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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Payra, Biswajit, Abhranil Dhar, Pankaj Singhania, Akshay Khatri, and Pranab Kumar Sahana. "Deceptive Brown Adipose Tissue." Journal of the ASEAN Federation of Endocrine Societies 39, no. 1 (May 25, 2024): 131–32. http://dx.doi.org/10.15605/jafes.039.01.21.

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12

Wilson, Shelagh. "Effect of the β-adrenoceptor agonist BRL 26830 on fatty acid synthesis and on the activities of pyruvate dehydrogenase and acetyl-CoA carboxylase in adipose tissues of the rat." Bioscience Reports 9, no. 1 (February 1, 1989): 111–17. http://dx.doi.org/10.1007/bf01117517.

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BRL 26830 is a thermogenic β-adrenoceptor agonist which stimulates lipolysis and fatty acid oxidation in vivo. It also stimulates insulin secretion, and hence promotes glucose utilisation in vivo. The effect of this agent on white and brown adipose tissue of the rat was investigated. BRL 26830 increased the rate of fatty acid synthesis in vivo in white adipose tissue by 135% but reduced the rate of fatty acid synthesis in vivo in brown adipose tissue by 78%. The increase was abolished in white adipose tissue of streptozotocin-diabetic rats, indicating that the effect involved a rise in circulating insulin levels. The reduction in fatty acid synthesis in brown adipose tissues was associated with a reduction in the activity of acetyl-CoA carboxylase in the tissue consistent with a direct β-adrenoceptor-mediated effect. BRL 26830 also increased the proportion of pyruvate dehydrogenase in its active form in vivo in brown adipose tissue and this increase was abolished in streptozotocin-diabetic rats. These findings illustrate different sensitivities of white and brown adipose tissues to combined β-adrenergic and insulin stimulation.
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13

Trayhurn, Paul, Norman J. Temple, and Johny Van Aerde. "Evidence from immunoblotting studies on uncoupling protein that brown adipose tissue is not present in the domestic pig." Canadian Journal of Physiology and Pharmacology 67, no. 12 (December 1, 1989): 1480–85. http://dx.doi.org/10.1139/y89-239.

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Adipose tissues and other tissues of the pig have been examined for the presence of the mitochondrial "uncoupling protein," characteristic of brown adipose tissue, in order to assess whether brown fat is present in this species. Mitochondria were prepared from various tissues and the proteins separated on the basis of molecular weight by sodium dodecyl sulphate – polyacrylamide gel electrophoresis. Immunoblotting procedures were then used to probe for uncoupling protein, employing a rabbit anti-(rat uncoupling protein) serum. Pigs were examined at 4 days, 4 weeks, and 8 weeks of age. No evidence for the presence of uncoupling protein was found at any of these ages. The protein was, however, readily detected in brown adipose tissue from rats, mice, golden hamsters, guinea pigs, Richardson's ground squirrel, and lambs. An additional group of pigs was acclimated to the cold (10 °C) for a period of 10 days prior to the examination of tissues, but again uncoupling protein was not detected in any tissue. These results indicate that uncoupling protein is either absent from adipose tissues of the pig or is present at such a low concentration that it is unlikely to support thermogenesis. It is concluded that the pig does not contain adipose tissue that is functionally "brown;" adipose tissues in this species appear to be exclusively "white."Key words: brown adipose tissue, white adipose tissue, uncoupling protein, thermogenesis, immunoblotting.
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14

Stepanchuk, A. P. "MORPHOLOGY OF HUMAN ADIPOSE TISSUE." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 2 (July 6, 2020): 171–75. http://dx.doi.org/10.31718/2077-1096.20.2.171.

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The risk of developing metabolic complications in obesity depends on the topography of excess adipose tissue. Adipose tissue is the main source of energy and also performs an endocrine function secreting substances that affect the sensitivity of tissues to insulin. The article describes the characteristics of histological preparations of adipose tissue samples taken from the omentum of middle-aged human cadavers with no confirmed diseases of the digestive system and of subcutaneous adipose tissue samples from interscapular region in the human dead foetuses. Microscopy of sections of adipose tissue from the omentum and subcutaneous adipose tissue from the interscapular region of the foetus revealed that it consisted of lobes and microvessels. Lobes of adipose tissue of a human large omentum consist of polygonal white adipocytes containing in their cytoplasm a nucleus displaced to the periphery and a fat drop. The subcutaneous adipose tissue taken from the interscapular region of the foetus consists of brown adipocytes with a nucleus located in the centre of the cytoplasm and surrounded by numerous fat droplets. Brown adipocytes when compared with white adipocyted are smaller and rounded in shape. Brown adipose tissue predominates in women than in men. Brown adipose tissue is not active all the time, but only at low ambient temperatures. In women, brown adipocytes are more saturated with mitochondria than in men. Adipose tissue of a human omentum can be a source of graft implant for restoring abdominal organ defects during extensive surgical operations.
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15

Kotzbeck, Petra, Antonio Giordano, Eleonora Mondini, Incoronata Murano, Ilenia Severi, Wiebe Venema, Maria Paola Cecchini, et al. "Brown adipose tissue whitening leads to brown adipocyte death and adipose tissue inflammation." Journal of Lipid Research 59, no. 5 (March 29, 2018): 784–94. http://dx.doi.org/10.1194/jlr.m079665.

