mmol/L vs. 6.4±1.6 mmol/L, P<0.01). Also, BAT was detected only in subjects with no history of diabetes meallitus (DM) (0 vs. 10%, P<0.01). Moreover, lower outdoor temperature (21.6±4.6。C vs. 23.4±4.7。C, P<0.005) resulted in higher prevalence of detected BAT. In the multiple logistic regression test, age and mean monthly temperatures were the significant independent predictors of the presence of BAT (P< 0.001 and P=0.001). Age was also significantly correlated to SUVmax (P< 0.001). The monthly prevalence of positive BAT correlated negatively with mean monthly temperature by Pearson’s correlation (r = -0.79; P<0.01). To summarize, BAT was more commonly found in young, female subjects with lower BMI and blood glucose levels, and non-diabetes subjects. Age was the most important factor associated with the prevalence of BAT in humans. Lower outdoor temperature in winter can increase the prevalence of BAT even in Hong Kong’s sub-tropical climates. Also, there was an association of BAT with normal BMI (<=23) and lower blood sugar levels supporting the notion that BAT may potentially be a therapeutic target for obesity and diabetes.
published_or_final_version
Diagnostic Radiology
Master
Master of Philosophy
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35

Mössenböck, Karin [Verfasser], and Stephan [Akademischer Betreuer] Herzig. "A Story in Brown and White Regulation of Metabolic Homeostasis by Brown Adipose tissue / Karin Mössenböck ; Betreuer: Stephan Herzig." Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180735242/34.

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36

Kates, Anna-Lisa. "Thyroid hormone metabolism in brown adipose tissue of lean and genetically obese (OBOB) mice." Thesis, University of Ottawa (Canada), 1989. http://hdl.handle.net/10393/21547.

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37

Zhou, Hongyi, Stephen M. Black, Tyler W. Benson, Neal L. Weintraub, and Weiqin Chen. "Berardinelli-Seip Congenital Lipodystrophy 2/Seipin Is Not Required for Brown Adipogenesis but Regulates Brown Adipose Tissue Development and Function." AMER SOC MICROBIOLOGY, 2016. http://hdl.handle.net/10150/621431.

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Brown adipose tissue (BAT) plays a unique role in regulating whole-body energy homeostasis by dissipating energy through thermogenic uncoupling. Berardinelli-Seip congenital lipodystrophy (BSCL) type 2 (BSCL2; also known as seipin) is a lipodystrophy-associated endoplasmic reticulum membrane protein essential for white adipocyte differentiation. Whether BSCL2 directly participates in brown adipocyte differentiation, development, and function, however, is unknown. We show that BSCL2 expression is increased during brown adipocyte differentiation. Its deletion does not impair the classic brown adipogenic program but rather induces premature activation of differentiating brown adipocytes through cyclic AMP (cAMP)/protein kinase A (PKA)-mediated lipolysis and fatty acid and glucose oxidation, as well as uncoupling. cAMP/PKA signaling is physiologically activated during neonatal BAT development in wild-type mice and greatly potentiated in mice with genetic deletion of Bscl2 in brown progenitor cells, leading to reduced BAT mass and lipid content during neonatal brown fat formation. However, prolonged overactivation of cAMP/PKA signaling during BAT development ultimately causes apoptosis of brown adipocytes through inflammation, resulting in BAT atrophy and increased overall adiposity in adult mice. These findings reveal a key cell-autonomous role for BSCL2 in controlling BAT mass/activity and provide novel insights into therapeutic strategies targeting cAMP/PKA signaling to regulate brown adipocyte function, viability, and metabolic homeostasis.
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38

Sabaté, Pérez Alba. "Regulation of brown adipose tissue metabolism by TP53INP2 = Regulació del metabolisme del teixit adipós marró per mitja de TP53INP2." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668259.

