Diet-induced Obesity and Brown Adipose Tissue

2015 ◽  
pp. 81-95
Author(s):  
Jean Himms-Hagen ◽  
Jingying Cui
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Brown Adipose

scholarly journals Effects of stem cells from inducible brown adipose tissue on diet-induced obesity in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Enrique Calvo ◽  
Noelia Keiran ◽  
Catalina Núñez-Roa ◽  
Elsa Maymó-Masip ◽  
Miriam Ejarque ◽  
...  
Keyword(s):  
Stem Cells ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Therapeutic Option ◽  
Metabolic Activation ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Obesity In Mice ◽  
Treatment Of Obesity ◽  
Visceral Adipose

AbstractAdipose-derived mesenchymal stem cells (ASCs) are a promising option for the treatment of obesity and its metabolic co-morbidities. Despite the recent identification of brown adipose tissue (BAT) as a potential target in the management of obesity, the use of ASCs isolated from BAT as a therapy for patients with obesity has not yet been explored. Metabolic activation of BAT has been shown to have not only thermogenic effects, but it also triggers the secretion of factors that confer protection against obesity. Herein, we isolated and characterized ASCs from the visceral adipose tissue surrounding a pheochromocytoma (IB-hASCs), a model of inducible BAT in humans. We then compared the anti-obesity properties of IB-hASCs and human ASCs isolated from visceral white adipose tissue (W-hASCs) in a murine model of diet-induced obesity. We found that both ASC therapies mitigated the metabolic abnormalities of obesity to a similar extent, including reducing weight gain and improving glucose tolerance. However, infusion of IB-hASCs was superior to W-hASCs in suppressing lipogenic and inflammatory markers, as well as preserving insulin secretion. Our findings provide evidence for the metabolic benefits of visceral ASC infusion and support further studies on IB-hASCs as a therapeutic option for obesity-related comorbidities.

scholarly journals Does a high-fat diet-induced obesity model brown adipose tissue thermogenesis? A systematic review

2019 ◽  
Author(s):  
Gabriela S. Perez ◽  
Gabriele D.S. Cordeiro ◽  
Lucimeire S. Santos ◽  
Djane D.A. Espírito-Santo ◽  
Gilson T. Boaventura ◽  
...  
Keyword(s):  
Systematic Review ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

scholarly journals Chronic dietary supplementation of proanthocyanidins corrects the mitochondrial dysfunction of brown adipose tissue caused by diet-induced obesity in Wistar rats

2011 ◽  
Vol 107 (2) ◽  
pp. 170-178 ◽  
Author(s):  
David Pajuelo ◽  
Helena Quesada ◽  
Sabina Díaz ◽  
Anabel Fernández-Iglesias ◽  
Anna Arola-Arnal ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Sirtuin 1 ◽  
Male Rats ◽  
Diet Induced Obesity ◽  
Brown Adipose

The present study aims to determine the effects of grape seed proanthocyanidin extract (GSPE) on brown adipose tissue (BAT) mitochondrial function in a state of obesity induced by diet. Wistar male rats were fed with a cafeteria diet (Cd) for 4 months; during the last 21 d, two groups were treated with doses of 25 and 50 mg GSPE/kg body weight. In the BAT, enzymatic activities of citrate synthase, cytochrome c oxidase (COX) and ATPase were determined and gene expression was analysed by real-time PCR. The mitochondrial function of BAT was determined in fresh mitochondria by high-resolution respirometry using both pyruvate and carnitine–palmitoyl-CoA as substrates. The results show that the Cd causes an important decrease in the gene expression of sirtuin 1, nuclear respiratory factor 1, isocitrate dehydrogenase 3γ and COX5α and, what is more telling, decreases the levels of mitochondrial respiration both with pyruvate and canitine–palmitoyl-CoA. Most of these parameters, which are indicative of mitochondrial dysfunction due to diet-induced obesity, are improved by chronic supplementation of GSPE. The beneficial effects caused by the administration of GSPE are exhibited as a protection against weight gain, in spite of the Cd the rats were fed. These data indicate that chronic consumption of a moderate dose of GSPE can correct an energy imbalance in a situation of diet-induced obesity, thereby improving the mitochondrial function and thermogenic capacity of the BAT.

scholarly journals Angiotensin 1–7 stimulates brown adipose tissue and reduces diet-induced obesity

2018 ◽  
Vol 314 (2) ◽  
pp. E131-E138 ◽  
Author(s):  
Hidechika Morimoto ◽  
Jun Mori ◽  
Hisakazu Nakajima ◽  
Yasuhiro Kawabe ◽  
Yusuke Tsuma ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Renin Angiotensin System ◽  
Hormone Sensitive Lipase ◽  
Brown Adipocyte ◽  
Metabolic Complications ◽  
Subcutaneous White Adipose Tissue ◽  
Beneficial Effects ◽  
Diet Induced Obesity ◽  
Brown Adipose

