scholarly journals TRPV1 Expression in Adipose Tissues Determines Metabolic Activity and Energy Expression to Counter Diet-Induced Obesity

2017 ◽  
Vol 112 (3) ◽  
pp. 408a-409a
Author(s):  
Baskaran Thyagarajan ◽  
Padmamalini Baskaran
Keyword(s):  
Metabolic Activity ◽  
Adipose Tissues ◽  
Energy Expression ◽  
Diet Induced Obesity

scholarly journals The depot-specific and essential roles of CBP/p300 in regulating adipose plasticity

2019 ◽  
Vol 240 (2) ◽  
pp. 257-269 ◽  
Author(s):  
Maria Namwanje ◽  
Longhua Liu ◽  
Michelle Chan ◽  
Nikki Aaron ◽  
Michael J Kraakman ◽  
...  
Keyword(s):  
Body Weight ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Knockout Mice ◽  
Metabolic Disorders ◽  
Physiological Effects ◽  
Double Knockout ◽  
Adipose Tissues ◽  
Diet Induced Obesity ◽  
Specific Deletion

Fat remodeling has been extensively explored through protein deacetylation, but not yet acetylation, as a viable therapeutic approach in the management of obesity and related metabolic disorders. Here, we investigated the functions of key acetyltransferases CBP/p300 in adipose remodeling and their physiological effects by generating adipose-specific deletion of CBP (Cbp-AKO), p300 (p300-AKO) and double-knockout (Cbp/p300-AKO) models. We demonstrated that Cbp-AKO exhibited marked brown remodeling of inguinal WAT (iWAT) but not epididymal WAT (eWAT) after cold exposure and that this pattern was exaggerated in diet-induced obesity (DIO). Despite this striking browning phenotype, loss of Cbp was insufficient to impact body weight or glucose tolerance. In contrast, ablation of p300 in adipose tissues had minimal effects on fat remodeling and adiposity. Surprisingly, double-knockout mice (Cbp/p300-AKO) developed severe lipodystrophy along with marked hepatic steatosis, hyperglycemia and hyperlipidemia. Furthermore, we demonstrated that pharmacological inhibition of Cbp and p300 activity suppressed adipogenesis. Collectively, these data suggest that (i) CBP, but not p300, has distinct functions in regulating fat remodeling and that this occurs in a depot-selective manner; (ii) brown remodeling occurs independently of the improvements in glucose metabolism and obesity and (iii) the combined roles of CBP and p300 are indispensable for normal adipose development.

scholarly journals Transketolase Deficiency in Adipose Tissues Protects Mice From Diet-Induced Obesity by Promoting Lipolysis

Diabetes ◽  
2020 ◽  
Vol 69 (7) ◽  
pp. 1355-1367 ◽  
Author(s):  
Na Tian ◽  
Qi Liu ◽  
Yakui Li ◽  
Lingfeng Tong ◽  
Ying Lu ◽  
...  
Keyword(s):  
Adipose Tissues ◽  
Diet Induced Obesity

scholarly journals Metabolic activity of the enteric microbiota influences the fatty acid composition of murine and porcine liver and adipose tissues

2009 ◽  
Vol 89 (5) ◽  
pp. 1393-1401 ◽  
Author(s):  
Rebecca Wall ◽  
R Paul Ross ◽  
Fergus Shanahan ◽  
Liam O’Mahony ◽  
Caitlin O’Mahony ◽  
...  
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Metabolic Activity ◽  
Porcine Liver ◽  
Adipose Tissues

Obesity enhances the recruitment of mesenchymal stem cell to visceral adipose tissue

2021 ◽  
Author(s):  
Agatha Assis-Ferreira ◽  
Roberta F.g. Saldanha-Gama ◽  
Natalia M de Brito ◽  
Mariana Renovato-Martins ◽  
Rafael L Simões ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Adipose Tissues ◽  
Migratory Response ◽  
Migratory Activity ◽  
Diet Induced Obesity ◽  
Pathway Activation ◽  
Tnf Α ◽  
Marrow Mesenchymal Stem Cells ◽  
Spontaneous Migration ◽  
Visceral Adipose

In obesity, high levels of TNF-α in the bone marrow microenvironment induces the bone marrow-mesenchymal stem cells (BM-MSCs) towards a pro-adipogenic phenotype. Here, we investigated the effect of obesity on the migratory potential of BM-MSCs and their fate towards the adipose tissues. BM-MSCs were isolated from male C57Bl/06 mice with high-fat diet-induced obesity. The migratory potential of the BM-MSCs, their presence in the subcutaneous (SAT) and the visceral adipose tissues (VAT), and the possible mechanisms involved were investigated. Obesity did not affect MSC content in the bone marrow but increased the frequency of MSCs in blood, SAT, and VAT. In these animals, the SAT adipocytes presented a larger area, without any changes in adipokine production or the SDF-1α gene expression. In contrast, in VAT, obesity increased leptin and IL-10 levels but did not modify the size of the adipocytes. The BM-MSCs from obese animals presented increased spontaneous migratory activity. Despite the augmented expression of CXCR4, these cells exhibited decreased migratory response toward SDF-1α, compared to that of BM-MSCs from lean mice. The PI3K-AKT pathway activation seems to mediate the migration of BM-MSCs from lean mice, but not from obese mice. Additionally, we observed an increase in the spontaneous migration of BM-MSCs from lean mice when they were co-cultured with BM-HCs from obese animals, suggesting a paracrine effect. We concluded that obesity increased the migratory potential of the BM-MSCs and induced their accumulation in VAT, which may represent an adaptive mechanism in response to chronic nutrient overload.