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Overweight and obesity have increased dramatically during recent decades becoming a major health problem for which therapeutic options are limited. Thus, there is an urgent need to develop new safe pharmacological therapies. Obesity results from the positive imbalance resulting from the increase of energy intake and/or decrease in energy expenditure, the latter consequence of impaired processes involved in basal metabolism, adaptive thermogenesis or associated with sedentary behaviour. The excess of energy is preferentially stored in white adipose tissue (WAT) within unilocular adipocytes. Another type of adipose tissue, the brown adipose tissue (BAT), is in charge of utilizing nutrients to produce heat in an attempt to maintain body temperature through non-shivering adaptive thermogenesis. Brown adipocytes are multilocular with many lipid droplets and mitochondria that express uncoupling protein-1 (UCP1), the final effector of heat dissipation. Upon adrenergic stimulation induced either by cold or by diet, the rise in intracellular cyclic AMP levels (cAMP) results in UCP1 activation increasing lipid oxidation uncoupled from ATP production. Functional BAT depots have recently been detected in lean adult humans that can be activated by cold exposure. Of relevance, human BAT activity correlates with lower body mass index and improved glycemia, indicating that strategies that could increase BAT mass and/or its activation could become promising targets to combat obesity and its metabolic complications. Tumour protein p53-inducible nuclear protein 2 (TP53INP2) promotes autophagy and stimulates a variety of nuclear hormone receptors, such as ecdysone receptors in flies, and thyroid hormone receptors, glucocorticoid receptors and PPAR receptors in mammalian cells. TP53INP2 is also a negative regulator of white adipogenesis through activation of TCF transcription factors. The transcription factor PPARγ plays a key role in the regulation of BAT thermogenesis, as well as in brown adipogenesis. However, the factors that modulate PPARγ activity in brown adipocytes are largely unknown. Here we document that the bifunctional protein TP53INP2 is a major regulator of BAT function and that its action is mediated by the regulation of PPARγ activity. TP53INP2 was upregulated under conditions of stimulated BAT thermogenesis, such as under low temperature or a high-fat diet. TP53INP2 deficiency reduced brown adipogenesis in cultured cells, and in vivo TP53INP2 ablation in Myf5+ precursor cells caused the dysregulation of BAT gene expression and enhanced lipid droplet accumulation in brown adipocytes. As a result, TP53INP2 depletion decreased BAT-specific thermogenic capacity, leading to positive energy balance and obesity. Furthermore, TP53INP2 loss-of-function in adult mice revealed that the protein is required for the maintenance of the differentiation state of brown adipocytes. Microarray gene expression profiling showed that the lack of TP53INP2 in BAT is linked to a reduced PPAR signalling pathway. In keeping with this, PPARγ activity was markedly decreased in TP53INP2 knockout brown preadipocytes. Under conditions of TP53INP2 deficiency, PPARγ proteasomal degradation was also impaired and this transcription factor showed a lower ubiquitination. Moreover, chronic exposure to the ligand rosiglitazone rescued brown adipogenesis. In all, we have identified a novel regulator of PPARγ activity and BAT metabolism. The expression of this regulator in BAT is induced under conditions of active thermogenesis, and its repression leads to energy imbalance, reduced thermogenesis and obesity.
TP53INP2 és una proteïna que promou autofàgia i estimula l’activitat de diferents receptors nuclears d’hormones, com ara el receptor d’ecdisona, el receptor d’hormona tiroïdal i els receptors de PPAR. També s’ha descrit que TP53INP2 és un regulador negatiu de l’adipogènesi del teixit adipós blanc per mitjà de ‘activació dels factors de transcripció TCF. Aquesta tesi doctoral s’ha centrat en l’estudi de la regulació de TP53INP2 en el teixit adipós marró i en la caracterització de la funció de TP53INP2 en el metabolisme d’aquest teixit. L’expressió de TP53INP2 en teixit adipós marró es veu augmentada en condicions de termogènesi activa, com ho són l’exposició a baixes temperatures o una alimentació rica en greixos. Per el contrari, la inhibició fisiològica de la termogènesi per exposició a un ambient termoneutral està acompanyada de la reducció de l’expressió de TP53INP2. Aquests resultats van suggerir que TP53INP2 podia ser necessari per a la regulació termogènica del teixit adipós marró. La pèrdua de funció de TP53INP2 en preadipòcits marrons va resultar en una disminució en la seva capacitat adipogènica. De la mateixa manera, l’ablació genètica de TP53INP2 en teixit adipós marró va donar lloc a una desregulació de l’expressió de gens adipogènics i termogènics, i a una reducció de la capacitat termogènica, la qual cosa va conduir a un balanç energètic positiu i obesitat. Estudis més detallats van mostrar que TP53INP2 és un regulador positiu de l’activitat PPARγ en el context de la cèl·lula adiposa marró, per mitjà de la modulació de la seva ubiqüitinació i conseqüent activitat. En resum, els resultats obtinguts en aquesta tesi doctoral demostren que TP53INP2 indueix l’adipogènesi i la termogènesi del teixit adipós marró per mitjà de l’activació de la via de senyalització de PPARγ D’aquesta manera, TP53INP2 indueix la despesa energètica i prevé el desenvolupament d’obesitat.
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39

Whittle, Andrew John. "A role for bone morphogenetic protein 8b in brown adipose tissue thermogenesis and energy homeostasis." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609416.

