Abstract
The purpose of the present study was to determine whether an anti-obesity effect of a Polygonum multiflorum Thunb. hot water extract (PW) was involved in the lipid metabolism of white adipose tissue (WAT) and brown adipose tissue (BAT) in high-fat diet (HFD)-induced C57BL/6N obese mice. Mice freely received a normal diet (NCD) or an HFD for 12 weeks; HFD-fed mice were orally given PW (100 or 300 mg/kg) or garcinia cambogia (GC, 200 mg/kg) once a day. After 12 weeks, PW (300 mg/kg) or GC significantly alleviated adiposity by reducing body weight, WAT weights, and food efficiency ratio. PW (300 mg/kg) improved hyperinsulinemia and enhanced insulin sensitivity. In addition, PW (300 mg/kg) significantly down-regulated expression of carbohydrate-responsive element-binding protein (ChREBP) and diacylglycerol O-acyltransferase 2 (DGAT2) genes in WAT compared with the untreated HFD group. HFD increased BAT gene levels such as adrenoceptor beta 3 (ADRB3), peroxisome proliferator-activated receptor γ (PPARγ), hormone-sensitive lipase (HSL), cluster of differentiation 36 (CD36), fatty acid-binding protein 4 (FABP4), PPARγ coactivator 1-α (PGC-1α), PPARα, and carnitine palmitoyltransferase 1B (CPT1B) compared with the NCD group; however, PW or GC effectively reversed those levels. These findings suggest that the anti-obesity activity of PW was mediated via suppression of lipogenesis in WAT, leading to the normalization of lipid metabolism in BAT.
Highlights
Obesity is a chronic complex disease caused by a persistent positive energy balance in which energy intake exceeds energy expenditure [1]
3 (ADRB3), peroxisome proliferator-activated receptor γ (PPARγ), hormone-sensitive lipase (HSL), cluster of differentiation 36 (CD36), fatty acid-binding protein 4 (FABP4), PPARγ coactivator 1-α (PGC-1α), PPARα, and carnitine palmitoyltransferase 1B (CPT1B) compared with the NCD group; PM hot water extract (PW) or garcinia cambogia (GC) effectively reversed those levels. These findings suggest that the anti-obesity activity of PW was mediated via suppression of lipogenesis in white adipose tissue (WAT), leading to the normalization of lipid metabolism in brown adipose tissue (BAT)
PW and GC did not affect food intake, but the food efficiency ratios (FER) in the NCD, PW300, and GC200 groups were reduced compared with the high-fat diet (HFD) group (Table 2)
Summary
Obesity is a chronic complex disease caused by a persistent positive energy balance in which energy intake exceeds energy expenditure [1]. WAT stores extra energy in a triglyceride (TG) form, while BAT is responsible for dissipation of energy as heat through thermogenesis to maintain body temperature and energy balance [2]. BAT activates thermogenesis in response to cold exposure and overfeeding, thereby contributing to the control of whole-body energy expenditure and body fat contents [3,4]. For this reason, activation of BAT is expected to provide a therapeutic effect on obesity and related metabolic disorders [5].
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