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Journal articles on the topic 'Thermogenic gene program'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Yi, Danielle, Hai P. Nguyen, and Hei Sook Sul. "Epigenetic dynamics of the thermogenic gene program of adipocytes." Biochemical Journal 477, no. 6 (2020): 1137–48. http://dx.doi.org/10.1042/bcj20190599.

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Brown adipose tissue (BAT) is a metabolically beneficial organ capable of burning fat by dissipating chemical energy into heat, thereby increasing energy expenditure. Moreover, subcutaneous white adipose tissue can undergo so-called browning/beiging. The recent recognition of the presence of brown or beige adipocytes in human adults has attracted much attention to elucidate the molecular mechanism underlying the thermogenic adipose program. Many key transcriptional regulators critical for the thermogenic gene program centering on activating the UCP1 promoter, have been discovered. Thermogenic

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2

Li, Siming, Lin Mi, Lei Yu, et al. "Zbtb7b engages the long noncoding RNA Blnc1 to drive brown and beige fat development and thermogenesis." Proceedings of the National Academy of Sciences 114, no. 34 (2017): E7111—E7120. http://dx.doi.org/10.1073/pnas.1703494114.

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Brown and beige adipocytes convert chemical energy into heat through uncoupled respiration to defend against cold stress. Beyond thermogenesis, brown and beige fats engage other metabolic tissues via secreted factors to influence systemic energy metabolism. How the protein and long noncoding RNA (lncRNA) regulatory networks act in concert to regulate key aspects of thermogenic adipocyte biology remains largely unknown. Here we developed a genome-wide functional screen to interrogate the transcription factors and cofactors in thermogenic gene activation and identified zinc finger and BTB domain

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3

Hoang, Anh Cuong, Haidong Yu, and Tamás Röszer. "Transcriptional Landscaping Identifies a Beige Adipocyte Depot in the Newborn Mouse." Cells 10, no. 9 (2021): 2368. http://dx.doi.org/10.3390/cells10092368.

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The present study sought to identify gene networks that are hallmarks of the developing inguinal subcutaneous adipose tissue (iWAT) and the interscapular brown adipose tissue (BAT) in the mouse. RNA profiling revealed that the iWAT of postnatal (P) day 6 mice expressed thermogenic and lipid catabolism transcripts, along with the abundance of transcripts associated with the beige adipogenesis program. This was an unexpected finding, as thermogenic BAT was believed to be the only site of nonshivering thermogenesis in the young mouse. However, the transcriptional landscape of BAT in P6 mice sugge

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Shao, Mengle, Jeff Ishibashi, Christine M. Kusminski, et al. "Zfp423 Maintains White Adipocyte Identity through Suppression of the Beige Cell Thermogenic Gene Program." Cell Metabolism 23, no. 6 (2016): 1167–84. http://dx.doi.org/10.1016/j.cmet.2016.04.023.

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5

Armengol, Jordi, Josep A. Villena, Elayne Hondares та ін. "Pref-1 in brown adipose tissue: specific involvement in brown adipocyte differentiation and regulatory role of C/EBPδ". Biochemical Journal 443, № 3 (2012): 799–810. http://dx.doi.org/10.1042/bj20111714.

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Pref-1 (pre-adipocyte factor-1) is known to play a central role in regulating white adipocyte differentiation, but the role of Pref-1 in BAT (brown adipose tissue) has not been analysed. In the present study we found that Pref-1 expression is high in fetal BAT and declines progressively after birth. However, Pref-1-null mice showed unaltered fetal development of BAT, but exhibited signs of over-activation of BAT thermogenesis in the post-natal period. In C/EBP (CCAAT/enhancer-binding protein) α-null mice, a rodent model of impaired fetal BAT differentiation, Pref-1 was dramatically overexpress

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6

Stadion, M., K. Schwerbel, A. Graja, et al. "Interferon activated gene 202b (Ifi202b) promotes Zfp432 expression and suppresses the thermogenic gene program resulting in obesity and insulin resistance." Diabetologie und Stoffwechsel 12, S 01 (2017): S1—S84. http://dx.doi.org/10.1055/s-0037-1601654.

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Koncarevic, Alan, Shingo Kajimura, Milton Cornwall-Brady та ін. "A Novel Therapeutic Approach to Treating Obesity through Modulation of TGFβ Signaling". Endocrinology 153, № 7 (2012): 3133–46. http://dx.doi.org/10.1210/en.2012-1016.