scholarly journals The Mediator subunit MED20 organizes the early adipogenic complex to promote development of adipose tissues and diet-induced obesity

Cell Reports ◽  
2021 ◽  
Vol 36 (1) ◽  
pp. 109314
Author(s):  
Wen-Shuai Tang ◽  
Li Weng ◽  
Xu Wang ◽  
Chang-Qin Liu ◽  
Guo-Sheng Hu ◽  
...  
Keyword(s):  
Adipose Tissues ◽  
Diet Induced Obesity

scholarly journals High-Fat Diet Alters the Expression of Reference Genes in Male Mice

2020 ◽  
Vol 7 ◽  
Author(s):  
Xiuqin Fan ◽  
Hongyang Yao ◽  
Xuanyi Liu ◽  
Qiaoyu Shi ◽  
Liang Lv ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Reference Genes ◽  
Molecular Mechanisms ◽  
Obese Mouse ◽  
Mrna Levels ◽  
High Fat ◽  
Adipose Tissues ◽  
Obesity Epidemic ◽  
Diet Induced Obesity

Quantitative PCR (qPCR), the most accurate and sensitive technique for quantifying mRNA expression, and choice of appropriate reference genes for internal error controlling in qPCR are essential to understanding the molecular mechanisms that drive the obesity epidemic and its comorbidities. In this study, using the high-fat diet (HFD)-induced obese mouse model, we assessed the expression of 10 commonly used reference genes to validate gene-expression stability in adipose tissue, liver, and muscle across different time points (4, 8, 12, and 16 weeks after HFD feeding) during the process of obesity. The data were analyzed by the GeNorm, NormFinder, BestKeeper, and Delta-Ct method, and the results showed that the most stable reference genes were different for a specific organ or tissue in a specific time point; however, PPIA, RPLP0, and YWHAZ were the top three most stable reference genes in qPCR experiments on adipose, hepatic tissues, and muscles of mice in diet-induced obesity. In addition, the mostly used genes ACTB and GAPDH were more unstable in the fat and liver, the ACTB mRNA levels were increased in four adipose tissues, and the GAPDH mRNA levels were decreased in four adipose tissues and liver after HFD feeding. These results suggest that PPIA, RPLP0, or YWHAZ may be more appropriate to be used as reference gene than ACTB and GAPDH in the adipose tissue and liver of mice during the process of high-fat diet-induced obesity.

Involvement of SIK2/TORC2 signaling cascade in the regulation of insulin-induced PGC-1α and UCP-1 gene expression in brown adipocytes

2009 ◽  
Vol 296 (6) ◽  
pp. E1430-E1439 ◽  
Author(s):  
Masaaki Muraoka ◽  
Aiko Fukushima ◽  
Say Viengchareun ◽  
Marc Lombès ◽  
Fukuko Kishi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transgenic Mice ◽  
Binding Protein ◽  
Uncoupling Protein ◽  
Brown Adipocytes ◽  
Adipose Tissues ◽  
Fatty Acid Binding ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
The Impact

Salt-inducible kinase 2 (SIK2) is expressed abundantly in adipose tissues and represses cAMP-response element-binding protein (CREB)-mediated gene expression by phosphorylating the coactivator transducer of regulated CREB activity (TORC2). Phosphorylation at Ser587 of SIK2 diminishes its TORC2 phosphorylation activity. In 3T3-L1 white adipocytes, SIK2 downregulates lipogenic gene in response to nutritional stresses. To investigate the impact of SIK2 on the function of brown adipose tissue (BAT), we used T37i brown adipocytes, mice with diet-induced obesity, and SIK2 mutant (S587A) transgenic mice. When T37i adipocytes were treated with insulin, the levels of peroxisome proliferator-activated receptor-coactivator-1α ( PGC-1α) and uncoupling protein-1 ( UCP-1) mRNA were increased, and the induction was inhibited by overexpression of SIK2 (S587A) mutant or dominant-negative CREB. Insulin enhanced SIK2 phosphorylation at Ser587, which was accompanied by decrease in phospho-TORC2. Similarly, the decrease in the level of SIK2 phosphorylation at Ser587 was observed in the BAT of mice with diet-induced obesity, which was negatively correlated with TORC2 phosphorylation. To confirm the negative correlation between SIK2 phosphorylation at Ser587 and TORC2 phosphorylation in BAT, SIK2 mutant (S587A) was overexpressed in adipose tissues by using the adipocyte fatty acid-binding protein 2 promoter. The expression of recombinant SIK2 (S587A) was restricted to BAT, and the levels of phospho-TORC2 were elevated in BAT of transgenic mice. Male transgenic mice developed high-fat diet-induced obesity, and their BAT expressed low levels of PGC-1α and UCP-1 mRNA, suggesting that SIK2-TORC2 cascade may be important for the regulation of PGC-1α and UCP-1 gene expression in insulin signaling in BAT.

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