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16

Silva, JE. "Brown Adipose Tissue: An Extrathyroidal Source of Triiodothyronine." Physiology 1, no. 4 (August 1, 1986): 119–22. http://dx.doi.org/10.1152/physiologyonline.1986.1.4.119.

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The role of brown adipose tissue in heat production is well known, but it is a novel concept that this tissue can activate the main secretory product of the thyroid gland, thyroxine, by converting it into the ten times more active triiodothyronine. The enzyme that catalyzes the reaction is present also in other tissues, but it is activated by the sympathetic nervous system only in brown adipose tissue. Thus sympathetic stimulation of brown adipose tissue results in increased production of triiodothyronine and activation of metabolism in other tissues.
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17

Karpathiou, Georgia, Jean Marc Dumollard, Zoe Evangelou, Anna Batistatou, Michel Peoc’h, and Alexandra Papoudou-Bai. "Cytoplasmic p16 Is Expressed in Normal Brown Fat and Hibernomas." International Journal of Surgical Pathology 28, no. 5 (February 5, 2020): 496–501. http://dx.doi.org/10.1177/1066896920904423.

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White adipose tissue browning has emerged as a putative therapy of obesity, and studies in mice have shown that Cdkn2a is implicated in white-to-brown transition. However, the role of Cdkn2a product p16 has been never studied in human brown fat tissue. The aim of the study is to investigate the expression of p16 in normal brown fat and in hibernoma, a lipoma containing brown fat-like adipocytes. Ten normal brown fat tissues and 5 hibernomas were immunohistochemically studied for p16 expression. Nearby white adipose tissue was used for comparison. All brown fat and hibernomas specimens express p16 in a cytoplasmic manner. Neighboring white adipose tissue is negative for p16 expression. Thus, cytoplasmic p16 may be associated with fat tissue browning.
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18

Trayhurn, P., and A. Howe. "Noradrenaline turnover in brown adipose tissue and the heart of fed and fasted golden hamsters." Canadian Journal of Physiology and Pharmacology 67, no. 2 (February 1, 1989): 106–9. http://dx.doi.org/10.1139/y89-018.

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The effect of fasting on sympathetic activity in tissues of the golden hamster has been investigated using measurements of noradrenaline turnover. Fasting for 60 h did not have a significant effect on noradrenaline turnover, both fractional and total, in brown adipose tissue or the heart. Fasting did, however, result in a functional atrophy of brown adipose tissue; tissue weight, protein content, and cytochrome oxidase activity were each reduced after a 60-h fast. These results suggest that the atrophy of brown adipose tissue induced by fasting in the golden hamster does not relate to a major decrease in sympathetic activity. The findings add further support for the view that the thermogenic capacity of brown adipose tissue is not primarily dependent on sympathetic activity in the golden hamster.
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19

Ito, Masahiro, Yosihisa Kawase, Kazuko Shichijo, Ichiro Sekine, Sinji Uchida, Masayori Ozaki, and Katuhiko Tuchiya. "Brown Adipose Tissue in SHRSP." Japanese Heart Journal 31, no. 4 (1990): 541. http://dx.doi.org/10.1536/ihj.31.541.

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20

Nuutila, Pirjo. "Brown adipose tissue in humans." Annals of Medicine 47, no. 2 (February 17, 2015): 122. http://dx.doi.org/10.3109/07853890.2015.1019917.

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21

Lecoultre, Virgile, and Eric Ravussin. "Brown adipose tissue and aging." Current Opinion in Clinical Nutrition and Metabolic Care 14, no. 1 (January 2011): 1–6. http://dx.doi.org/10.1097/mco.0b013e328341221e.

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22

Lidell, M. E., and S. Enerbäck. "Brown adipose tissue and bone." International Journal of Obesity Supplements 5, S1 (August 2015): S23—S27. http://dx.doi.org/10.1038/ijosup.2015.7.

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23

Enerbäck, S. "Brown adipose tissue in humans." International Journal of Obesity 34, S1 (October 2010): S43—S46. http://dx.doi.org/10.1038/ijo.2010.183.

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24

Holloway, Brian R. "Reactivation of brown adipose tissue." Proceedings of the Nutrition Society 48, no. 2 (July 1989): 225–30. http://dx.doi.org/10.1079/pns19890033.

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25

Lean, M. E. J. "Brown adipose tissue in humans." Proceedings of the Nutrition Society 48, no. 2 (July 1989): 243–57. http://dx.doi.org/10.1079/pns19890036.

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26

Tews, D., and M. Wabitsch. "Renaissance of Brown Adipose Tissue." Hormone Research in Paediatrics 75, no. 4 (2011): 231–39. http://dx.doi.org/10.1159/000324806.

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27

Mulya, Anny, and John P. Kirwan. "Brown and Beige Adipose Tissue." Endocrinology and Metabolism Clinics of North America 45, no. 3 (September 2016): 605–21. http://dx.doi.org/10.1016/j.ecl.2016.04.010.