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40

Jones, Terence A. "Characterisation and identification of brown adipose tissue on positron-emission tomography and magnetic resonance imaging." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/71009/.

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Characterisation and identification of brown adipose tissue on positron-emission tomography and magnetic resonance imaging Since the first published description of brown adipose tissue (BAT) in 1551 its reputation has changed from that of a mere curiosity of little physiological significance in adult humans, to meriting reclassification as a metabolic organ in its own right. Obesity is a major global public health problem. Modulation of non-shivering thermogenesis through BAT manipulation presents an attractive therapeutic target for inducing weight loss. Testing the efficacy of such pharmacological agents requires the development of a reliable imaging biomarker to enable BAT quantification. In this thesis we have evaluated the effectiveness of positron-emission tomography (PET) and magnetic resonance (MR) imaging in quantifying BAT. Retrospective analysis of 3,295 consecutive PET scans performed at University Hospitals Coventry & Warwickshire NHS Trust (Coventry, UK) in 2007-2012 showed 18F-FDG uptake consistent with BAT in 5.3% of scans. Gender (female), age (younger), BMI (lower), serum glucose (lower), time of day (earlier), and temperature (lower) were all significant predictors of BAT prevalence. Regression analysis showed patients’ age and preceding day’s minimum temperature to correlate most strongly with BAT volume, while the impact of other factors is less clear. We also showed the pattern of BAT uptake within individuals to be consistent across serial PET scans. Quantitative colocalisation techniques showed this degree of colocalisation to be significant in 14/15 patients, implying fixed BAT deposits in adult humans. Concerns over the high ionising radiation dose of PET scans has stimulated research into MR as an alternative means of detecting BAT, with the potential to identify BAT irrespective of its activation state. Using IDEAL FSE sequences acquired on a 3 Tesla clinical MR scanner, we found BAT to have a significantly lower fat fraction than white adipose tissue in rats post mortem and adult humans in vivo. Our efforts to identify BAT prospectively using fat fraction yielded inconsistent results.
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41

Troike, Katie M. "White Adipose Tissue Beiging in Mice With Increased Growth Hormone Action." Ohio University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1497354961246326.

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42

Pence, Sydney W. "Novel regulation of BAT thermogenesis induced by hypothalamic Apolipoprotein AIV." Ohio University Honors Tutorial College / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1524828526830907.

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43

DiStefano, Marina T. "A Role for the Lipid Droplet Protein HIG2 in Promoting Lipid Deposition in Liver and Adipose Tissue: A Dissertation." eScholarship@UMMS, 2016. http://escholarship.umassmed.edu/gsbs_diss/830.

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Chronic exposure of humans or rodents to high calorie diets leads to hypertriglyceridemia and ectopic lipid deposition throughout the body, resulting in metabolic disease. Cellular lipids are stored in organelles termed lipid droplets (LDs) that are regulated by tissue-specific LD proteins. These proteins are critical for lipid homeostasis, as humans with LD protein mutations manifest metabolic dysfunction. Identification of novel components of the LD machinery could shed light on human disease mechanisms and suggest potential therapeutics for Type 2 Diabetes. Microarray analyses pinpointed the largely unstudied Hypoxia-Inducible Gene 2 (Hig2) as a gene that was highly expressed in obese human adipocytes. Imaging studies demonstrated that Hig2 localized to LDs in mouse hepatocytes and the human SGBS adipocyte cell line. Thus, this work examined the role of Hig2 as a LD protein in liver and adipose tissue. Hig2 deficiency reduced triglyceride deposition in hepatocytes; conversely, ectopic Hig2 expression promoted lipid deposition. Furthermore, liver-specific Hig2-deficient mice displayed improved glucose tolerance and reduced liver triglyceride content. Hig2 deficiency increased lipolysis and -oxidation, accounting for the reduced triglyceride accumulation. Similarly, adipocyte-specific Hig2-deficient mice displayed improved glucose tolerance, reduced adipose tissue weight and brown adipose tissue that was largely cleared of lipids. These improvements were abrogated when the animals were placed in thermoneutral housing and brown adipocyte-specific Hig2-deficient mice also displayed improved glucose tolerance, suggesting that active brown fat largely mediates the metabolic phenotype of Hig2 deletion. Thus, this work demonstrates that Hig2 localizes to LDs in liver and adipose tissue and promotes glucose intolerance.
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44

Wikström, Jakob D. "Mitochondrial form and function in pancreatic β-cells and brown adipocytes." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-39336.

