Dissertations / Theses on the topic 'Brown adipose tissue'
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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.
Full textDeiuliis, 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.
Full textHansen, 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.
Full textAt the time of doctoral defence the following papers were unpublished and had a status as follows: Paper 1: Manuscript; Paper 3: Manuscript; Paper 4: Manuscript; Paper 5: Manuscript
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.
Full textAt the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 1: Manuscript.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.
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.
Full textRobb, Louise. "The effect of exercise on rat brown adipose tissue." Thesis, University of Ottawa (Canada), 1989. http://hdl.handle.net/10393/5739.
Full textGibbins, 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.
Full textShaikh, Muhammad Iqbal. "Alpha-2 adrenoreceptors in brown adipose tissue of infant rats." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/27195.
Full textGraduate and Postdoctoral Studies
Graduate
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.
Full textHarper, Mary Ellen. "Ion transport and brown adipose tissue activity in energy balance." Thesis, University of Ottawa (Canada), 1991. http://hdl.handle.net/10393/7486.
Full textOguri, Yasuo. "Tetrahydrobiopterin activates brown adipose tissue and regulates systemic energy metabolism." Kyoto University, 2018. http://hdl.handle.net/2433/232086.
Full textvon, 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.
Full textAt 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.
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.
Full textTitle from first page of PDF file (viewed July 9, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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.
Full textMelnyk, 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.
Full textMercer, 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.
Full textReddy, Narendra Lakshmana. "Novel insights in imaging and function of human brown adipose tissue." Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/69397/.
Full textOjha, Shalini. "Pericardial fat is a nutritionally regulated depot of brown adipose tissue." Thesis, University of Nottingham, 2015. http://eprints.nottingham.ac.uk/30678/.
Full textSarapio, 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.
Full textThe 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.
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.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-25T23:51:50Z (GMT). No. of bitstreams: 1 Leite_JulianaPaula_M.pdf: 4915396 bytes, checksum: 09ea43792fb47457eab9ac0df46c3416 (MD5) Previous issue date: 2014
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
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.
Full textObesity 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.
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.
Full textChen, 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.
Full textPeachey, 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.
Full textKUO, 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.
Full textNnodim, 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.
Full textCarvalho, 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.
Full textPeroxisome 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.
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.
Full textSigurdson, 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.
Full textLiu, 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.
Full textMilner, 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.
Full textEFREMOVA, 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.
Full textAfter 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.
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.
Full textLeung, 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.
Full textpublished_or_final_version
Diagnostic Radiology
Master
Master of Philosophy
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.
Full textKates, 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.
Full textZhou, 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.
Full textSabaté, 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.
Full textTP53INP2 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.
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.
Full textJones, 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/.
Full textTroike, 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.
Full textPence, 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.
Full textDiStefano, 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.
Full textWikström, 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.
Full textAt the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 3: Manuscript. Paper 4: Manuscript.
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.
Full textKim, 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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