scholarly journals Withaferin A Promotes White Adipose Browning and Prevents Obesity Through Sympathetic Nerve-Activated Prdm16-FATP1 Axis

2021 ◽  
Author(s):  
Bingbing Guo ◽  
Jiarui Liu ◽  
Bingwei Wang ◽  
Chenyu Zhang ◽  
Zhijie Su ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Sympathetic Nerve ◽  
High Fat Diet ◽  
Respiratory Exchange Ratio ◽  
Withaferin A ◽  
High Fat ◽  
Leptin Signaling ◽  
Effective Strategies ◽  
Prevalence Of Obesity ◽  
Chemical Denervation

The increasing prevalence of obesity has resulted in demands for the development of new effective strategies for obesity treatment. The Withaferin A (WA) shows a great potential for prevention of obesity by sensitizing leptin signaling in the hypothalamus. However, the mechanism underlying the weight- and adiposity-reducing effects of WA remains to be elucidated. Here, we report that WA treatment induced white adipose tissue (WAT) browning, elevated energy expenditure (EE), decreased respiratory exchange ratio (RER), and prevented high-fat diet (HFD)-induced obesity. The sympathetic chemical denervation dampened the WAT browning and also impeded the reduction of adiposity in WA-treated mice. WA markedly up-regulated the levels of Prdm16 and FATP1 (Slc27a1) in the inguinal WAT (iWAT), and this was blocked by sympathetic denervation. Prdm16 or FATP1 knockdown in iWAT abrogated the WAT browning-inducing effects of WA, and restored the weight gain and adiposity in WA-treated mice. Together, these findings suggest that WA induces WAT browning through the sympathetic nerve-adipose axis; and the adipocytic Prdm16-FATP1 pathway mediates the promotive effects of WA on white adipose browning.

scholarly journals Withaferin A Promotes White Adipose Browning and Prevents Obesity Through Sympathetic Nerve-Activated Prdm16-FATP1 Axis

2021 ◽  
Author(s):  
Bingbing Guo ◽  
Jiarui Liu ◽  
Bingwei Wang ◽  
Chenyu Zhang ◽  
Zhijie Su ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Sympathetic Nerve ◽  
High Fat Diet ◽  
Respiratory Exchange Ratio ◽  
Withaferin A ◽  
High Fat ◽  
Leptin Signaling ◽  
Effective Strategies ◽  
Prevalence Of Obesity ◽  
Chemical Denervation

The increasing prevalence of obesity has resulted in demands for the development of new effective strategies for obesity treatment. The Withaferin A (WA) shows a great potential for prevention of obesity by sensitizing leptin signaling in the hypothalamus. However, the mechanism underlying the weight- and adiposity-reducing effects of WA remains to be elucidated. Here, we report that WA treatment induced white adipose tissue (WAT) browning, elevated energy expenditure (EE), decreased respiratory exchange ratio (RER), and prevented high-fat diet (HFD)-induced obesity. The sympathetic chemical denervation dampened the WAT browning and also impeded the reduction of adiposity in WA-treated mice. WA markedly up-regulated the levels of Prdm16 and FATP1 (Slc27a1) in the inguinal WAT (iWAT), and this was blocked by sympathetic denervation. Prdm16 or FATP1 knockdown in iWAT abrogated the WAT browning-inducing effects of WA, and restored the weight gain and adiposity in WA-treated mice. Together, these findings suggest that WA induces WAT browning through the sympathetic nerve-adipose axis; and the adipocytic Prdm16-FATP1 pathway mediates the promotive effects of WA on white adipose browning.

scholarly journals Withaferin A promotes white adipose browning and prevents obesity through sympathetic nerve-activated Prdm16-FATP1 axis

2021 ◽  
Author(s):  
Ruimao Zheng ◽  
Bingbing Guo ◽  
Jiarui Liu ◽  
Bingwei Wang ◽  
Chenyu Zhang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Sympathetic Nerve ◽  
High Fat Diet ◽  
Respiratory Exchange Ratio ◽  
Withaferin A ◽  
High Fat ◽  
Leptin Signaling ◽  
Prevalence Of Obesity ◽  
Chemical Denervation ◽  
New Strategies

