Relevant bibliographies by topics / Brown adipose tissue

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Brown adipose tissue'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Brown adipose tissue"

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Radhina, Afifa. "Proses Pencokelatan Jaringan Adiposa." Indonesian Journal of Health Science 1, no. 2 (December 24, 2021): 42–46. http://dx.doi.org/10.54957/ijhs.v1i2.104.

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Obesity is a common, serious, and detrimental condition. In 2014, more than 1.9 billion adults were overweight. Obesity is associated with many diseases and the increase in obesity has become a major health problem. Obesity is caused by an imbalance between energy intake and energy consumption. Adipose tissue is an endocrine organ that secretes many hormones and cytokines that can affect metabolism. There are two types of adipose tissue in the body with different functions, namely white adipose tissue and brown adipose tissue. White fat has a major function in storing energy and is increased in obesity, while brown fat produces heat (thermogenesis) and then increases energy consumption. Therefore, brown fat and the induction of brown fat-like properties in white fat, have been considered as targets in the fight against obesity. The complex process of cell differentiation leading to the appearance of active brown adipocytes has been identified. There are classic brown adipocytes and cream adipocytes. Beige adipocytes are brown adipocytes that appear on precursor cells of white adipose tissue due to stimuli. Brown adipocytes are equipped with mitochondria containing uncoupling protein 1 (UCP1), which, when activated, controls ATP synthesis and stimulates respiratory chain activity. The browning process of adipose tissue is controlled by factors such as exercise. Obesitas merupakan keadaan yang umum, serius, dan merugikan. Tahun 2014, lebih dari 1,9 milyar orang dewasa mengalami kelebihan berat badan. Obesitas berasosiasi dengan banyak penyakit dan peningkatan obesitas telah menjadi masalah kesehatan utama. Obesitas disebabkan oleh ketidakseimbangan antara energi yang masuk dan konsumsi energi. Jaringan adiposa dalam tubuh ada dua tipe yang fungsinya berbeda, yakni jaringan adiposa putih dan jaringan adiposa cokelat. Lemak putih berfungsi utama dalam menyimpan energi dan meningkat pada obesitas, sedangkan lemak cokelat menghasilkan panas (termogenesis) dan kemudian meningkatkan konsumsi energi. Oleh karena itu, lemak cokelat dan induksi sifat seperti lemak cokelat pada lemak putih, telah dipertimbangkan sebagai target dalam melawan obesitas. Tujuan penelitian ini adalah untuk mengetahui proses pencoklatan jaringan adiposa putih. Metode penelitian yang digunakan adalah metode penelusuran ilmiah. Hasil penelitian diperoleh bahwa adiposit krem merupakan adiposit cokelat yang muncul pada sel prekursor dari jaringan adiposa putih karena adanya stimuli. Adiposit krem sama seperti adiposit cokelat dilengkapi dengan mitokondria yang mengandung uncoupling protein 1 (UCP1), yang ketika teraktivasi akan mengendalikan sintesis ATP dan menstimulasi aktivitas rantai respirasi. Beberapa regulator seperti PPAR γ, PGC-1α, dan PRDM16 muncul sebagai pelaku utama dalam proses diferensiasi adiposit krem.
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Sidossis, Labros S. "Brown adipose tissue." Current Opinion in Clinical Nutrition and Metabolic Care 15, no. 6 (November 2012): 521–22. http://dx.doi.org/10.1097/mco.0b013e328358020d.

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TYLER, DAVID. "Brown Adipose Tissue." Biochemical Society Transactions 15, no. 6 (December 1, 1987): 1198. http://dx.doi.org/10.1042/bst0151198.

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Townsend, Kristy, and Yu-Hua Tseng. "Brown adipose tissue." Adipocyte 1, no. 1 (January 2012): 13–24. http://dx.doi.org/10.4161/adip.18951.

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Tam, Charmaine S., Virgile Lecoultre, and Eric Ravussin. "Brown Adipose Tissue." Circulation 125, no. 22 (June 5, 2012): 2782–91. http://dx.doi.org/10.1161/circulationaha.111.042929.

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Blackburn, Susan. "Brown Adipose Tissue." Journal of Perinatal & Neonatal Nursing 25, no. 3 (2011): 222–23. http://dx.doi.org/10.1097/jpn.0b013e31821a6481.

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Nuutila, Pirjo. "Brown adipose tissue." Best Practice & Research Clinical Endocrinology & Metabolism 30, no. 4 (August 2016): 469. http://dx.doi.org/10.1016/j.beem.2016.09.004.

