scholarly journals Epigallocatechin-3-Gallate Reduces Visceral Adiposity Partly through the Regulation of Beclin1-Dependent Autophagy in White Adipose Tissues

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3072
Author(s):  
Cheoljun Choi ◽  
Hyun-Doo Song ◽  
Yeonho Son ◽  
Yoon Keun Cho ◽  
Sang-Yeop Ahn ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
White Adipose Tissue ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Autophagic Flux ◽  
Tissue Mass ◽  
Egcg Treatment ◽  
Adipose Tissue Mass

Epigallocatechin-3-gallate (EGCG) is a primary bioactive phytochemical in green tea. Its therapeutic potential in metabolic diseases has been reported; however, the molecular mechanisms of the anti-obesity effect of EGCG have not been fully elucidated. In this study, we examined the effects of EGCG on lipid metabolism and autophagy in adipose tissue. After 8 weeks of high-fat diet feeding, mice were treated with EGCG (20 mg/kg/day) for 2 weeks to test in vivo anti-obesity effects of EGCG. EGCG treatment improved glucose tolerance and caused body weight loss. Interestingly, reduced adipose tissue mass was more prominent in visceral compared to subcutaneous white adipose tissue. Mechanistically, EGCG treatment increased autophagic flux in white adipose tissue through the AMP-activated protein kinase-mediated signaling pathway. Adipocyte-specific knockout of Beclin1 mitigated the effects of EGCG on visceral adipose tissue mass and glucose tolerance, indicating that the anti-obesity effect of EGCG requires Beclin1-dependent autophagy. Collectively, our data demonstrated that EGCG has anti-obesity effects through the upregulation of Beclin1-dependent autophagy and lipid catabolism in white adipose tissue (WAT).

scholarly journals MED19 Regulates Adipogenesis and Maintenance of White Adipose Tissue Mass by Mediating PPARγ-Dependent Gene Expression

Cell Reports ◽  
2020 ◽  
Vol 33 (1) ◽  
pp. 108228 ◽  
Author(s):  
John M. Dean ◽  
Anyuan He ◽  
Min Tan ◽  
Jun Wang ◽  
Dongliang Lu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Tissue Mass ◽  
Adipose Tissue Mass

scholarly journals Individual housing of male C57BL/6J mice after weaning impairs growth and predisposes for obesity

2019 ◽  
Author(s):  
Lidewij Schipper ◽  
Steffen van Heijningen ◽  
Giorgio Karapetsas ◽  
Eline M. van der Beek ◽  
Gertjan van Dijk
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Intake ◽  
White Adipose Tissue ◽  
Body Weight Gain ◽  
Tissue Mass ◽  
Individual Housing ◽  
Adipose Tissue Mass ◽  
Obesogenic Diet

AbstractIndividual housing from weaning onwards resulted in reduced growth rate during adolescence in male C57Bl/6J mice that were housed individually, while energy intake and energy expenditure were increased compared to socially housed counterparts. At 6 weeks of age, these mice had reduced lean body mass, but significantly higher white adipose tissue mass compared to socially housed mice. Body weight gain of individually housed animals exceeded that of socially housed mice during adulthood, with elevations in both energy intake and expenditure. At 18 weeks of age, individually housed mice showed higher adiposity and higher mRNA expression of UCP-1 in inguinal white adipose tissue. Exposure to an obesogenic diet starting at 6 weeks of age further amplified body weight gain and adipose tissue deposition. This study shows that post-weaning individual housing of male mice results in impaired adolescent growth and higher susceptibility to obesity in adulthood. Mice are widely used to study obesity and cardiometabolic comorbidities. For (metabolic) research models using mice, (social) housing practices should be carefully considered and regarded as a potential confounder due to their modulating effect on metabolic health outcomes.

scholarly journals Resistin expression and plasma concentration peak at different times during pregnancy in rats

2005 ◽  
Vol 185 (3) ◽  
pp. 551-559 ◽  
Author(s):  
Sergio Caja ◽  
Izaskun Martínez ◽  
María Abelenda ◽  
Marisa Puerta
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Plasma Concentration ◽  
White Adipose Tissue ◽  
Post Partum ◽  
Time Lag ◽  
Simultaneous Increase ◽  
Tissue Mass ◽  
Pregnant Rats ◽  
Adipose Tissue Mass

