Resveratrol attenuates inflammation and oxidative stress in epididymal white adipose tissue: Implications for its involvement in improving steroidogenesis in diet-induced obese mice

2015 ◽  
Vol 82 (4) ◽  
pp. 321-328 ◽  
Author(s):  
Zheng-mei Lv ◽  
Qi Wang ◽  
Yuan-hua Chen ◽  
Sheng-hua Wang ◽  
Dao-qi Huang
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Obese Mice ◽  
Epididymal White Adipose Tissue ◽  
And Oxidative Stress

scholarly journals Metformin induces oxidative stress in white adipocytes and raises uncoupling protein 2 levels

2008 ◽  
Vol 199 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Andrea Anedda ◽  
Eduardo Rial ◽  
M Mar González-Barroso
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Protein Levels ◽  
White Adipocytes ◽  
Epididymal White Adipose Tissue ◽  
Amp Activated Protein Kinase

Metformin is a drug widely used to treat type 2 diabetes. It enhances insulin sensitivity by improving glucose utilization in tissues like liver or muscle. Metformin inhibits respiration, and the decrease in cellular energy activates the AMP-activated protein kinase that in turn switches on catabolic pathways. Moreover, metformin increases lipolysis and β-oxidation in white adipose tissue, thereby reducing the triglyceride stores. The uncoupling proteins (UCPs) are transporters that lower the efficiency of mitochondrial oxidative phosphorylation. UCP2 is thought to protect against oxidative stress although, alternatively, it could play an energy dissipation role. The aim of this work was to analyse the involvement of UCP2 on the effects of metformin in white adipocytes. We studied the effect of this drug in differentiating 3T3-L1 adipocytes and found that metformin causes oxidative stress since it increases the levels of reactive oxygen species (ROS) and lowers the aconitase activity. Variations in UCP2 protein levels parallel those of ROS. Metformin also increases lipolysis in these cells although only when the levels of ROS and UCP2 have decreased. Hence, UCP2 does not appear to be needed to facilitate fatty acid oxidation. Furthermore, treatment of C57BL/6 mice with metformin also augmented the levels of UCP2 in epididymal white adipose tissue. We conclude that metformin treatment leads to the overexpression of UCP2 in adipocytes to minimize the oxidative stress that is probably due to the inhibition of respiration caused by the drug.

scholarly journals Exercise Training Attenuates the Dysregulated Expression of Adipokines and Oxidative Stress in White Adipose Tissue

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Takuya Sakurai ◽  
Junetsu Ogasawara ◽  
Ken Shirato ◽  
Tetsuya Izawa ◽  
Shuji Oh-ishi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Exercise Training ◽  
White Adipose Tissue ◽  
Monocyte Chemoattractant Protein 1 ◽  
Enhanced Production ◽  
Lifestyle Related Diseases ◽  
Inflammatory Changes ◽  
The Impact ◽  
And Oxidative Stress

Obesity-induced inflammatory changes in white adipose tissue (WAT), which caused dysregulated expression of inflammation-related adipokines involving tumor necrosis factor-αand monocyte chemoattractant protein-1, contribute to the development of insulin resistance. Moreover, current literature reports state that WAT generates reactive oxygen species (ROS), and the enhanced production of ROS in obese WAT has been closely associated with the dysregulated expression of adipokines in WAT. Therefore, the reduction in excess WAT and oxidative stress that results from obesity is thought to be one of the important strategies in preventing and improving lifestyle-related diseases. Exercise training (TR) not only brings about a decrease in WAT mass but also attenuates obesity-induced dysregulated expression of the adipokines in WAT. Furthermore, some reports indicate that TR affects the generation of oxidative stress in WAT. This review outlines the impact of TR on the expression of inflammation-related adipokines and oxidative stress in WAT.

scholarly journals Retention of sedentary obese visceral white adipose tissue phenotype with intermittent physical activity despite reduced adiposity

2015 ◽  
Vol 309 (5) ◽  
pp. R594-R602 ◽  
Author(s):  
Katherine S. Wainright ◽  
Nicholas J. Fleming ◽  
Joe L. Rowles ◽  
Rebecca J. Welly ◽  
Terese M. Zidon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Immune Cell ◽  
Regular Physical Activity ◽  
Metabolic Phenotype ◽  
Running Wheels ◽  
The Impact ◽  
And Oxidative Stress