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28

Perdikari, Aliki, Germán Gastón Leparc, Miroslav Balaz, Nuno D. Pires, Martin E. Lidell, Wenfei Sun, Francesc Fernandez-Albert, et al. "BATLAS: Deconvoluting Brown Adipose Tissue." Cell Reports 25, no. 3 (October 2018): 784–97. http://dx.doi.org/10.1016/j.celrep.2018.09.044.

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29

Virtanen, Kirsi A., and Pirjo Nuutila. "Brown adipose tissue in humans." Current Opinion in Lipidology 22, no. 1 (February 2011): 49–54. http://dx.doi.org/10.1097/mol.0b013e3283425243.

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30

de Meis, Leopoldo. "Brown Adipose Tissue Ca2+-ATPase." Journal of Biological Chemistry 278, no. 43 (August 11, 2003): 41856–61. http://dx.doi.org/10.1074/jbc.m308280200.

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31

Pauli, José Rodrigo. "A Palette of Adipose Tissue: Multiple Functionality and Extraordinary Plasticity." Trends in Anatomy and Physiology 4, no. 1 (February 17, 2021): 1–4. http://dx.doi.org/10.24966/tap-7752/100013.

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After the knowledge of adipose tissue as an endocrine organ and its role as a regulator of metabolisms, studies have advanced on its biological function. Previously, only two adipose tissues were identified in mammals, white and brown adipose tissue. White adipocytes store lipids mainly with the function of energy reserve and brown for thermal homeostasis. Due to the plasticity of adipose tissue and its ability to proliferate and differentiate, the third type of adipocyte, beige, emerged. Beige adipocytes originate from white adipocytes that have acquired phenotypic brown characteristics in response to different stimuli, this process is known as browning. More recently, the plastic properties allowed the identification of the fourth type of adipose tissue, the pink.
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32

Symonds, Michael E. "Brown Adipose Tissue Growth and Development." Scientifica 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/305763.

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Brown adipose tissue is uniquely able to rapidly produce large amounts of heat through activation of uncoupling protein (UCP) 1. Maximally stimulated brown fat can produce 300 watts/kg of heat compared to 1 watt/kg in all other tissues. UCP1 is only present in small amounts in the fetus and in precocious mammals, such as sheep and humans; it is rapidly activated around the time of birth following the substantial rise in endocrine stimulatory factors. Brown adipose tissue is then lost and/or replaced with white adipose tissue with age but may still contain small depots of beige adipocytes that have the potential to be reactivated. In humans brown adipose tissue is retained into adulthood, retains the capacity to have a significant role in energy balance, and is currently a primary target organ in obesity prevention strategies. Thermogenesis in brown fat humans is environmentally regulated and can be stimulated by cold exposure and diet, responses that may be further modulated by photoperiod. Increased understanding of the primary factors that regulate both the appearance and the disappearance of UCP1 in early life may therefore enable sustainable strategies in order to prevent excess white adipose tissue deposition through the life cycle.
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de Jong, Jasper M. A., Ola Larsson, Barbara Cannon, and Jan Nedergaard. "A stringent validation of mouse adipose tissue identity markers." American Journal of Physiology-Endocrinology and Metabolism 308, no. 12 (June 15, 2015): E1085—E1105. http://dx.doi.org/10.1152/ajpendo.00023.2015.

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The nature of brown adipose tissue in humans is presently debated: whether it is classical brown or of brite/beige nature. The dissimilar developmental origins and proposed distinct functions of the brown and brite/beige tissues make it essential to ascertain the identity of human depots with the perspective of recruiting and activating them for the treatment of obesity and type 2 diabetes. For identification of the tissues, a number of marker genes have been proposed, but the validity of the markers has not been well documented. We used established brown (interscapular), brite (inguinal), and white (epididymal) mouse adipose tissues and corresponding primary cell cultures as validators and examined the informative value of a series of suggested markers earlier used in the discussion considering the nature of human brown adipose tissue. Most of these markers unexpectedly turned out to be noninformative concerning tissue classification ( Car4, Cited1, Ebf3, Eva1, Fbxo31, Fgf21, Lhx8, Hoxc8, and Hoxc9). Only Zic1 (brown), Cd137, Epsti1, Tbx1, Tmem26 (brite), and Tcf21 (white) proved to be informative in these three tissues. However, the expression of the brite markers was not maintained in cell culture. In a more extensive set of adipose depots, these validated markers provide new information about depot identity. Principal component analysis supported our single-gene conclusions. Furthermore, Zic1, Hoxc8, Hoxc9, and Tcf21 displayed anteroposterior expression patterns, indicating a relationship between anatomic localization and adipose tissue identity (and possibly function). Together, the observed expression patterns of these validated marker genes necessitates reconsideration of adipose depot identity in mice and humans.
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34

Schimmel, R. J., and L. McCarthy. "Brown adipose tissue in cafeteria-fed hamsters." American Journal of Physiology-Endocrinology and Metabolism 248, no. 2 (February 1, 1985): E230—E235. http://dx.doi.org/10.1152/ajpendo.1985.248.2.e230.