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Cinti, Saverio. "The adipose organ: morphological perspectives of adipose tissues." Proceedings of the Nutrition Society 60, no. 3 (August 2001): 319–28. http://dx.doi.org/10.1079/pns200192.

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Anatomically, an organ is defined as a series of tissues which jointly perform one or more interconnected functions. The adipose organ qualifies for this definition as it is made up of two tissue types, the white and brown adipose tissues, which collaborate in partitioning the energy contained in lipids between thermogenesis and the other metabolic functions. In rats and mice the adipose organ consists of several subcutaneous and visceral depots. Some areas of these depots are brown and correspond to brown adipose tissue, while many are white and correspond to white adipose tissue. The number of brown adipocytes found in white areas varies with age, strain of animal and environmental conditions. Brown and white adipocyte precursors are morphologically dissimilar. Together with a rich vascular supply, brown areas receive abundant noradrenergic parenchymal innervation. The gross anatomy and histology of the organ vary considerably in different physiological (cold acclimation, warm acclimation, fasting) and pathological conditions such as obesity; many important genes, such as leptin and uncoupling protein-1, are also expressed very differently in the two cell types. These basic mechanisms should be taken into account when addressing the physiopathology of obesity and its treatment.
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Mund, Ross A., and William H. Frishman. "Brown Adipose Tissue Thermogenesis." Cardiology in Review 21, no. 6 (2013): 265–69. http://dx.doi.org/10.1097/crd.0b013e31829cabff.

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Enerbäck, Sven. "Human Brown Adipose Tissue." Cell Metabolism 11, no. 4 (April 2010): 248–52. http://dx.doi.org/10.1016/j.cmet.2010.03.008.

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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.

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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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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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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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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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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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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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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.
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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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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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Books on the topic "Brown adipose tissue"

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Guertin, David A., and Christian Wolfrum, eds. Brown Adipose Tissue. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2087-8.

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Pfeifer, Alexander, Martin Klingenspor, and Stephan Herzig, eds. Brown Adipose Tissue. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-10513-6.

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Paul, Trayhurn, and Nicholls David G, eds. Brown adipose tissue. London: E. Arnold, 1986.

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Paul, Trayhurn, and Nicholls David G, eds. Brown adipose tissue. London: Edward Arnold, 1986.

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Rehnmark, Stefan. Adrenergic regulation of proliferation and differentiation in brown adipose tissue. Stockholm: [s.n.], 1991.

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The good fat revoultion: A 30-day plan that triggers brown fat---the secret to losing weight and living healthier. New York: St. Martin's Press, 2009.

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The missing piece to the weight loss puzzle. [England?]: Bedford Kennsington, 1995.

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Fat management: The thermogenic factor. Lehi, Utah: Victory Publications, 1994.

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Lee, Seoeun. Sympathetic Innervation of Brown Adipose Tissue - a Platform to Uncover Fundamental Principles of Developmental Programming. [New York, N.Y.?]: [publisher not identified], 2020.

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Lerea, Jaclyn Sadie. Early intervention in a mouse model of childhood obesity: Effects on brown adipose tissue function. [New York, N.Y.?]: [publisher not identified], 2016.

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Book chapters on the topic "Brown adipose tissue"

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Villarroya, Francesc, Aleix Gavaldà-Navarro, Marion Peyrou, Joan Villarroya, and Marta Giralt. "Brown Adipokines." In Brown Adipose Tissue, 239–56. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_119.

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Klingenspor, Martin, and Tobias Fromme. "Brown Adipose Tissue." In Adipose Tissue Biology, 39–69. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0965-6_3.

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Klingenspor, Martin, Andrea Bast, Florian Bolze, Yongguo Li, Stefanie Maurer, Sabine Schweizer, Monja Willershäuser, and Tobias Fromme. "Brown Adipose Tissue." In Adipose Tissue Biology, 91–147. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52031-5_4.

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Pavelka, Margit, and Jürgen Roth. "Brown Adipose Tissue." In Functional Ultrastructure, 292–93. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_150.

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Gupta, Amit. "Brown Adipose Tissue." In PET/MR Imaging, 227–28. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65106-4_97.

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Goody, Deborah, and Alexander Pfeifer. "BAT Exosomes: Metabolic Crosstalk with Other Organs and Biomarkers for BAT Activity." In Brown Adipose Tissue, 337–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_114.

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Yao, Xi, Barbara Salingova, and Christian Dani. "Brown-Like Adipocyte Progenitors Derived from Human iPS Cells: A New Tool for Anti-obesity Drug Discovery and Cell-Based Therapy?" In Brown Adipose Tissue, 97–105. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_115.

