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Dietary Supplementation of Chinese Ginseng Prevents Obesity and Metabolic Syndrome in High-Fat Diet-Fed Mice

Xiaoxiao Li,Jing Luo,Pon Velayutham Anandh Babu,Wei Zhang,Elizabeth Gilbert,Mark Cline,Ryan McMillan,Matthew Hulver,Hana Alkhalidy,Wei Zhen,Haiyan Zhang,Dongmin Liu 한국식품영양과학회 2014 Journal of medicinal food Vol.17 No.12
Obesity and diabetes are growing health problems worldwide. In this study, dietary provision of Chinese ginseng (0.5 g/kg diet) prevented body weight gain in high-fat (HF) diet-fed mice. Dietary ginseng supplementation reduced body fat mass gain, improved glucose tolerance and whole body insulin sensitivity, and prevented hypertension in HF dietinduced obese mice. Ginseng consumption led to reduced concentrations of plasma insulin and leptin, but had no effect on plasma adiponectin levels in HF diet-fed mice. Body temperature was higher in mice fed the ginseng-supplemented diet but energy expenditure, respiration rate, and locomotive activity were not significantly altered. Dietary intake of ginseng increased fatty acid oxidation in the liver but not in skeletal muscle. Expression of several transcription factors associated with adipogenesis (C/EBPa and PPARc) were decreased in the adipose tissue of HF diet-fed mice, effects that were mitigated in mice that consumed the HF diet supplemented with ginseng. Abundance of fatty acid synthase (FASN) mRNA was greater in the adipose tissue of mice that consumed the ginseng-supplemented HF diet as compared with control or un-supplemented HF diet-fed mice. Ginseng treatment had no effect on the expression of genes involved in the regulation of food intake in the hypothalamus. These data suggest that Chinese ginseng can potently prevent the development of obesity and insulin resistance in HF diet-fed mice.
2
Fiber hypertrophy and increased oxidative capacity can occur simultaneously in pig glycolytic skeletal muscle

Scheffler, T. L.,Scheffler, J. M.,Park, S.,Kasten, S. C.,Wu, Y.,McMillan, R. P.,Hulver, M. W.,Frisard, M. I.,Gerrard, D. E. American Physiological Society 2014 American journal of physiology. Cell physiology Vol.306 No.4
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An inverse relationship between skeletal muscle fiber cross-sectional area (CSA) and oxidative capacity suggests that muscle fibers hypertrophy at the expense of oxidative capacity. Therefore, our objective was to utilize pigs possessing mutations associated with increased oxidative capacity [AMP-activated protein kinase (AMPKγ3R200Q)] or fiber hypertrophy [ryanodine receptor 1 (RyR1R615C)] to determine if these events occur in parallel. Longissimus muscle was collected from wild-type (control), AMPKγ3R200Q, RyR1R615C, and AMPKγ3R200Q-RyR1R615C pigs. Regardless of AMPK genotype, RyRR615C increased fiber CSA by 35%. In contrast, AMPKγ3R200Q pig muscle exhibited greater citrate synthase and β-hydroxyacyl CoA dehydrogenase activity. Isolated mitochondria from AMPKγ3R200Q muscle had greater maximal, ADP-stimulated oxygen consumption rate. Additionally, AMPKγ3R200Q muscle contained more (∼50%) of the mitochondrial proteins succinate dehydrogenase and cytochrome c oxidase and more mitochondrial DNA. Surprisingly, RyR1R615C increased mitochondrial proteins and DNA, but this was not associated with improved oxidative capacity, suggesting that altered energy metabolism in RyR1R615C muscle influences mitochondrial proliferation and protein turnover. Thus pigs that possess both AMPKγ3R200Q and RyRR615C exhibit increased muscle fiber CSA as well as greater oxidative capacity. Together, our findings support the notion that hypertrophy and enhanced oxidative capacity can occur simultaneously in skeletal muscle and suggest that the signaling mechanisms controlling these events are independently regulated.

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