Resistin has been proposed as both an anti-adipogenic factor and an inducer of insulin resistance. During late pregnancy, white adipose tissue mass increases and insulin sensitivity decreases. To check for the involvement of resistin in these processes, we measured plasma resistin in pregnant and non-pregnant rats and in lactating dams. Plasma resistin increased by day 15 of pregnancy and remained high 5 days post partum. The simultaneous increase in plasma resistin concentration and the decrease in insulin sensitivity is compatible with resistin depressing maternal insulin sensitivity. Resistin expression increased 5–15 times in visceral white adipose tissue depots by day 8 of pregnancy but was similar to pre-pregnancy values by day 19. Resistin expression in the placenta and mammary gland was similar to that in the parametrial adipose depot by day 8 but was almost null by day 19. There was therefore a time-lag between the peaks in expression and in plasma concentration. White adipose tissue mass increased without changes in adipocyte size once peaks in resistin expression had passed, which is compatible with an anti-adipogenic role for enhanced resistin expression. A bolus injection of chorionic gonadotrophin – which peaks in early pregnancy – to non-pregnant rats increased resistin expression in white adipose tissue, indicating that this hormone is involved in controlling resistin expression. Resistin was not detected in cerebrospinal fluid. Our results have suggested a role for resistin in pregnancy.

Activation of adipose tissue glycerokinase contributes to increased white adipose tissue mass in mice fed a high-fat diet

Endocrine ◽  
2020 ◽  
Vol 69 (1) ◽  
pp. 79-91
Author(s):  
Samyra Lopes Buzelle ◽  
Franciele Przygodda ◽  
Rafael Rossi-Valentim ◽  
Graziella Nascimento Ferreira ◽  
Maria Antonieta Rissato Garófalo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
High Fat ◽  
Tissue Mass ◽  
Adipose Tissue Mass

scholarly journals High Dietary Sodium Intake Increases White Adipose Tissue Mass and Plasma Leptin in Rats*

Obesity ◽  
2007 ◽  
Vol 15 (9) ◽  
pp. 2200-2208 ◽  
Author(s):  
Miriam H. Fonseca-Alaniz ◽  
Luciana C. Brito ◽  
Cristina N. Borges-Silva ◽  
Julie Takada ◽  
Sandra Andreotti ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
Plasma Leptin

scholarly journals Glucocorticoid antagonism limits adiposity rebound and glucose intolerance in young male rats following the cessation of daily exercise and caloric restriction

2016 ◽  
Vol 311 (1) ◽  
pp. E56-E68 ◽  
Author(s):  
Trevor Teich ◽  
Emily C. Dunford ◽  
Deanna P. Porras ◽  
Jacklyn A. Pivovarov ◽  
Jacqueline L. Beaudry ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Receptor Antagonist ◽  
Caloric Restriction ◽  
Mass Gain ◽  
Male Rats ◽  
Tissue Mass ◽  
Adiposity Rebound ◽  
Adipose Tissue Mass

Severe caloric restriction (CR), in a setting of regular physical exercise, may be a stress that sets the stage for adiposity rebound and insulin resistance when the food restriction and exercise stop. In this study, we examined the effect of mifepristone, a glucocorticoid (GC) receptor antagonist, on limiting adipose tissue mass gain and preserving whole body insulin sensitivity following the cessation of daily running and CR. We calorically restricted male Sprague-Dawley rats and provided access to voluntary running wheels for 3 wk followed by locking of the wheels and reintroduction to ad libitum feeding with or without mifepristone (80 mg·kg−1·day−1) for 1 wk. Cessation of daily running and CR increased HOMA-IR and visceral adipose mass as well as glucose and insulin area under the curve during an oral glucose tolerance test vs. pre-wheel lock exercised rats and sedentary rats (all P < 0.05). Insulin sensitivity and glucose tolerance were preserved and adipose tissue mass gain was attenuated by daily mifepristone treatment during the post-wheel lock period. These findings suggest that following regular exercise and CR there are GC-induced mechanisms that promote adipose tissue mass gain and impaired metabolic control in healthy organisms and that this phenomenon can be inhibited by the GC receptor antagonist mifepristone.

scholarly journals Regulation of adiposity by mTORC1

2017 ◽  
Vol 15 (4) ◽  
pp. 507-511 ◽  
Author(s):  
Juliana Magdalon ◽  
William Tadeu Festuccia
Keyword(s):  
Adipose Tissue ◽  
Metabolic Diseases ◽  
Therapeutic Strategies ◽  
Health Concern ◽  
Nonshivering Thermogenesis ◽  
Public Health Concern ◽  
Tissue Mass ◽  
Mechanistic Target Of Rapamycin ◽  
Adipose Tissue Mass

ABSTRACT Obesity is characterized by an excessive increase in the adipose tissue mass, and is associated with higher incidence of several chronic metabolic diseases, such as type 2 diabetes. Therefore, its increasing prevalence is a public health concern, and it is important to better understand its etiology to develop new therapeutic strategies. Evidence accumulated over the years indicates that obesity is associated with a marked activation in adipose tissue of the mechanistic target of rapamycin complex 1 (mTORC1), a signaling pathway that controls lipid metabolism, and adipocyte formation and maintenance. Curiously, mTORC1 is also involved in the control of nonshivering thermogenesis and recruitment as well as browning of white adipose tissue. In this review, we explored mTORC1 functions in adipocytes and presented evidence, suggesting that mTORC1 may either increase or reduce adiposity, depending on the conditions and activation levels.