The increasing prevalence of obesity causes demands for new strategies for obesity treatment. Withaferin A (WA) shows a great potential for obesity prevention by sensitizing leptin signaling in hypothalamus. However, the mechanism underlying weight- and adiposity-reducing effects of WA remains elusive. We report that WA induced white adipose tissue (WAT) browning, elevated energy expenditure (EE), decreased respiratory exchange ratio (RER), and prevented high-fat diet (HFD)-induced obesity. Sympathetic chemical denervation dampened WAT browning and impeded reduction of adiposity in WA-treated mice. WA up-regulated the levels of Prdm16 and FATP1 (Slc27a1) in the inguinal WAT (iWAT), and this was blocked by sympathetic denervation. Prdm16 or FATP1 knockdown in iWAT abrogated WAT browning-inducing effects of WA, and restored weight gain and adiposity in WA-treated mice. Together, these findings suggest that WA induces WAT browning through the sympathetic nerve-adipose axis; and the adipocytic Prdm16-FATP1 pathway mediates the promotive effects of WA on WAT browning.

scholarly journals Adipose tissue-derived autotaxin causes cardiomyopathy in obese mice

2019 ◽  
Vol 63 (2) ◽  
pp. 113-121 ◽  
Author(s):  
Yousheng Xu ◽  
Yongshun Wang ◽  
Jingjin Liu ◽  
Wei Cao ◽  
Lili Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Cardiac Fibrosis ◽  
Left Ventricular ◽  
Obese Mice ◽  
High Fat ◽  
Structural Disorders ◽  
Pathophysiological Role ◽  
Prevalence Of Obesity

The prevalence of obesity is dramatic increased and strongly associated with cardiovascular disease. Adipokines, secreted from adipose tissues, are critical risk factors for the development of cardiomyopathy. Present study aimed to investigate the pathophysiological role of autotaxin in obesity-related cardiomyopathy. In high-fat diet-fed mice, autotaxin was mainly synthesized and secreted from adipocytes. The increased accumulation of cardiac autotaxin was positively associated with cardiac dysfunction in obese mice. Interestingly, specific blockage of adipose tissue autotaxin effectively protected against high-fat diet-induced cardiac structural disorders, left ventricular hypertrophy and dysfunction. Inhibition of autotaxin further improved high-fat diet-induced cardiac fibrosis and mitochondrial dysfunction, including improvement of mitochondrial structure, mass and activities. Our findings demonstrated intervention of adipose tissue biology could influence cardiac modification in obese mice, and adipocyte-derived autotaxin was a potential diagnostic marker and therapeutic target for obesity-related cardiomyopathy.

Inhibition of Adipose Tissue Angiogenesis Prevents Rebound Weight Regain after Calorie Restriction Independent of Hypothalamic Melanocortin System in Obese Mice Fed a High-Fat Diet

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 287-LB
Author(s):  
HYE-JIN LEE ◽  
MUN-GYU SONG ◽  
NA-HEE HA ◽  
BO-YEONG JIN ◽  
SANG-HYUN CHOI ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Calorie Restriction ◽  
High Fat Diet ◽  
Weight Regain ◽  
Obese Mice ◽  
High Fat ◽  
Melanocortin System

scholarly journals Anti-Obesity and Hypocholesterolemic Actions of Protamine-Derived Peptide RPR (Arg-Pro-Arg) and Protamine in High-Fat Diet-Induced C57BL/6J Mice

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2501
Author(s):  
Maihemuti Mijiti ◽  
Ryosuke Mori ◽  
Bingyu Huang ◽  
Kenichiro Tsukamoto ◽  
Keisuke Kiriyama ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Fecal Excretion ◽  
Control Group ◽  
High Fat ◽  
Tissue Weight ◽  
Cholesterol Levels ◽  
Adipose Tissue Weight ◽  
Fas Mrna ◽  
Hypocholesterolemic Peptide

Dietary protamine can ameliorate hyperlipidemia; however, the protamine-derived active peptide and its hypolipidemic mechanism of action are unclear. Here, we report the discovery of a novel anti-obesity and hypocholesterolemic peptide, RPR (Arg-Pro-Arg), derived from protamine in mice fed a high-fat diet for 50 days. Serum cholesterol levels were significantly lower in the protamine and RPR groups than in the control group. White adipose tissue weight was significantly decreased in the protamine and RPR groups. The fecal excretion of cholesterol and bile acid was significantly higher in the protamine and RPR groups than in the control group. We also observed a significant decrease in the expression of hepatic SCD1, SREBP1, and adipocyte FAS mRNA, and significantly increased expression of hepatic PPARα and adipocyte PPARγ1 mRNA in the protamine group. These findings demonstrate that the anti-obesity effects of protamine are linked to the upregulation of adipocyte PPARγ1 and hepatic PPARα and the downregulation of hepatic SCD1 via SREBP1 and adipocyte FAS. RPR derived from protamine has a crucial role in the anti-obesity action of protamine by evaluating the effective dose of adipose tissue weight loss.