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Obesity results from disproportionately high energy intake relative to energy expenditure. Many therapeutic strategies have focused on the intake side of the equation, including pharmaceutical targeting of appetite and digestion. An alternative approach is to increase energy expenditure through physical activity or adaptive thermogenesis. A pharmacological way to increase muscle mass and hence exercise capacity is through inhibition of the activin receptor type IIB (ActRIIB). Muscle mass and strength is regulated, at least in part, by growth factors that signal via ActRIIB. Administration of a

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8

Dinas, Petros C., Argyro Krase, Eleni Nintou, et al. "Thermogenic Capacity of Human White-Fat: The Actual Picture†." Proceedings 25, no. 1 (2019): 2. http://dx.doi.org/10.3390/proceedings2019025002.

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AIM: Cold exposure and exercise may increase thermogenic capacity of white adipose tissue (WAT), which could subsequently enhance energy expenditure and body weight loss. We aimed to identify possible alterations in uncoupling protein 1 (UCP1)—the main biomarker of thermogenic activation—in human WAT due to both cold exposure and exercise, as well as the link between environmental temperature and thermogenic capacity of human WAT. MATERIAL & METHOD: We conducted four human experimental studies and two systematic reviews and meta-analyses—PROSPERO registration CRD42019120116, CRD42019120213

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9

Mao, Xiaoxiang, Dandan Huang, Caijun Rao, et al. "Enoyl coenzyme A hydratase 1 combats obesity and related metabolic disorders by promoting adipose tissue browning." American Journal of Physiology-Endocrinology and Metabolism 318, no. 3 (2020): E318—E329. http://dx.doi.org/10.1152/ajpendo.00424.2019.

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Browning of white adipose tissue (WAT) has been recognized as an important strategy for the treatment of obesity, insulin resistance, and diabetes. Enoyl coenzyme A hydratase 1 (ECH1) is a widely known enzyme involved in lipid metabolism. However, whether and how ECH1 is implicated in browning of WAT remain obscure. Adeno-associated, virus-mediated genetic engineering of ECH1 in adipose tissue was used in investigations in mouse models of obesity induced by a high-fat diet (HFD) or browning induced by cold exposure. Metabolic parameters showed that ECH1 overexpression decreased weight gain and

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10

Xiong, Yan, Feng Yue, Zhihao Jia, et al. "A novel brown adipocyte-enriched long non-coding RNA that is required for brown adipocyte differentiation and sufficient to drive thermogenic gene program in white adipocytes." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1863, no. 4 (2018): 409–19. http://dx.doi.org/10.1016/j.bbalip.2018.01.008.

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11

Rodríguez-Cuenca, S., M. Monjo, M. Gianotti, A. M. Proenza та P. Roca. "Expression of mitochondrial biogenesis-signaling factors in brown adipocytes is influenced specifically by 17β-estradiol, testosterone, and progesterone". American Journal of Physiology-Endocrinology and Metabolism 292, № 1 (2007): E340—E346. http://dx.doi.org/10.1152/ajpendo.00175.2006.

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Control of mitochondrial biogenesis in brown adipose tissue (BAT), as part of the thermogenesis program, is a complex process that requires the integration of multiple transcription factors to orchestrate mitochondrial and nuclear gene expression. Despite the knowledge of the role of sex hormones on BAT physiology, little is known about the effect of these hormones on the mitochondrial biogenic program. The aim of this study was to determine the effect of testosterone, 17β-estradiol, and progesterone on the expression of nuclear factors involved in the control of mitochondrial biogenesis and t

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12

Villanueva, Claudio J., Laurent Vergnes, Jiexin Wang та ін. "Adipose Subtype-Selective Recruitment of TLE3 or Prdm16 by PPARγ Specifies Lipid Storage versus Thermogenic Gene Programs". Cell Metabolism 17, № 3 (2013): 423–35. http://dx.doi.org/10.1016/j.cmet.2013.01.016.

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13

Yamaguchi, Shintaro, Michael P. Franczyk, Maria Chondronikola, et al. "Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice." Proceedings of the National Academy of Sciences 116, no. 47 (2019): 23822–28. http://dx.doi.org/10.1073/pnas.1909917116.

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Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme for cellular energy metabolism. The aim of the present study was to determine the importance of brown and white adipose tissue (BAT and WAT) NAD+ metabolism in regulating whole-body thermogenesis and energy metabolism. Accordingly, we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice because NAMPT is the rate-limiting NAD+ biosynthetic enzyme. We found ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene pr

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14

Verdeguer, Francisco, Meghan S. Soustek, Maximilian Hatting, et al. "Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity." Molecular and Cellular Biology, October 26, 2015, MCB.00722–15. http://dx.doi.org/10.1128/mcb.00722-15.