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Hamsters consuming a “cafeteria diet” had more brown adipose tissue than did chow-fed hamsters. The growth of the brown fat depots in cafeteria-fed hamsters was accompanied by increases in tissue protein and cytochrome oxidase. To assess the thermogenic capacity of brown fat mitochondria, the binding of GDP to isolated mitochondria was measured. Mitochondrial GDP binding was not affected by feeding the cafeteria diet for 4 wk, but more prolonged cafeteria feeding for 8 wk did, however, increase the binding of GDP to isolated mitochondria. The morphology of brown adipose tissue was altered during cafeteria feeding. The brown adipose tissue of cafeteria-fed hamsters had more large unilocular cells than did the brown adipose tissue of chow-fed hamsters. In addition, the average adipocyte diameter was greater in brown adipose tissue of cafeteria-fed hamsters. These data support the presence of a dietary regulation of brown adipose tissue growth in hamsters. The growth of brown adipose tissue in hamsters eating the cafeteria diet appears to result largely from proliferation of adipocytes, as evidenced by the increases in tissue protein and cytochrome oxidase during cafeteria feeding, but some hypertrophy of the adipocytes also occurs. A dietary regulation of brown fat thermogenic capacity is also apparent but this regulation is evident only after more prolonged periods of cafeteria feeding. Hamsters eating a cafeteria diet increase their caloric intake but have the same or greater body weight gain efficiency as do chow-fed animals. The absence of dietary stimulation of thermogenesis may underlie the similar efficiencies of weight gain in chow- and cafeteria-fed hamsters.
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Krause, Kerstin. "Novel Aspects of White Adipose Tissue Browning by Thyroid Hormones." Experimental and Clinical Endocrinology & Diabetes 128, no. 06/07 (November 7, 2019): 446–49. http://dx.doi.org/10.1055/a-1020-5354.

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AbstractThyroid hormones are essential for the full thermogenic capacity of brown adipose tissue. The thermogenic response of brown adipocytes to thyroid hormones is resulting from the synergistic interaction of thyroid hormones with the sympathetic nervous system. In recent years, evidence has been provided that thyroid hormones also induce the browning of white adipose tissues. This review will provide a brief overview about the recent findings regarding the effects of thyroid hormones on adipose tissue thermogenesis including central and peripheral regulation of white adipose tissue browning.
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36

de Jong, Jasper M. A., Wenfei Sun, Nuno D. Pires, Andrea Frontini, Miroslav Balaz, Naja Z. Jespersen, Amir Feizi, et al. "Human brown adipose tissue is phenocopied by classical brown adipose tissue in physiologically humanized mice." Nature Metabolism 1, no. 8 (August 2019): 830–43. http://dx.doi.org/10.1038/s42255-019-0101-4.

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37

Kalmykova, O., and M. Dzerzhynsky. "The effects of melatonin administration in different times of day on the brown adipose tissue in rats with high-calorie diet-induced obesity." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 77, no. 1 (2019): 55–61. http://dx.doi.org/10.17721/1728_2748.2019.77.55-61.

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The aim of our study was to determine morpho-functional state (area of nucleus, brown adipocytes and also area and number of lipid droplets in each cells, general optical density of tissue) of brown adipose tissue in rats with high-calorie (high fat) dietinduced obesity after melatonin administration in different time of the day (morning and evening). Melatonin was administered daily by gavage for 7 weeks in dose 30 mg/kg either 1 h after lights-on (ZT01) or 1 h before lights-off (ZT11) rats with high-calorie diet (HCD). Besides morphometric parameters as well were measured related visceral fat weight and related brown adipose tissue mass. Rats with HCD had huge changes in brown adipocytes morphology, which summarized in become resembles of classical white adipocytes: grown lipid droplets and cells area, but goes down lipid droplets number and optical density of brown adipose tissue. In general brown adipose tissue with above mentioned characteristic from HCD rats lose their ability to conduct strongly thermoproduction function. After melatonin used in rats with HCD arise leveling of pathological changes, which associated with consumption of HCD. Namely, in groups HCD ZT01 and HCD ZT11 we obtain decreased cells and lipid droplets area, increased lipid droplets number and optical density of brown adipose tissue, in relation to group HCD. Therese received changes has evidence about functionally active brown adipose tissue state, which can also dissipate of exceed energy (lipids – triacylglycerols) amount into whole organism during heat production for avoid to its storage in white adipose tissue and in outside adipose tissue. In addition, evening administration of melatonin (group HCD ZT11) demonstrate more activated state of brown adipose tissueand also related visceral weight gain less, than morning(group HCD ZT01). In conclusions, melatonin influence on morpho-functional state brown adipose tissue in rats with HCD, moreover evening administration can use for obesity therapy via its strong action on activate brown adipocytes.
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38

Zakharova, A. N., K. G. Milovanova, A. A. Orlova, O. V. Kollantay, I. Yu Shuvalov, and L. V. Kapilevich. "Oxidative phosphorylation in brown adipose tissue in a type II diabetes mellitus mouse model after forced treadmill running." Bulletin of Siberian Medicine 23, no. 1 (April 10, 2024): 48–55. http://dx.doi.org/10.20538/1682-0363-2024-1-48-55.

