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)

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Summary

Introduction

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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