scholarly journals Reduced cortical BACE1 content with one bout of exercise is accompanied by declines in AMPK, Akt, and MAPK signaling in obese, glucose-intolerant mice

2015 ◽  
Vol 119 (10) ◽  
pp. 1097-1104 ◽  
Author(s):  
R. E. K. MacPherson ◽  
P. Baumeister ◽  
W. T. Peppler ◽  
D. C. Wright ◽  
J. P. Little
Keyword(s):  
High Fat Diet ◽  
Recovery Period ◽  
Significant Risk ◽  
Mapk Signaling ◽  
Treadmill Running ◽  
High Fat ◽  
Cellular Mechanisms ◽  
Ampk Signaling ◽  
Erk Phosphorylation ◽  
Single Bout

Obesity and type 2 diabetes are significant risk factors in the development of neurodegenerative diseases, such as Alzheimer's disease. A variety of cellular mechanisms, such as altered Akt and AMPK and increased inflammatory signaling, contribute to neurodegeneration. Exercise training can improve markers of neurodegeneration, but the underlying mechanisms remain unknown. The purpose of this study was to determine the effects of a single bout of exercise on markers of neurodegeneration and inflammation in brains from mice fed a high-fat diet. Male C57BL/6 mice were fed a low (LFD; 10% kcal from lard)- or a high-fat diet (HFD; 60% kcal from lard) for 7 wk. HFD mice underwent an acute bout of exercise (treadmill running: 15 m/min, 5% incline, 120 min) followed by a recovery period of 2 h. The HFD increased body mass and glucose intolerance (both P < 0.05). This was accompanied by an approximately twofold increase in the phosphorylation of Akt, ERK, and GSK in the cortex ( P < 0.05). Following exercise, there was a decrease in beta-site amyloid precursor protein cleaving enzyme 1 (BACE1; P < 0.05) and activity ( P < 0.001). This was accompanied by a reduction in AMPK phosphorylation, indicative of a decline in cellular stress ( P < 0.05). Akt and ERK phosphorylation were decreased following exercise in HFD mice to a level similar to that of the LFD mice ( P < 0.05). This study demonstrates that a single bout of exercise can reduce BACE1 content and activity independent of changes in adiposity. This effect is associated with reductions in Akt, ERK, and AMPK signaling in the cortex.

scholarly journals BabaoDan attenuates high-fat diet-induced non-alcoholic fatty liver disease via activation of AMPK signaling

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Dandan Sheng ◽  
Shanmin Zhao ◽  
Lu Gao ◽  
Huifei Zheng ◽  
Wenting Liu ◽  
...  
Keyword(s):  
Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
High Fat ◽  
Adipose Tissues ◽  
Alcoholic Fatty Liver ◽  
Ampk Signaling ◽  
Tnf Α ◽  
Alcoholic Fatty Liver Disease

Abstract Background Babaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD. Methods C57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin–eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis. Results We found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway. Conclusion In summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling.

scholarly journals Hedgehog signaling via Gli2 prevents obesity induced by high-fat diet in adult mice

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Yu Shi ◽  
Fanxin Long
Keyword(s):  
High Fat Diet ◽  
Hedgehog Signaling ◽  
Significant Risk ◽  
Whole Body ◽  
Postnatal Life ◽  
High Fat ◽  
Fat Depots ◽  
Diet Induced Obesity ◽  
Hh Signaling

Obesity poses a significant risk of developing type II diabetes and other diseases. Hedgehog (Hh) signaling has been shown to inhibit adipose tissue development, but its effect on diet-induced obesity during postnatal life is not known. Here by inducing expression of constitutively active Smoothened (SmoM2) or Gli2 (ΔNGli2) in the adipocyte lineage of postnatal mice, we show that targeted activation of Hh signaling suppresses high-fat-diet-induced obesity and improves whole-body glucose tolerance and insulin sensitivity. Both SmoM2 and ΔNGli2 induce the expression of Wnt6, a known anti-adipogenic factor, in fat depots of the mouse. Hh-Gli2 signaling inhibits not only adipocyte differentiation but also lipogenesis in adipocytes in vitro. Finally, pharmacological inhibition of Porcupine, an acyltransferase essential for Wnt secretion, alleviates both anti-adipogenic and anti-lipogenic effects of Hh in cell culture models. Overall, targeted activation of Hh signaling ameliorates diet-induced obesity and may be explored for pharmaceutical development.

Oat β-glucan inhibits adipogenesis and hepatic steatosis in high fat diet-induced hyperlipidemic mice via AMPK signaling

2018 ◽  
Vol 41 ◽  
pp. 72-82 ◽  
Author(s):  
Bo Liu ◽  
Tao Yang ◽  
Yi Luo ◽  
Linna Zeng ◽  
Limin Shi ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
High Fat ◽  
Ampk Signaling
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