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Aim. To study the effect of forced exercises on the content and parameters of oxidative phosphorylation in brown adipose tissue of mice with type II diabetes mellitus.Materials and methods. To model the disease, we used a high-fat diet and physical exercises in the form of forced treadmill running for 4 weeks. The content of oxidative phosphorylation enzymes in brown adipose tissue was determined by Western blotting.Results. Modeling diabetes in experimental animals was accompanied by expansion of adipose tissue. However, in brown adipose tissue, the content of all oxidative phosphorylation components decreases. Apparently, during type II diabetes mellitus modeling in mice, there is a decrease in the “energy efficiency” in brown adipose tissue, which is partially offset by an increase in its content in the body. Regular physical activity in mice with type II diabetes mellitus, in contrast to healthy animals, contributes to a decrease in the content of brown adipose tissue. At the same time, the content of most oxidative phosphorylation components in brown adipose tissue increases, in some casesб it even exceeds the baseline values. The latter is typical of a variable load mode – when the execution time of exercises periodically changes.Conclusion. The obtained results suggest that metabolic rearrangements in brown adipose tissue may serve as some of the mechanisms of preventive and projective effects of physical activity in type 2 diabetes mellitus.
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39

Gburcik, Valentina, William P. Cawthorn, Jan Nedergaard, James A. Timmons, and Barbara Cannon. "An essential role for Tbx15 in the differentiation of brown and “brite” but not white adipocytes." American Journal of Physiology-Endocrinology and Metabolism 303, no. 8 (October 15, 2012): E1053—E1060. http://dx.doi.org/10.1152/ajpendo.00104.2012.

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The transcription factor Tbx15 is expressed predominantly in brown adipose tissue and in those white adipose depots that are capable of giving rise to brown-in-white (“brite”/“beige”) adipocytes. Therefore, we have investigated a possible role here of Tbx15 in brown and brite adipocyte differentiation in vitro. Adipocyte precursors were isolated from interscapular and axilliary brown adipose tissues, inguinal white (“brite”) adipose tissue, and epididymal white adipose tissue in 129/Sv mouse pups and differentiated in culture. Differentiation was enhanced by chronic treatment with the PPARγ agonist rosiglitazone plus the sympathetic neurotransmitter norepinephrine. Using short interfering RNAs (siRNA) directed toward Tbx15 in these primary adipocyte cultures, we decreased Tbx15 expression >90%. This resulted in reduced expression levels of adipogenesis markers (PPARγ, aP2). Importantly, Tbx15 knockdown reduced the expression of brown phenotypic marker genes (PRDM16, PGC-1α, Cox8b/Cox4, UCP1) in brown adipocytes and even more markedly in inguinal white adipocytes. In contrast, Tbx15 knockdown had no effect on white adipocytes originating from a depot that is not brite competent in vivo (epididymal). Therefore, Tbx15 may be essential for the development of the adipogenic and thermogenic programs in adipocytes/adipomyocytes capable of developing brown adipocyte features.
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40

Gui, Yaoting, Zhiming Cai, Josef V. Silha, and Liam J. Murphy. "Variations in parametrial white adipose tissue mass during the mouse estrous cycle: relationship with the expression of peroxisome proliferator-activated receptor-γ and retinoic acid receptor-α." Canadian Journal of Physiology and Pharmacology 84, no. 8-9 (September 2006): 887–92. http://dx.doi.org/10.1139/y06-032.

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Estrogen and progestin participate in the regulation of adipose tissue metabolism, and peroxisome proliferator-activated receptor-gamma (PPARγ) and retinoic acid receptor-alpha (RXRα) are absolutely required for adipose tissue development. The present study is to investigate the changes in parametrial fat mass and expression of PPARγ and RXRα during estrous cycle in mice. Parametrial white adipose tissues (WAT), inter-scapula brown adipose tissues, and uteri from female mice were weighed. Blood samples were collected for the measurement of 17 β-estradiol and progesterone levels. An RNase protection assay and Western blot analysis were used to compare the expression of PPARγ and RXRα in adipose tissue. The mass of parametrial WAT in diestrus was significantly higher compared with estrus. However, there is no significant difference on the mass of brown adipose tissues during estrous cycle. The expression of PPARγ in WAT in diestrus was significantly higher than that in estrus. The expression of RXRα during estrous cycle was unchanged in both white and brown adipose tissues. In conclusion, the variation in parametrial WAT mass during the mouse estrous cycle correlates with changes in the expression of PPARγ in WAT.
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41

Kates, Anna-Lisa, Ian R. A. Park, Jean Himms-Hagen, and Rudolf W. Mueller. "Thyroxine 5′-deiodinase in brown adipose tissue of the cynomolgus monkey Macaca fascicularis." Biochemistry and Cell Biology 68, no. 1 (January 1, 1990): 231–37. http://dx.doi.org/10.1139/o90-031.