Regular physical activity is effective in reducing visceral white adipose tissue (AT) inflammation and oxidative stress, and these changes are commonly associated with reduced adiposity. However, the impact of multiple periods of physical activity, intercalated by periods of inactivity, i.e., intermittent physical activity, on markers of AT inflammation and oxidative stress is unknown. In the present study, 5-wk-old male C57BL/6 mice were randomized into three groups ( n = 10/group): sedentary, regular physical activity, and intermittent physical activity, for 24 wk. All animals were singly housed and fed a diet containing 45% kcal from fat. Regularly active mice had access to voluntary running wheels throughout the study period, whereas intermittently active mice had access to running wheels for 3-wk intervals (i.e., 3 wk on/3 wk off) throughout the study. At death, regular and intermittent physical activity was associated with similar reductions in visceral AT mass (approximately −24%, P < 0.05) relative to sedentary. However, regularly, but not intermittently, active mice exhibited decreased expression of visceral AT genes related to inflammation (e.g., monocyte chemoattractant protein 1), immune cell infiltration (e.g., CD68, CD11c, F4/80, CD11b/CD18), oxidative stress (e.g., p47 phagocyte oxidase), and endoplasmic reticulum stress (e.g., CCAAT enhancer-binding protein homologous protein; all P < 0.05). Furthermore, regular, but not intermittent, physical activity was associated with a trend toward improvement in glucose tolerance ( P = 0.059). Collectively, these findings suggest that intermittent physical activity over a prolonged period of time may lead to a reduction in adiposity but with retention of a sedentary obese white AT and metabolic phenotype.

scholarly journals Ursodeoxycholic Acid Regulates Hepatic Energy Homeostasis and White Adipose Tissue Macrophages Polarization in Leptin-Deficiency Obese Mice

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 253 ◽  
Author(s):  
Yu-Sheng Chen ◽  
Hsuan-Miao Liu ◽  
Tzung-Yan Lee
Keyword(s):  
Adipose Tissue ◽  
Mitochondrial Dysfunction ◽  
Ursodeoxycholic Acid ◽  
White Adipose Tissue ◽  
Whole Body ◽  
Bile Acid Metabolism ◽  
Obese Mice ◽  
Alcoholic Fatty Liver ◽  
Tissue Macrophage ◽  
Stat3 Phosphorylation

Obesity has been shown to play a role in the pathogenesis of several forms of metabolic syndrome, including non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes. Ursodeoxycholic acid (UDCA) has been shown to possess antioxidant and anti-inflammatory properties and prevents mitochondrial dysfunction in the progression of obesity-associated diseases. The aim of the study was to evaluate the mechanisms of UDCA during obesity-linked hepatic mitochondrial dysfunction and obesity-associated adipose tissue macrophage-induced inflammation in obese mice. UDCA significantly decreased lipid droplets, reduced free fatty acids (FFA) and triglycerides (TG), improved mitochondrial function, and enhanced white adipose tissue browning in ob/ob mice. This is associated with increased hepatic energy expenditure, mitochondria biogenesis, and incorporation of bile acid metabolism (Abca1, Abcg1 mRNA and BSEP, FGFR4, and TGR5 protein). In addition, UDCA downregulated NF-κB and STAT3 phosphorylation by negative regulation of the expression of SOCS1 and SOCS3 signaling. These changes were accompanied by decreased angiogenesis, as shown by the downregulation of VEGF, VCAM, and TGF-βRII expression. Importantly, UDCA is equally effective in reducing whole body adiposity. This is associated with decreased adipose tissue expression of macrophage infiltration (CD11b, CD163, and CD206) and lipogenic capacity markers (lipofuscin, SREBP-1, and CD36). Furthermore, UDCA significantly upregulated adipose browning in association with upregulation of SIRT-1-PGC1-α signaling in epididymis adipose tissue (EWAT). These results suggest that multi-targeted therapies modulate glucose and lipid biosynthesis fluxes, inflammatory response, angiogenesis, and macrophage differentiation. Therefore, it may be suggested that UDCA treatment may be a novel therapeutic agent for obesity.

AT1 receptor antagonist induces thermogenic beige adipocytes in the inguinal white adipose tissue of obese mice

Endocrine ◽  
2016 ◽  
Vol 55 (3) ◽  
pp. 786-798 ◽  
Author(s):  
Francielle Graus-Nunes ◽  
Tamiris Lima Rachid ◽  
Felipe de Oliveira Santos ◽  
Sandra Barbosa-da-Silva ◽  
Vanessa Souza-Mello
Keyword(s):  
Adipose Tissue ◽  
Receptor Antagonist ◽  
White Adipose Tissue ◽  
At1 Receptor ◽  
Obese Mice ◽  
Beige Adipocytes

scholarly journals Visceral and Subcutaneous Adipose Tissue Volumes Are Cross-Sectionally Related to Markers of Inflammation and Oxidative Stress

Circulation ◽  
2007 ◽  
Vol 116 (11) ◽  
pp. 1234-1241 ◽  
Author(s):  
Karla M. Pou ◽  
Joseph M. Massaro ◽  
Udo Hoffmann ◽  
Ramachandran S. Vasan ◽  
Pal Maurovich-Horvat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Markers Of Inflammation ◽  
Subcutaneous Adipose ◽  
And Oxidative Stress
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