Dietary apple polyphenols promote fat browning in high‐fat diet‐induced obese mice through activation of adenosine monophosphate‐activated protein kinase α

2020 ◽  
Vol 100 (6) ◽  
pp. 2389-2398 ◽  
Author(s):  
Tiande Zou ◽  
Bo Wang ◽  
Shuo Li ◽  
Yue Liu ◽  
Jinming You
Keyword(s):  
Protein Kinase ◽  
High Fat Diet ◽  
Adenosine Monophosphate ◽  
Obese Mice ◽  
High Fat

scholarly journals Antiobesity Effect ofAstilbe chinensisFranch. et Savet. Extract through Regulation of Adipogenesis and AMP-Activated Protein Kinase Pathways in 3T3-L1 Adipocyte and High-Fat Diet-Induced C57BL/6N Obese Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xian Hua Zhang ◽  
Zhiqiang Wang ◽  
Bueom-Goo Kang ◽  
Seung Hwan Hwang ◽  
Jae-Young Lee ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Lipid Content ◽  
High Fat Diet ◽  
Binding Protein ◽  
Resistance Index ◽  
Nonesterified Fatty Acid ◽  
Dependent Manner ◽  
Obese Mice ◽  
High Fat ◽  
Amp Activated Protein Kinase

Astilbe chinensisFranch. et Savat. (AC) has been used in traditional medicine for the treatment of chronic bronchitis, arthralgia, and gastralgia. In this study, we investigated the antiobesity effect of AC extract on 3T3-L1 preadipocytes and high-fat-diet-fed C57BL/6N obese mice. We found that AC extracts dramatically decreased the lipid content of 3T3-L1 cells in a concentration-dependent manner without cytotoxicity. The action mechanism of AC extract was demonstrated to be the inhibition of lipid accumulation and dose-dependent decrease in the expression of CCAAT/enhancer-binding proteinα(C/EBPα), peroxisome proliferator-activated receptor-γ(PPAR-γ), and sterol regulatory element-binding protein 1 (SREBP1). Furthermore, AC extract increased the mitochondrial phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), mitochondrial biogenesis, and lipolysis-related factors. In amice model of high-fat-diet-induced obesity, the mice administered AC extract experienced significant decrease of 64% in weight gain, 55% in insulin resistance index, 22% in plasma triglycerides (TG), 56% in total cholesterol (TC), and 21% in nonesterified fatty acid (NEFA) levels compared with those in the high-fat diet-fed control mice. Collectively, these results indicated that AC extract exerted antiobesogenic activity through the modulation of the AMPK signaling pathway, inhibition of adipogenesis, decreased lipid content, and reduced adipocyte size.

scholarly journals Effects of different intensities of physical exercise on insulin sensitivity and protein kinase B/Akt activity in skeletal muscle of obese mice

2014 ◽  
Vol 12 (1) ◽  
pp. 82-89 ◽  
Author(s):  
Rodolfo Marinho ◽  
Leandro Pereira de Moura ◽  
Bárbara de Almeida Rodrigues ◽  
Luciana Santos Souza Pauli ◽  
Adelino Sanchez Ramos da Silva ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Protein Kinase ◽  
High Fat Diet ◽  
Protein Kinase B ◽  
Whole Body ◽  
Control Group ◽  
Standard Diet ◽  
Obese Mice ◽  
High Fat

Objective : To investigate the effects of different intensities of acute exercise on insulin sensitivity and protein kinase B/Akt activity in skeletal muscle of obese mice. Methods : Swiss mice were randomly divided into four groups, and fed either a standard diet (control group) or high fat diet (obese sedentary group and obese exercise group 1 and 2) for 12 weeks. Two different exercise protocols were used: swimming for 1 hour with or without an overload of 5% body weight. The insulin tolerance test was performed to estimate whole-body sensitivity. Western blot technique was used to determine protein levels of protein kinase B/Akt and phosphorylation by protein Kinase B/Akt in mice skeletal muscle. Results : A single bout of exercise inhibited the high fat diet-induced insulin resistance. There was increase in phosphorylation by protein kinase B/Akt serine, improve in insulin signaling and reduce of fasting glucose in mice that swam for 1 hour without overload and mice that swan for 1 hour with overload of 5%. However, no significant differences were seen between exercised groups. Conclusion : Regardless of intensity, aerobic exercise was able to improve insulin sensitivity and phosphorylation by protein kinase B/Ak, and proved to be a good form of treatment and prevention of type 2 diabetes.

Protein kinase Cδ contributes to phenylephrine-mediated contraction in the aortae of high fat diet-induced obese mice

2014 ◽  
Vol 446 (4) ◽  
pp. 1179-1183 ◽  
Author(s):  
Limei Liu ◽  
Jian Liu ◽  
Yuansheng Gao ◽  
Xiaoxing Yu ◽  
Dou Dou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Protein Kinase Cδ

scholarly journals Metformin Protects Endothelial Function in Diet-Induced Obese Mice by Inhibition of Endoplasmic Reticulum Stress Through 5′ Adenosine Monophosphate–Activated Protein Kinase–Peroxisome Proliferator–Activated Receptor δ Pathway

2014 ◽  
Vol 34 (4) ◽  
pp. 830-836 ◽  
Author(s):  
Wai San Cheang ◽  
Xiao Yu Tian ◽  
Wing Tak Wong ◽  
Chi Wai Lau ◽  
Susanna Sau-Tuen Lee ◽  
...  
Keyword(s):  
Er Stress ◽  
High Fat Diet ◽  
Adenosine Monophosphate ◽  
Peroxisome Proliferator ◽  
Obese Mice ◽  
High Fat ◽  
Peroxisome Proliferator Activated Receptor ◽  
Aortic Endothelial Cells ◽  
Stress Markers ◽  
Endothelium Dependent Relaxation

Objective— 5′ Adenosine monophosphate–activated protein kinase (AMPK) interacts with peroxisome proliferator–activated receptor δ (PPARδ) to induce gene expression synergistically, whereas the activation of AMPK inhibits endoplasmic reticulum (ER) stress. Whether the vascular benefits of antidiabetic drug metformin (AMPK activator) in diabetes mellitus and obesity is mediated by PPARδ remains unknown. We aim to investigate whether PPARδ is crucial for metformin in ameliorating ER stress and endothelial dysfunction induced by high-fat diet. Approach and Results— Acetylcholine-induced endothelium-dependent relaxation in aortae was measured on wire myograph. ER stress markers were determined by Western blotting. Superoxide production in mouse aortae and NO generation in mouse aortic endothelial cells were assessed by fluorescence imaging. Endothelium-dependent relaxation was impaired and ER stress markers and superoxide level were elevated in aortae from high-fat diet–induced obese mice compared with lean mice. These effects of high-fat diet were reversed by oral treatment with metformin in diet-induced obese PPARδ wild-type mice but not in diet-induced obese PPARδ knockout littermates. Metformin and PPARδ agonist GW1516 reversed tunicamycin (ER stress inducer)-induced ER stress, oxidative stress, and impairment of endothelium-dependent relaxation in mouse aortae as well as NO production in mouse aortic endothelial cells. Effects of metformin were abolished by cotreatment of GSK0660 (PPARδ antagonist), whereas effects of GW1516 were unaffected by compound C (AMPK inhibitor). Conclusions— Metformin restores endothelial function through inhibiting ER stress and oxidative stress and increasing NO bioavailability on activation of AMPK/PPARδ pathway in obese diabetic mice.

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