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This thesis is focused on the role of mitochondria in pancreatic β-cells and brown adipose tissue (BAT). Two main aspects of mitochondria were explored; mitochondrial functional efficiency and the interrelationship between mitochondrial shape and function. Mitochondria in β-cells were found to exhibit heterogeneity in mitochondrial membrane potential. This functional diversity decreased when cells were challenged with glucose stimuli, suggesting that at higher fuel levels low-activity mitochondria are recruited into a pool of high-activity mitochondria. Glucolipotoxic conditions increased the functional diversity suggesting that this may be of importance for diabetes pathophysiology. To examine mitochondrial efficiency in intact islets a high throughput islet respirometry method was developed. Due to increased uncoupling, islets from a diabetic animal model exhibit lower respiratory efficiency. Glucose, free fatty acids and amino acids all decreased respiratory efficiency. A large portion of the respiratory efficiency was mediated by reactive oxygen species and the adenine nucleotide translocase. In β-cells mitochondria were found to undergo cycles of fusion and fission. During glucolipotoxicity mitochondria fragmented and lost their fusion ability. Knock down of the fission protein Fis1 rescued the β-cells from glucolipotoxic induced cell death. BAT mitochondria also showed fusion and fission. The mitochondrial dynamics proteins Mfn2 and Drp1 were shown to strongly affect BAT mitochondrial morphology. In response to a combination of adrenergic and free fatty acid stimuli mitochondria drastically changed from long filamentous structures to fragmented spheres. Inhibiting fission by the negative form of Drp1 decreased BAT response to adrenergic stimuli by half. In conclusion, mitochondrial efficiency may be of importance for normal as well as compromised β-cell and islet function. Mitochondrial morphology appears critical for mitochondrial function in β-cells and BAT.
At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.
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45

Ntinas, Petros. "Function and activation of human adipose tissue : the role of genes in the link between physical activity and brown adipose-like phenotype." Thesis, University of Wolverhampton, 2017. http://hdl.handle.net/2436/620509.

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Background: Excess white adipose tissue (WAT) in humans is considered as a harmful health index. However, increased brown adipose tissue (BAT) and brown-like adipose tissue activity are associated with increased resting energy expenditure (REE) that may help to control body weight. Exercise may enhance browning formation of WAT and reduce WAT that may lead to health improvements. Aims: a) to examine the effects of physical activity on the link between peroxisome proliferator-activated receptor gamma co-activator 1-alpha (PGC-1α) and fibronectin type III domaincontaining protein 5 (FNDC5) genes in muscle, circulating Irisin and uncoupling protein one (UCP1) of WAT in humans (study 1); b) to examine the relationship between UCP1 mRNA and protein expression as well as PGC-1α, peroxisome proliferatoractivated receptor alpha (PPARα) and PPARγ genes with physical activity levels in WAT of healthy men (study 2); c) to examine the effects of different types of exercise and de-training on the UCP1 mRNA and protein expression (study 3), and d) on leptin mRNA in WAT of healthy men (study 4). Method: Study 1: A systematic review was conducted using the Preferred Reporting Items for Systematic Reviews and Meta- Analyses. Studies 2-4: The total of 46 healthy men subjected to measurements for physical activity levels, diet, anthropometry, body composition, REE, peak oxygen consumption, 1-repetition maximum and provided subcutaneous fat biopsies to determine mRNA and protein expression of six genes in one cross-sectional study and one randomized controlled trial. Results: Study 1: No link was found between PGC- 1α and FNDC5, circulating Irisin and UCP1 of WAT in response to physical activity. Study 2: The mRNA of, UCP1, PGC-1α, PPARα and PPARγ genes of WAT were not associated with physical activity levels. The UCP1 protein expression however, was negatively associated with physical activity levels. Studies 3-4: Different types of chronic exercise and de-training do not affect UCP1 mRNA and protein expression 3 and leptin mRNA in WAT. However, effect size analyses demonstrated increased UCP1 mRNA and protein expression, PPARγ and leptin in response to chronic exercise. Conclusions: There is no evidence to support the link between PGC-1α and FNDC5 in human muscle or the link between FNDC5 and circulating Irisin and UCP1 in WAT in response to exercise. There are no effects of exercise and de-training on browning formation of WAT and no link between browning formation indices and REE, body weight as well as leptin mRNA in healthy men. Further research is required to elaborate the aforementioned phenomena.
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46

Kim, Dongho, and n/a. "Regulation of mouse UCP2 and UCP3 gene expression." University of Otago. Department of Biochemistry, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070424.131549.