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Mitochondrial oxidative and thermogenic function in brown and beige adipose tissues modulate rates of energy expenditure. It is unclear, however, how beige or white adipose tissue contributes to brown fat thermogenic function or compensate for partial deficiencies in this tissue and protect against obesity. Here, we show that the transcription factor YY1 in brown adipose tissue activates the canonical thermogenic and uncoupling gene expression program. In contrast, YY1 represses a series of secreted proteins including FGF21, BMP8b, GDF15, Angptl6, Neuromedin B and Nesfatin linked to energy exp

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15

Yi, Danielle, Hai P. Nguyen, Jennie Dinh, et al. "Dot1l interacts with Zc3h10 to activate Ucp1 and other thermogenic genes." eLife 9 (October 27, 2020). http://dx.doi.org/10.7554/elife.59990.

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Brown adipose tissue is a metabolically beneficial organ capable of dissipating chemical energy into heat, thereby increasing energy expenditure. Here, we identify Dot1l, the only known H3K79 methyltransferase, as an interacting partner of Zc3h10 that transcriptionally activates the Ucp1 promoter and other BAT genes. Through a direct interaction, Dot1l is recruited by Zc3h10 to the promoter regions of thermogenic genes to function as a coactivator by methylating H3K79. We also show that Dot1l is induced during brown fat cell differentiation and by cold exposure and that Dot1l and its H3K79 met

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16

Huang, Paul, and Sylvia Lee-Huang. "Abstract 13115: Nitric Oxide Differentially Regulates White and Brown Adipogenesis Through Effects on Thermogenesis and Mitochondrial Biogenesis (Best of Basic Science Abstract)." Circulation 132, suppl_3 (2015). http://dx.doi.org/10.1161/circ.132.suppl_3.13115.

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Introduction: In addition to its roles as a vascular signaling molecule, nitric oxide (NO) plays roles in metabolism. Mice deficient in eNOS are overweight and develop insulin resistance. It is not known whether the metabolic effects are due to primary roles of NO, or to increased visceral adiposity, leading to secondary metabolic changes. Hypothesis: We hypothesized that NO plays distinct and separable primary roles in white and brown adipogenesis, which underlie the effects on adiposity, energy metabolism, and expression of thermogenic genes. Methods: We exposed wild-type and mice carrying s

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17

Artsi, Hanna, Irina Gurt, Madi El-Haj, et al. "Sirt1 Promotes a Thermogenic Gene Program in Bone Marrow Adipocytes: From Mice to (Wo)Men." Frontiers in Endocrinology 10 (February 28, 2019). http://dx.doi.org/10.3389/fendo.2019.00126.

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18

Colitti, Monica, Federico Boschi та Tommaso Montanari. "Dynamic of lipid droplets and gene expression in response to β-aminoisobutyric acid treatment on 3T3-L1 cells". European Journal of Histochemistry 62, № 4 (2018). http://dx.doi.org/10.4081/ejh.2018.2984.

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Research on adipobiology has recognized the browning process of white adipocytes as a potential therapeutic strategy for the treatment of obesity and related morbidities. Physical exercise stimulates the secretion of myokines, such as b-aminoisobutyric acid (BAIBA), which in turn promotes adaptive thermogenesis. White adipocyte conversion to brown cells involves dynamic changes in lipid droplet (LD) dimension and in the transcription of brown-specific marker genes. This study analyzes the effect of different doses of BAIBA and at different days of development on 3T3-L1 cells by evaluating morp

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19

Shi, Fubiao, and Sheila Collins. "Second messenger signaling mechanisms of the brown adipocyte thermogenic program: an integrative perspective." Hormone Molecular Biology and Clinical Investigation, September 26, 2017. http://dx.doi.org/10.1515/hmbci-2017-0062.

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Abstractβ-adrenergic receptors (βARs) are well established for conveying the signal from catecholamines to adipocytes. Acting through the second messenger cyclic adenosine monophosphate (cAMP) they stimulate lipolysis and also increase the activity of brown adipocytes and the ‘browning’ of adipocytes within white fat depots (so-called ‘brite’ or ‘beige’ adipocytes). Brown adipose tissue mitochondria are enriched with uncoupling protein 1 (UCP1), which is a regulated proton channel that allows the dissipation of chemical energy in the form of heat. The discovery of functional brown adipocytes i

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20

Park, Sung-Soo, Yeon-Joo Lee, Hyuno Kang та ін. "Lactobacillus amylovorus KU4 ameliorates diet-induced obesity in mice by promoting adipose browning through PPARγ signaling". Scientific Reports 9, № 1 (2019). http://dx.doi.org/10.1038/s41598-019-56817-w.