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Brown adipose tissue was identified in axillary, interscapular, subscapular, and cervical fat deposits of male and female cynomolgus monkeys (Macaca fascicularis) by histological and immunological techniques. Histology included staining of mitochondria with a Novelli stain and identification of mitochondria-rich multilocular cells. Immunological detection involved separation of homogenate proteins by sodium dodecyl sulphate – polyacrylamide gel chromatography, blotting on to nitrocellulose membranes, and identification of the specific uncoupling protein, unique to brown adipose tissue, with an antiserum to purified hamster uncoupling protein followed by detection with 125I-labelled protein A. The activity of thyroxine 5′-deiodinase in monkey brown adipose tissue homogenates was much higher than that seen previously in brown adipose tissue of rats, mice, and hamsters. This is the first demonstration of the presence of this enzyme in brown adipose tissue of a primate species.Key words: uncoupling protein, primate, 3,5,3′-triiodothyronine, thermogenesis; white adipose tissue.
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42

Bazin, R., D. Ricquier, F. Dupuy, J. Hoover-Plow, and M. Lavau. "Thermogenic and lipogenic activities in brown adipose tissue of I-strain mice." Biochemical Journal 231, no. 3 (November 1, 1985): 761–64. http://dx.doi.org/10.1042/bj2310761.

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The thermogenic capacity of brown adipose tissue has been investigated in I-strain mice to determine whether this tissue could play a role in the lower efficiency of food utilization reported in this strain of mice. (1) As compared with C57BL mice (a control strain), interscapular-brown-adipose-tissue weight and lipid percentage were decreased by 40% and 13% respectively in I-strain mice. (2) Mitochondrial protein content and cytochrome c oxidase activity were similar in the two strains, but the number of mitochondrial GDP-binding sites and uncoupling-protein content were increased by 2-fold in I-strain mice. (3) Fatty acid synthetase and citrate-cleavage enzyme (units/mg of protein) were 3-fold higher in the brown adipose tissue of I-strain mice. These results indicate that I-strain mice possess a very active brown adipose tissue. This enhanced capacity of energy dissipation in brown adipose tissue could contribute to the decreased capacity of I-strain mice to store adipose tissue.
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43

Porter, Craig, Elisabet Børsheim, and Labros S. Sidossis. "Does Adipose Tissue Thermogenesis Play a Role in Metabolic Health?" Journal of Obesity 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/204094.

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The function ascribed to brown adipose tissue in humans has long been confined to thermoregulation in neonates, where this thermogenic capacity was thought lost with maturation. Recently, brown adipose tissue depots have been identified in adult humans. The significant oxidative capacity of brown adipocytes and the ability of their mitochondria to respire independently of ATP production, has led to renewed interest in the role that these adipocytes play in human energy metabolism. In our view, there is a need for robust physiological studies determining the relationship between molecular signatures of brown adipose tissue, adipose tissue mitochondrial function, and whole body energy metabolism, in order to elucidate the significance of thermogenic adipose tissue in humans. Until such information is available, the role of thermogenic adipose tissue in human metabolism and the potential that these adipocytes may prevent or treat obesity and metabolic diseases in humans will remain unknown. In this article, we summarize the recent literature pertaining to brown adipose tissue function with the aims of drawing the readers’ attention to the lack of data concerning the role of brown adipocytes in human physiology, and to the potential limitations of current research strategies.
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44

Imai-Matsumura, Kyoko, and Teruo Nakayama. "The central efferent mechanism of brown adipose tissue thermogenesis induced by preoptic cooling." Canadian Journal of Physiology and Pharmacology 65, no. 6 (June 1, 1987): 1299–303. http://dx.doi.org/10.1139/y87-206.

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This study was performed to investigate central efferent mechanisms for brown adipose tissue thermogenesis. In unanesthetized rats, the effects of local anesthesia of the ventromedial hypothalamus, anterior hypothalamus, and lateral hypothalamus were observed on the brown adipose tissue thermogenesis induced by preoptic cooling. Rats had a thermode, thermocouple, and bilateral injection cannulae chronically implanted in the hypothalamus and a thermocouple beneath the interscapular brown adipose tissue. The experiments were done at an ambient temperature of 24–25 °C. Preoptic cooling increased brown adipose tissue and colonic temperatures without shivering. Injecting lidocaine bilaterally into the ventromedial hypothalamus during preoptic cooling reduced brown adipose tissue temperature (Tbat). The mean maximum decrease of Tbat was 0.51 ± 0.26 °C and occurred 5–8 min after lidocaine injection. When lidocaine was injected into the anterior hypothalamus, Tbat increased. The mean maximum increase of Tbat was 0.85 ± 0.29 °C and occurred 4–9 min after lidocaine injection. In the lateral hypothalamus, lidocaine had no effect on Tbat∙Tbat was not influenced by injection of saline into the ventromedial, anterior, or lateral hypothalamus. The efferent pathway from preoptic to brown adipose tissue may thus traverse the medial part of hypothalamus. The ventromedial hypothalamus facilititates and anterior hypothalamus inhibits brown adipose tissue thermogenesis induced by preoptic cooling.
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45

Gómez-Hernández, Almudena, Nuria Beneit, Sabela Díaz-Castroverde, and Óscar Escribano. "Differential Role of Adipose Tissues in Obesity and Related Metabolic and Vascular Complications." International Journal of Endocrinology 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/1216783.