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Uncoupling protein, UCP, present in the inner mitochondrial membrane of brown adipose tissue (BAT) contributes to adaptive thermogenesis. UCP functions as a proton pore and can dissipate the proton electrochemical gradient established by the respiratory chain during fuel oxidation, and thus generates heat without producing ATP. However, the brown adipose tissue thermogenesis is not likely to be a major mechanism in controlling energy expenditure for humans because adults have only residual amounts of the tissue. Two new members of the UCP family have been identified based on their high sequence homology to UCP in BAT and named UCP2 and UCP3. The original UCP was renamed UCP1. At the amino acid level, human UCP2 and UCP3 are 59% and 57% identical to UCP1, respectively. In contrast to UCP1, UCP2 is expressed in many tissues such as brown adipose tissue, white adipose tissue, muscle, spleen and macrophages. UCP3 is expressed preferentially in skeletal muscle in humans, and brown adipose tissue and skeletal muscle in rodents. Since their identification many functional studies, including transgenic animals and ectopic expression of UCP2 or UCP3 in yeast, showed uncoupling activity of UCP2 and UCP3. A number of studies have been done that show increased expression of UCP2 and UCP3 by fasting, high-fat diets and suckling of newborn mice. A common characteristic of these circumstances is an associated increase in plasma free fatty acid levels. This study aimed to investigate effects of fatty acids, peroxisome proliferator-activated receptors (PPARs) and other transcription factors on UCP2 and UCP3 gene expression and to explore the molecular mechanism of their regulation through analysis of the promoter of the UCP2 and UCP3 genes. The 3.1 kb and 3.2 kb 5�-flanking regions of the mouse UCP2 and UCP3 genes, respectively, were cloned and used to construct promoter reporter gene (firefly luciferase) plasmids. The cloned region of the UCP2 and UCP3 genes contained putative binding motifs for several transcription factors, including PPAR, myogenin, and MyoD. Luciferase assays of both constructs showed basal promoter activity with 20~190-fold induction for the UCP2 promoter and 1.3~23-fold induction for the UCP3 promoter in several transfected cell lines, including 3T3-L1, C2C12, L6, COS7 and HepG2. Oleic acid (0.3 mM) up-regulated endogenous UCP2 mRNA by 2.3-fold in 3T3-L1 preadipocytes but not in C2C12 myotubes, and UCP3 mRNA by 2.5-fold in C2C12 myotubes. Responsiveness of the cloned promoter to oleic acid reflected the tissue-specific responsiveness of their endogenous genes but with less fold induction, 1.4-fold for UCP2 promoter in 3T3-L1 preadipocytes and 1.5-fold for UCP3 promoter in C2C12 myotubes. Forced expression of PPAR isotypes (PPARα, PPAR[delta] and PPARγ) showed tissue and isotype-specific activation of the UCP2 promoter. UCP2 promoter activity was induced by 2-fold by PPARγ in 3T3-L1 and by 2.8-fold by PPAR[delta] in C2C12. Treatment of oleic acid (0.3 mM) brought about further induction of the UCP2 promoter activity only in 3T3-L1. In contrast, all three isotypes induced activation of the UCP3 promoter in 3T3-L1, C2C12 and HepG2 cells. Treatment with oleic acid (0.3 mM) or isotype-specific agonist (10 [mu]M) resulted in further increased activity of the UCP3 promoter in 3T3-L1 and HepG2 cells. In particular, rosiglitazone (10 [mu]M) induced a 41-fold increase in UCP3 promoter activity in PPARγ transfected HepG2 cells, and this induction returned to basal level by treatment with bisphenol A diglycidyl ether (BADGE) (50 [mu]M), an antagonist for PPARγ. In addition, UCP3 promoter activity increased up to 20-fold 4 days after induction of C2C12 myoblasts differentiation, whereas UCP2 promoter activity increased only up to 2-fold. Forced expression of myogenin and MyoD in C2C12 myoblasts to mimic differentiation, induced UCP3 promoter activity in an additive manner, consistent with UCP3 being regulated by muscle differentiation. In the present study, it has been shown that UCP2 and UCP3 genes are regulated differently by fatty acids. The tissue-type dependence in regulation of endogenous UCP2 and UCP3 paralleled the cell type-specific effect of oleic acid on the promoter-reporter constructs, suggesting that fatty acid effects are at the transcriptional level. UCP2 and UCP3 promoters showed differences in their response to PPARs. Mediation of the fatty acid effect through PPARs has been also demonstrated, but direct binding of PPARs and particular regulatory motifs on the cloned promoter region have not yet been investigated.
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47

Leslie, P. J. "Aspects of energy expenditure in diabetic and non-diabetic man : the role of brown adipose tissue." Thesis, University of Edinburgh, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.653823.