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Gaudry, Michael J., Kevin L. Campbell, and Martin Jastroch. "Evolution of UCP1." In Brown Adipose Tissue, 127–41. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_116.

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Reverte-Salisa, Laia, Abhishek Sanyal, and Alexander Pfeifer. "Role of cAMP and cGMP Signaling in Brown Fat." In Brown Adipose Tissue, 161–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_117.

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Lidell, Martin E. "Brown Adipose Tissue in Human Infants." In Brown Adipose Tissue, 107–23. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_118.

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Conference papers on the topic "Brown adipose tissue"

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Colebeck, E., and E. Topsakal. "Microwave dielectric properties of brown adipose tissue (BAT)." In 2013 US National Committee of URSI National Radio Science Meeting (USNC-URSI NRSM). IEEE, 2013. http://dx.doi.org/10.1109/usnc-ursi-nrsm.2013.6525127.

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Son’kin, VD, EB Akimov, RS Andreev, AV Yakushkin, and AV Kozlov. "Brown Adipose Tissue Participate in Lactate Utilization during Muscular Work." In International Congress on Sport Sciences Research and Technology Support. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0005080100970102.

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Chen, Changshen. "Investigation of Potential Inhibitors of Brown Adipose Tissue Induced Thermogenesis." In ICBBB '21: 2021 11th International Conference on Bioscience, Biochemistry and Bioinformatics. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3448340.3448349.

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Gohlke, S., C. Mancini, J. Gerdes, and T. Schulz. "Ciliary dysfunction impairs metabolic activation of brown and white adipose tissue." In Abstracts des Adipositas-Kongresses 2020 zur 36. Jahrestagung der Deutschen Adipositas Gesellschaft e.V. (DAG). © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1714481.

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Mrzilkova, Jana. "3D vasculature analysis of mouse brown adipose tissue in micro-CT." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.185.

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Tabei, Shirin, Britta Wilms, Valin Sulivani, Leonie Dräger, Katarzyna Worobiec, Svenja Meyhöfer, and Sebastian M. Meyhöfer. "Effects of subchronic activation of brown adipose tissue in humans (#67)." In Abstracts des Adipositas-Kongresses 2022 zur 38. Jahrestagung der Deutschen Adipositas Gesellschaft e.V. DAG. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1755682.

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Gifford, Aliya, Theodore F. Towse, Ronald C. Walker, Malcom J. Avison, and E. B. Welch. "Progress toward automatic classification of human brown adipose tissue using biomedical imaging." In SPIE Medical Imaging, edited by Barjor Gimi and Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2082955.

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Fuse, Sayuri, Takafumi Hamaoka, Miyuki Kuroiwa, Ryotaro Kime, Tasuki Endo, Riki Tanaka, Shiho Amagasa, and Yuko Kurosawa. "Identification of human brown/beige adipose tissue using near-infrared time-resolved spectroscopy." In Biophotonics in Exercise Science, Sports Medicine, Health Monitoring Technologies, and Wearables, edited by Babak Shadgan and Amir H. Gandjbakhche. SPIE, 2020. http://dx.doi.org/10.1117/12.2545273.

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Lenihan-Geels, G., F. Garcia-Carrizo, C. Li, M. Oster, A. Prokesch, M. Schupp, and T. Schulz. "P53 regulates the lipid metabolism response to metabolic stress in brown adipose tissue." In Abstracts des Adipositas-Kongresses 2020 zur 36. Jahrestagung der Deutschen Adipositas Gesellschaft e.V. (DAG). © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1714476.

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Hofmann, L., J. Meyer, J. Pappisch, T. Kerkhoff, N. Linder, H. Busse, S. Hesse, et al. "Brown adipose tissue activity predicts cachexia and survival in patients with lung cancer." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2707.

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Reports on the topic "Brown adipose tissue"

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Van Eenige, Robin, Wietse In Het Panhuis, Milena Schönke, Céline Jouffe, Thomas Devilee, Ricky Siebeler, Trea Streefland, et al. Angiopoietin-like 4 dictates the day-night rhythm of metabolic brown adipose tissue activity. Peeref, June 2023. http://dx.doi.org/10.54985/peeref.2306p7202701.

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Tabei, Shirin, Rodrigo Chamorro, Sebastian M. Meyhöfer, and Britta Wilms. Metabolic effects of brown adipose tissue activity due to cold exposure in humans: A systematic review and meta-analysis of RCTs and non-RCTs. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2023. http://dx.doi.org/10.37766/inplasy2023.12.0043.

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You might also be interested in the extended bibliographies on the topic 'Brown adipose tissue' for particular source types:
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