Abstract 58: Adipose-Specific Deletion of ARV1 Results in Decreased HDL Cholesterol, Reduced White Adipose Tissue Mass and Improved Glucose Tolerance in Mice

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
William R Lagor ◽  
Fumin Tong ◽  
David W Fields ◽  
Wen Lin ◽  
Jeffrey T Billheimer ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Lipoprotein Metabolism ◽  
Hdl Cholesterol ◽  
Sphingolipid Metabolism ◽  
Chow Diet ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
Important Player ◽  
Specific Deletion

ACAT related enzyme 2 required for viability 1 (ARV1) was identified as a gene required for viability in yeast in the absence of cholesterol esterification. ARV1 encodes a putative lipid transporter believed to be important in trafficking of lipids from the ER to the Golgi. ARV1 deficient yeast exhibit profound alterations in cholesterol, phospholipid, and sphingolipid metabolism, accompanied by a constitutively activated unfolded protein response and impaired GPI anchor synthesis. To study the role of ARV1 in mammalian lipid metabolism, we have generated mice with an adipose specific deletion of ARV1 using Cre/loxP technology with Cre expression driven by the Ap2 promoter. ARV1 adipose specific knockout (ASKO) mice exhibited significant reductions in plasma total cholesterol (↓21%, p < 0.05), HDL cholesterol (↓25%, p < 0.01), and phospholipid (↓17.6%, p < 0.05) levels, while fasting triglyceride levels were unaffected. ARV1 ASKO mice also had substantial reductions in epididymal adipose (WT: 0.41 +/- 0.07 g vs. KO: 0.10 +/- 0.07 g, p = 0.0002) and subcutaneous adipose tissue mass (WT: 0.32 +/- 0.03 g vs. KO: 0.11 +/- 0.08 g; p= 0.0002) on a chow diet. In contrast to nearly every other lipodystrophic mouse model, the reduced fat mass in these animals was paradoxically accompanied by improved glucose tolerance (WT AUC: 32,055 vs. KO AUC: 21,470 mg/dl*minutes, p<0.05). These data identify mammalian ARV1 as an important player in adipose tissue biology, and support an important role for adipose tissue in circulating lipoprotein metabolism.

scholarly journals Oxygenated Water Inhibits Adipogenesis and Attenuates Hepatic Steatosis in High-Fat Diet-Induced Obese Mice

2020 ◽  
Vol 21 (15) ◽  
pp. 5493
Author(s):  
Yuh-Jen Cheng ◽  
Chao-Chi Liu ◽  
Fang-Yeh Chu ◽  
Ching-Ping Yang ◽  
Chiao-Wan Hsiao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Hepatic Steatosis ◽  
Molecular Mechanisms ◽  
Metabolic Effects ◽  
Metabolic Function ◽  
Tissue Mass ◽  
Lipid Contents ◽  
Oxygenated Water

The expansion of adipose tissue mass is the primary characteristic of the process of becoming obesity, which causes chronic adipose inflammation and is closely associated with type 2 diabetes mellitus (T2DM). Adipocyte hypertrophy restricts oxygen availability, leading to microenvironmental hypoxia and adipose dysfunction. This study aimed at investigating the effects of oxygenated water (OW) on adipocyte differentiation (adipogenesis) and the metabolic function of mature adipocytes. The effects of OW on adipogenesis and the metabolic function of mature adipocytes were examined. Meanwhile, the in vivo metabolic effects of long-term OW consumption on diet-induced obesity (DIO) mice were investigated. OW inhibited adipogenesis and lipid accumulation through down-regulating critical adipogenic transcription factors and lipogenic enzymes. While body weight, blood and adipose parameters were not significantly improved by long-term OW consumption, transient circulatory triglyceride-lowering and glucose tolerance-improving effects were identified. Notably, hepatic lipid contents were significantly reduced, indicating that the DIO-induced hepatic steatosis was attenuated, despite no improvements in fibrosis and lipid contents in adipose tissue being observed in the OW-drinking DIO mice. The study provides evidence regarding OW’s effects on adipogenesis and mature adipocytes, and the corresponding molecular mechanisms. OW exhibits transient triglyceride-lowering and glucose tolerance-improving activity as well as hepatic steatosis-attenuating functions.

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