The renin-angiotensin system is a key regulator of metabolism with beneficial effects of the angiotensin 1–7 (Ang 1–7) peptide. We hypothesized that the antiobesity effect of Ang 1–7 was related to the stimulation of brown adipose tissue (BAT). We administered Ang 1–7 (0.54 mg kg−1 day−1) for 28 days via implanted micro-osmotic pumps to mice with high-fat diet (HFD)-induced obesity. Ang 1–7 treatment reduced body weight, upregulated thermogenesis, and ameliorated impaired glucose homeostasis without affecting food consumption. Furthermore, Ang 1–7 treatment enlarged BAT and the increased expression of UCP1, PRDM16, and prohibitin. Alterations in PRDM16 expression correlated with increased AMPK and phosphorylation of mTOR. Ang 1–7 treatment elevated thermogenesis in subcutaneous white adipose tissue without altering UCP1 expression. These changes occurred in the context of decreased lipid accumulation in BAT from HFD-fed mice, preserved insulin signaling concomitant with phosphorylation of hormone-sensitive lipase and decreased expression of perilipin. These data suggest that Ang 1–7 induces brown adipocyte differentiation leading to upregulation of thermogenesis and improved metabolic profile in diet-induced obesity. Enhancing Ang 1–7 action represents a promising therapy to increase BAT and to reduce the metabolic complications associated with diet-induced obesity.

Short-term resistance to diet-induced obesity in A/J mice is not associated with regulation of hypothalamic neuropeptides

2004 ◽  
Vol 287 (4) ◽  
pp. E662-E670 ◽  
Author(s):  
John W. Bullen ◽  
Mary Ziotopoulou ◽  
Linda Ungsunan ◽  
Jatin Misra ◽  
Ilias Alevizos ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Microarray Analysis ◽  
Energy Homeostasis ◽  
Uncoupling Protein ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Hypothalamic Neuropeptides ◽  
Fat Feeding

To investigate the mechanisms underlying long-term resistance of the A/J mouse strain to diet-induced obesity, we studied, over a period of 4 wk, the expression of uncoupling proteins in brown adipose tissue and the expression of hypothalamic neuropeptides known to regulate energy homeostasis and then used microarray analysis to identify other potentially important hypothalamic peptides. Despite increased caloric intake after 2 days of high-fat feeding, body weights of A/J mice remained stable. On and after 1 wk of high-fat feeding, A/J mice adjusted their food intake to consume the same amount of calories as mice fed a low-fat diet; thus their body weight and insulin, corticosterone, free fatty acid, and glucose levels remained unchanged for 4 wk. We found no changes in hypothalamic expression of several orexigenic and/or anorexigenic neuropeptides known to play an important role in energy homeostasis for the duration of the study. Uncoupling protein-2 mRNA expression in brown adipose tissue, however, was significantly upregulated after 2 days of high-fat feeding and tended to remain elevated for the duration of the 4-wk study. Gene array analysis revealed that several genes are up- or downregulated in response to 2 days and 1 wk of high-fat feeding. Real-time PCR analysis confirmed that expression of the hypothalamic IL-1 pathway (IL-1β, IL-1 type 1 and 2 receptors, and PPM1b/PP2C-β, a molecule that has been implicated in the inhibition of transforming growth factor-β-activated kinase-1-mediated IL-1 action) is altered after 2 days, but not 1 wk, of high-fat feeding. The role of additional molecules discovered by microarray analysis needs to be further explored in the future.

scholarly journals Deletion of Letmd1 leads to the disruption of mitochondrial function in brown adipose tissue

2020 ◽  
Author(s):  
Runjie Song ◽  
Yaqi Du ◽  
Peng Li ◽  
Huijiao Liu ◽  
Han Zheng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Energy Homeostasis ◽  
Mitochondrial Calcium ◽  
List Type ◽  
Insulin Resistant ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Clinical Biomarker ◽  
Mitochondrial Membrane Protein

AbstractHuman cervical cancer oncogene (HCCR-1), also named as LETMD1, is a LETM-domain containing outer mitochondrial membrane protein which plays an important role in the carcinogenesis of cancers. Surprisingly, we found that loss of Letmd1 in mice leads to multiply severe abnormities, such as the brown adipose tissue (BAT) whitening, disruption of thermogenesis, cold-induced death, diet-induced obesity, hyperglycinemia and insulin resistance. Mechanistically, deletion of Letmd1 in BAT causes the reduction of mitochondrial calcium ion, which in turn results in the suppressed fission of mitochondria, and ultimately leads to the depletion of Ucp1-mediated BAT heat production. This study indicates that LETMD1 plays a crucial role in controlling BAT thermogenesis and energy homeostasis by regulating mitochondrial structures and functions, and also provides a novel insight for the clinical biomarker and therapeutical target of oncogene for the metabolic disorders.HighlightsLetmd1 is an oncogene and also highly expressed in brown adipose tissue (BAT) of human and mice.Loss of Letmd1 leads to BAT whitening, diet-induced obesity, hyperglycemia and insulin resistant.Letmd1 knockout causes the disruption of thermogenesis and death at 4°C exposure.Deletion of Letmd1 results in mitochondrial calcium homeostasis disorders.Graphic abstract

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