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AbstractBrowning of white adipose tissue (WAT) is currently considered a potential therapeutic strategy to treat diet-induced obesity. While some probiotics have protective effects against diet-induced obesity, the role of probiotics in adipose browning has not been explored. Here, we show that administration of the probiotic bacterium Lactobacillus amylovorus KU4 (LKU4) to mice fed a high-fat diet (HFD) enhanced mitochondrial levels and function, as well as the thermogenic gene program (increased Ucp1, PPARγ, and PGC-1α expression and decreased RIP140 expression), in subcutaneous inguinal WAT

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21

Auclair, Martine, Natacha Roblot, Emilie Capel, Bruno Fève та Benedicte Antoine. "Pharmacological modulation of RORα controls the fat browning, adaptive thermogenesis and body weight in mice". American Journal of Physiology-Endocrinology and Metabolism, 30 листопада 2020. http://dx.doi.org/10.1152/ajpendo.00131.2020.

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Beiging is an attractive therapeutic strategy to fight against obesity and its side metabolic complications. The loss of function of the nuclear transcription factor RORa has been related to a lean phenotype with higher thermogenesis in sg/sg mice lacking this protein. Here we show that pharmacological modulation of RORa activity exerts reciprocal and cell-autonomous effect on UCP1 expression ex vivo, in cellulo and in vivo. The RORa inverse-agonist SR3335 up-regulated UCP1 expression in brown and subcutaneous white adipose tissue (scWAT) explants of WT mice, while the RORa agonist SR1078 had

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22

Li, Yu, Xiaodan Ping, Yankang Zhang та ін. "Comparative Transcriptome Profiling of Cold Exposure and β3-AR Agonist CL316,243-Induced Browning of White Fat". Frontiers in Physiology 12 (4 травня 2021). http://dx.doi.org/10.3389/fphys.2021.667698.

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Beige adipocytes are newly identified thermogenic-poised adipocytes that could be activated by cold or β3-adrenergic receptor (β3-AR) signaling and offer therapeutic potential for treating obesity and metabolic diseases. Here we applied RNA-sequencing analysis in the beige fat of mice under cold exposure or β3-AR agonist CL316,243 (CL) treatment to provide a comparative and comprehensive analysis for the similarity and heterogeneity of these two stimulants. Importantly, via KEGG analysis, we found that cold and CL commonly induced oxidative phosphorylation. Meanwhile, cold increased glycerolip

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23

Bast-Habersbrunner, Andrea, Christoph Kiefer, Peter Weber, et al. "The Long Noncoding RNA Ctcflos Orchestrates Transcriptional and Post-Transcriptional Alternative Splicing Programs Essential for Thermogenic Gene Expression in Brite Adipocytes." SSRN Electronic Journal, 2020. http://dx.doi.org/10.2139/ssrn.3606292.

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24

Chinnasamy, Prameladevi, Aparna Srinivasan, Isabel Casimiro, Dario F. Riascos-Bernal, and Nicholas E. Sibinga. "Abstract 51: Allograft Inflammatory Factor-1 Deficiency Prevents Obesity and Insulin Resistance by Promoting Brown and Beige Adipocyte Thermogenic Programs." Arteriosclerosis, Thrombosis, and Vascular Biology 36, suppl_1 (2016). http://dx.doi.org/10.1161/atvb.36.suppl_1.51.

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Objectives: Human population studies link sequence variants near the allograft inflammatory factor (Aif)-1 locus with obesity, adipose inflammation, and diabetes, conditions strongly associated with cardiovascular disease. We assessed possible causal roles of Aif-1 in these conditions using mouse models. Hypothesis: Aif-1 promotes obesity, adipose inflammation, and glucose intolerance. Methods: We generated Aif-1-deficient ( aif-1 -/- ) mice and fed them a normal or high fat diet (ND or HFD, respectively) for 16 weeks. Body composition was analyzed by microCT scan, tissues by macroscopic and m

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25

Rubio, Blanca M., Cristina Mora, Lorena Mazuecos, et al. "SUN-570 The Crosstalk Between Central Leptin and PPARbeta/delta Protects the Heart Against Oxidative Stress Damage and the Development of Hypertrophy." Journal of the Endocrine Society 4, Supplement_1 (2020). http://dx.doi.org/10.1210/jendso/bvaa046.1932.

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Abstract Cardiovascular disease is a common cause of morbidity and mortality in obese people with type 2 diabetes, which is often associated with increased levels of leptin. While many studies hint at the existence of important roles for both hyperleptinemia and leptin resistance in obesity and diabetes-associated cardiovascular disease, others support that leptin has cardioprotective effects. Leptin action comprises direct effects on cardiac tissue and indirect effects mediated via the sympathetic nervous system. Since the molecular underpinnings of leptin-regulated pathways in cardiac tissue

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