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INTRODUCTION: Abnormalities of energy expenditure (EE) in obesity and type II diabetes mellitus have been described in animal models and adult man and it has been suggested that these abnormalities predispose to weight gain. In rodents there is evidence for a requirement for insulin in regulatory thermogenesis mediated via brown adipose tissue (BAT). The hypotheses that, firstly, insulin has a role in the control of EE and, secondly, that this is mediated by BAT in adult man were tested in the present studies. METHODS: Three components of daily EE resting metabolic rate (RMR), and the thermic responses to a mixed liquid meal (32.6 KJ/kg) and to an infusion of noradrenaline (NA), 0.1 μg/kg/min, were measured using indirect calorimetry in type I and type II diabetic subjects. The components of EE were measured in 9 lean type I diabetics initially while poorly controlled on conventional therapy (CT), HbA_1 12.1±0.7%; (mean±SEM), and then when optimally controlled on continuous subcutaneous insulin infusion (CSII) (HbA_1 7.5±0.2%). The response to fat supplementation for one week (5.23 MJ/day) was assessed and the results compared to 8 non-diabetic control subjects. These parameters were also measured in 8 type II diabetics controlled on diet and oral hypoglycaemic agents (HbA1 8.6±0.7%) in order to ascertain whether the alterations in body weight during metformin therapy (weight loss) or sulphonylurea therapy (weight gain) were reflected in alterations of EE. An estimation of the thermogenic potential of BAT in adult man was attempted by histological (light and electron microscopy) and biochemical (GDP binding, cytochrome c oxidase activity and respiration of isolated mitochondria and adipocytes) studies on perirenal BAT obtained at post mortem and during surgery. RESULTS: Poorly controlled type I diabetic subjects had a significantly (p< .01)) raised RMR (4.92±0.27 KJ/min) which returned to predicted value (4.6±0.34 KJ/min) on attainment of optimal glycaemic control. This decrease in RMR may partly explain the mean gain in weight (3.5 kg) observed during CSII. The thermic response to infused NA was decreased by over 50% during CT (27.1±3.4 KJ controls vs. 11.1±3.7 KJ diabetic CT; p< 01) and did not significantly improve during CSII (13.4±3.7 KJ). A blunted thermic response to a meal was observed during fat supplementation with CT (44.8±14.0 KJ) but CSII corrected this (71±9.9 KJ). Hence insulin has a role in the control of EE but precise replacement does not correct all these abnormalities in Type I diabetes mellitus. 2. Type II diabetic subjects had a normal RMR and thermic responses and these were similar whether on metformin or sulphonylurea therapy. This suggests that alterations in EE do not account for the changes in weight during treatment with these agents. 3. Histological and biochemical studies demonstrated the presence of functional BAT in adult man with activity equivalent to the partially cold-adapted guinea pig suggesting some potential for thermogenesis in adult man. However, it was calculated that this tissue can account for only 0.2% of the rise in oxygen consumption during NA infusion and suggests that this tissue has little energetic significance in adult man. CONCLUSIONS: These data suggest that although type I diabetes mellitus may be associated with abnormalities of EE these are unlikely to be mediated through BAT metabolism in man.
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48

Allars, J. M. "Regulation of diet induced brown adipose tissue thermogenesis in the genetically obese (fa/fa) Zucker rat." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377433.

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49

Ölkrug, Rebecca [Verfasser], and Gerhard [Akademischer Betreuer] Heldmaier. "New perspectives on the significance of brown adipose tissue in mammals / Rebecca Ölkrug. Betreuer: Gerhard Heldmaier." Marburg : Philipps-Universität Marburg, 2013. http://d-nb.info/1036727661/34.

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50

Sherman, Shermel B. "Tibia Morphology & Bone Marrow Adipose Tissue Phenotype is Controlled by Sex Steroids in C57BL/6 Mice." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1461972446.

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