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    Anti Obesity effects of Ashwagandha

    https://drive.google.com/file/d/1KRs...ew?usp=sharing

    Withania somnifera Extract Enhances Energy Expenditure via Improving Mitochondrial Function in Adipose Tissue and Skeletal Muscle

    Abstract: Withania somnifera (WS), commonly known as ashwagandha, possesses diverse biological functions. WS root has mainly been used as an herbal medicine to treat anxiety and was recently reported to have an anti-obesity effect, however, the mechanisms underlying its action remain to be explored. We hypothesized that WS exerts its anti-obesity effect by enhancing energy expenditure through improving the mitochondrial function of brown/beige adipocytes and skeletal muscle. Male C57BL/6J mice were fed a high-fat diet (HFD) containing 0.25% or 0.5% WS 70% ethanol extract (WSE) for 10 weeks. WSE (0.5%) supplementation significantly suppressed the increases in body weight and serum lipids, and lipid accumulation in the liver and adipose tissue induced by HFD. WSE supplementation increased oxygen consumption and enhanced mitochondrial activity in brown fat and skeletal muscle in the HFD-fed mice. In addition, it promoted browning of subcutaneous fat by increasing mitochondrial uncoupling protein 1 (UCP1) expression. Withaferin A (WFA), a major compound of WS, enhanced the differentiation of pre-adipocytes into beige adipocytes and oxygen consumption in C2C12 murine myoblasts. These results suggest that WSE ameliorates diet-induced obesity by enhancing energy expenditure via promoting mitochondrial function in adipose tissue and skeletal muscle, and WFA is a key regulator in this function.


    We investigated whether WSE supplementation would exhibit an anti-obesity effect in HFD-fed mice. HFD effectively induced a body weight gain at 10 weeks, and the two HFD + WSE groups (0.25% or 0.5% WSE) had a significantly reduced body weight gain when compared with the HFD group (Figure 1A). Food intake per day was not different in all groups (Supplementary Figure S1A). WSE supplementation significantly suppressed the increase in serum triglyceride induced by HFD, and the serum high-density lipoprotein/total cholesterol ratio was significantly increased by this supplementation (Figure 1B). Both WSE + HFD groups showed decreased liver and white adipose tissue (WAT) weights, but increased muscle per body weight when compared with the HFD group (Supplementary Figure S1B). When we measured adipocyte size using H&E staining, we found that WSE supplementation significantly reduced adipocyte size in epididymal WAT when compared with the size observed in the HFD group (Supplementary Figure S1C,D). WSE supplementation also reduced hepatic lipid accumulation (Supplementary Figure S1E,F) and the expression of lipid metabolism-related genes, such as cluster of differentiation 36 (CD36), stearoyl-CoA desaturase 1 (SCD1), and sterol regulatory element-binding protein 1c (SREBP1c) at 10 weeks (Supplementary Figure S1G). We evaluated the effect of WSE on insulin resistance in HFD-fed mice using an oral glucose tolerance test (OGTT) and intraperitoneal insulin tolerance test (IPITT). The 0.5% WSE supplementation, but not the 0.25% WSE, showed a significant reduction in the glucose level in OGTT when compared with the HFD group (Supplementary Figure S2A,B). In the IPITT, the 0.25% and 0.5% WSE groups showed a significant reduction in the glucose level when compared with the HFD group (Supplementary Figure S2C,D). Taken together, these finding showed that WSE exhibited an anti-obesity effect and improved insulin resistance in the HFD-fed mice. WS reportedly enhances muscle activity by increasing muscle mass and strength [22,23].

    BAT is rich in mitochondria, which are essential for non-shivering thermogenesis [9]. H&E staining of BAT showed that WSE supplementation resulted in a reduction in lipid accumulation induced by HFD (Figure 2A). Immunohistochemical and immunoblot analyses revealed that UCP1 expression was increased by WSE supplementation when compared with the level in mice fed the HFD (Figure 2A,B). The HFD decreased the expression of BAT-enriched genes, including UCP1,
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