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This review focuses on the contribution of white, brown, and perivascular adipose tissues to the pathophysiology of obesity and its associated metabolic and vascular complications. Weight gain in obesity generates excess of fat, usually visceral fat, and activates the inflammatory response in the adipocytes and then in other tissues such as liver. Therefore, low systemic inflammation responsible for insulin resistance contributes to atherosclerotic process. Furthermore, an inverse relationship between body mass index and brown adipose tissue activity has been described. For these reasons, in recent years, in order to combat obesity and its related complications, as a complement to conventional treatments, a new insight is focusing on the role of the thermogenic function of brown and perivascular adipose tissues as a promising therapy in humans. These lines of knowledge are focused on the design of new drugs, or other approaches, in order to increase the mass and/or activity of brown adipose tissue or the browning process of beige cells from white adipose tissue. These new treatments may contribute not only to reduce obesity but also to prevent highly prevalent complications such as type 2 diabetes and other vascular alterations, such as hypertension or atherosclerosis.
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46

Snoke, Deena B., Austin Angelotti, Kamil Borkowski, Rachel M. Cole, John W. Newman, and Martha A. Belury. "Linoleate-Rich Safflower Oil Diet Increases Linoleate-Derived Bioactive Lipid Mediators in Plasma, and Brown and White Adipose Depots of Healthy Mice." Metabolites 12, no. 8 (August 12, 2022): 743. http://dx.doi.org/10.3390/metabo12080743.

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Polyunsaturated fats are energy substrates and precursors to the biosynthesis of lipid mediators of cellular processes. Adipose tissue not only provides energy storage, but influences whole-body energy metabolism through endocrine functions. How diet influences adipose–lipid mediator balance may have broad impacts on energy metabolism. To determine how dietary lipid sources modulate brown and white adipose tissue and plasma lipid mediators, mice were fed low-fat (15% kcal fat) isocaloric diets, containing either palm oil (POLF) or linoleate-rich safflower oil (SOLF). Baseline and post body weight, adiposity, and 2-week and post fasting blood glucose were measured and lipid mediators were profiled in plasma, and inguinal white and interscapular brown adipose tissues. We identified over 30 species of altered lipid mediators between diets and found that these changes were unique to each tissue. We identified changes to lipid mediators with known functional roles in the regulation of adipose tissue expansion and function, and found that there was a relationship between the average fold difference in lipid mediators between brown adipose tissue and plasma in mice consuming the SOLF diet. Our findings emphasize that even with a low-fat diet, dietary fat quality has a profound effect on lipid mediator profiles in adipose tissues and plasma.
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47

Petito, Giuseppe, Federica Cioffi, Nunzia Magnacca, Pieter de Lange, Rosalba Senese, and Antonia Lanni. "Adipose Tissue Remodeling in Obesity: An Overview of the Actions of Thyroid Hormones and Their Derivatives." Pharmaceuticals 16, no. 4 (April 10, 2023): 572. http://dx.doi.org/10.3390/ph16040572.

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Metabolic syndrome and obesity have become important health issues of epidemic proportions and are often the cause of related pathologies such as type 2 diabetes (T2DM), hypertension, and cardiovascular disease. Adipose tissues (ATs) are dynamic tissues that play crucial physiological roles in maintaining health and homeostasis. An ample body of evidence indicates that in some pathophysiological conditions, the aberrant remodeling of adipose tissue may provoke dysregulation in the production of various adipocytokines and metabolites, thus leading to disorders in metabolic organs. Thyroid hormones (THs) and some of their derivatives, such as 3,5-diiodo-l-thyronine (T2), exert numerous functions in a variety of tissues, including adipose tissues. It is known that they can improve serum lipid profiles and reduce fat accumulation. The thyroid hormone acts on the brown and/or white adipose tissues to induce uncoupled respiration through the induction of the uncoupling protein 1 (UCP1) to generate heat. Multitudinous investigations suggest that 3,3′,5-triiodothyronine (T3) induces the recruitment of brown adipocytes in white adipose depots, causing the activation of a process known as “browning”. Moreover, in vivo studies on adipose tissues show that T2, in addition to activating brown adipose tissue (BAT) thermogenesis, may further promote the browning of white adipose tissue (WAT), and affect adipocyte morphology, tissue vascularization, and the adipose inflammatory state in rats receiving a high-fat diet (HFD). In this review, we summarize the mechanism by which THs and thyroid hormone derivatives mediate adipose tissue activity and remodeling, thus providing noteworthy perspectives on their efficacy as therapeutic agents to counteract such morbidities as obesity, hypercholesterolemia, hypertriglyceridemia, and insulin resistance.
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48

CANNON, BARBARA, and JAN NEDERGAARD. "Brown Adipose Tissue: Function and Physiological Significance." Physiological Reviews 84, no. 1 (January 2004): 277–359. http://dx.doi.org/10.1152/physrev.00015.2003.