Inhibitory Effects of Fermented Ougan (Citrus reticulata cv. Suavissima) Juice on High-Fat Diet-induced Obesity Associated with White Adipose Tissue Browning and Gut Microbiota Modulation in Mice

2021 ◽  
Author(s):  
Xiao Guo ◽  
Xuedan Cao ◽  
Xiugui Fang ◽  
Ailing Guo ◽  
Erhu Li
Keyword(s):  
Adipose Tissue ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Citrus Reticulata ◽  
Inhibitory Effects ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Tissue Browning

In this study, Ougan juice (OJ) and lactic acid bacteria fermented Ougan juice (FOJ) were investigated individually for their capability of preventing obesity in high-fat diet (HFD)-fed C57BL/6J mice. After...

Trans-palmitoleic Acid Reduces Adiposity via Increased Lipolysis in a Rodent Model of Diet-Induced Obesity

2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Rodent Model ◽  
Adipocyte Size ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Visceral Adipose

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

Irisin induces white adipose tissue browning in mice as assessed by magnetic resonance imaging

2021 ◽  
pp. 153537022110060
Author(s):  
Yue Chen ◽  
Jie Ding ◽  
Yufei Zhao ◽  
Shenghong Ju ◽  
Hui Mao ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Adipose Tissue ◽  
Magnetic Resonance ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Chow Diet ◽  
Resonance Imaging ◽  
High Fat ◽  
White Adipocytes ◽  
Fat Fraction

This study aimed to track and evaluate the effect of low-dose irisin on the browning of white adipose tissue (WAT) in mice using magnetic resonance imaging (MRI) noninvasively in vivo. Mature white adipocytes extracted from mice were cultured, induced and characterized before being treated by irisin. The volume and fat fraction of WAT were quantified using MRI in normal chow diet and high fat mice after injection of irisin. The browning of cultured white adipocytes and WAT in mice were validated by immunohistochemistry and western blotting for uncoupling protein 1 (UCP1) and deiodinase type II (DIO2). The serum indexes were examined with high fat diet after irisin intervention. UCP1 and DIO2 in adipocytes showed increases responding to the irisin treatment. The size of white adipocytes in mice receiving irisin intervention was reduced. MRI measured volumes and fat fraction of WAT were significantly lower after Irisin treatment. Blood glucose and cholesterol levels were reduced in high fat diet mice after irisin treatment. Irisin intervention exerted browning of WAT, resulting reduction of volume and fat fraction of WAT as measured by MRI. Furthermore, it improved the condition of mice with diet-induced obesity and related metabolic disorders.

scholarly journals Partial Deficiency of Zfp217 Resists High-Fat Diet-Induced Obesity by Increasing Energy Metabolism in Mice

2021 ◽  
Vol 22 (10) ◽  
pp. 5390
Author(s):  
Qianhui Zeng ◽  
Nannan Wang ◽  
Yaru Zhang ◽  
Yuxuan Yang ◽  
Shuangshuang Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Chow Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Partial Deficiency

Obesity-induced adipose tissue dysfunction and disorders of glycolipid metabolism have become a worldwide research priority. Zfp217 plays a crucial role in adipogenesis of 3T3-L1 preadipocytes, but about its functions in animal models are not yet clear. To explore the role of Zfp217 in high-fat diet (HFD)-induced obese mice, global Zfp217 heterozygous knockout (Zfp217+/−) mice were constructed. Zfp217+/− mice and Zfp217+/+ mice fed a normal chow diet (NC) did not differ significantly in weight gain, percent body fat mass, glucose tolerance, or insulin sensitivity. When challenged with HFD, Zfp217+/− mice had less weight gain than Zfp217+/+ mice. Histological observations revealed that Zfp217+/− mice fed a high-fat diet had much smaller white adipocytes in inguinal white adipose tissue (iWAT). Zfp217+/− mice had improved metabolic profiles, including improved glucose tolerance, enhanced insulin sensitivity, and increased energy expenditure compared to the Zfp217+/+ mice under HFD. We found that adipogenesis-related genes were increased and metabolic thermogenesis-related genes were decreased in the iWAT of HFD-fed Zfp217+/+ mice compared to Zfp217+/− mice. In addition, adipogenesis was markedly reduced in mouse embryonic fibroblasts (MEFs) from Zfp217-deleted mice. Together, these data indicate that Zfp217 is a regulator of energy metabolism and it is likely to provide novel insight into treatment for obesity.

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