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Cannon, Barbara, and Jan Nedergaard. Brown Adipose Tissue: Function and Physiological Significance. Physiol Rev 84: 277–359, 2004; 10.1152/physrev.00015.2003.—The function of brown adipose tissue is to transfer energy from food into heat; physiologically, both the heat produced and the resulting decrease in metabolic efficiency can be of significance. Both the acute activity of the tissue, i.e., the heat production, and the recruitment process in the tissue (that results in a higher thermogenic capacity) are under the control of norepinephrine released from sympathetic nerves. In thermoregulatory thermogenesis, brown adipose tissue is essential for classical nonshivering thermogen-esis (this phenomenon does not exist in the absence of functional brown adipose tissue), as well as for the cold acclimation-recruited norepinephrine-induced thermogenesis. Heat production from brown adipose tissue is activated whenever the organism is in need of extra heat, e.g., postnatally, during entry into a febrile state, and during arousal from hibernation, and the rate of thermogenesis is centrally controlled via a pathway initiated in the hypothalamus. Feeding as such also results in activation of brown adipose tissue; a series of diets, apparently all characterized by being low in protein, result in a leptin-dependent recruitment of the tissue; this metaboloregulatory thermogenesis is also under hypothalamic control. When the tissue is active, high amounts of lipids and glucose are combusted in the tissue. The development of brown adipose tissue with its characteristic protein, uncoupling protein-1 (UCP1), was probably determinative for the evolutionary success of mammals, as its thermogenesis enhances neonatal survival and allows for active life even in cold surroundings.
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49

Spaanderman, Dieuwertje C. E., Mark Nixon, Jacobus C. Buurstede, Hetty H. C. M. Sips, Maaike Schilperoort, Eline N. Kuipers, Emma A. Backer, et al. "Androgens modulate glucocorticoid receptor activity in adipose tissue and liver." Journal of Endocrinology 240, no. 1 (January 2019): 51–63. http://dx.doi.org/10.1530/joe-18-0503.

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Glucocorticoid signaling is context dependent, and in certain scenarios, glucocorticoid receptors (GRs) are able to engage with other members of the nuclear receptor subfamily. Glucocorticoid signaling can exert sexually dimorphic effects, suggesting a possible interaction with androgen sex hormones. We therefore set out to determine the crosstalk between glucocorticoids and androgens in metabolic tissues including white adipose tissue, liver and brown adipose tissue. Thereto we exposed male C57BL/6J mice to elevated levels of corticosterone in combination with an androgen receptor (AR) agonist or an AR antagonist. Systemic and local glucocorticoid levels were determined by mass spectrometry, and tissue expression of glucocorticoid-responsive genes and protein was measured by RT-qPCR and Western blot, respectively. To evaluate crosstalk in vitro, cultured white and brown adipocytes were exposed to a combination of corticosterone and an AR agonist. We found that AR agonism potentiated transcriptional response to GR in vitro in white and brown adipocytes and in vivo in white and brown adipose tissues. Conversely, AR antagonism substantially attenuated glucocorticoid signaling in white adipose tissue and liver. In white adipose tissue, this effect could partially be attributed to decreased 11B-hydroxysteroid dehydrogenase type 1-mediated glucocorticoid regeneration upon AR antagonism. In liver, attenuated GR activity was independent of active glucocorticoid ligand levels. We conclude that androgen signaling modulates GR transcriptional output in a tissue-specific manner.
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50

Revelli, J. P., R. Pescini, P. Muzzin, J. Seydoux, M. G. Fitzgerald, C. M. Fraser, and J. P. Giacobino. "Changes in β1- and β2-adrenergic receptor mRNA levels in brown adipose tissue and heart of hypothyroid rats." Biochemical Journal 277, no. 3 (August 1, 1991): 625–29. http://dx.doi.org/10.1042/bj2770625.

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The aim of the present work was to study the effect of hypothyroidism on the expression of the beta-adrenergic receptor (beta-AR) in interscapular brown adipose tissue and heart. The total density of plasma membrane beta-AR per tissue is decreased by 44% in hypothyroid rat interscapular brown adipose tissue and by 55% in hypothyroid rat heart compared with euthyroid controls. The effects of hypothyroidism on the density of both beta 1- and beta 2-AR subtypes were also determined in competition displacement experiments. The densities of beta 1- and beta 2-AR per tissue are decreased by 50% and 48% respectively in interscapular brown adipose tissue and by 52% and 54% in the heart. Northern blot analysis of poly(A)+ RNA from hypothyroid rat interscapular brown adipose tissue demonstrated that the levels of beta 1- and beta 2-AR mRNA per tissue are decreased by 73% and 58% respectively, whereas in hypothyroid heart, only the beta 1-AR mRNA is decreased, by 43%. The effect of hypothyroidism on the beta 1-AR mRNA is significantly more marked in the interscapular brown adipose tissue than in the heart. These results indicate that beta-AR mRNA levels are differentially regulated in rat interscapular brown adipose tissue and heart, and suggest that the decrease in beta-AR number in interscapular brown adipose tissue and heart of hypothyroid animals may in part be explained by a decreased steady-state level of beta-AR mRNA.
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