Abstract

Obesity is intimately related to a chronic inflammatory state, with augmentation of macrophage infiltration and pro-inflammatory cytokine secretion in white adipose tissue (WAT) and mitochondrial dysfunction in skeletal muscle. The specific aim of this study is to evaluate effects of tartary buckwheat extract (TB) on obesity-induced adipose tissue inflammation and muscle peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α/sirtulin 1 (SIRT1) pathway in rats fed a high-fat diet. Sprague-Dawley rats were divided into four groups and fed either a normal diet (NOR), 45% high-fat diet (HF), HF + low dose of TB (TB-L; 5 g/kg diet), or HF + high dose of TB (TB-H; 10 g/kg diet) for 13 weeks. TB significantly reduced adipose tissue mass with decreased adipogenic gene expression of PPAR-γ and aP2. Serum nitric oxide levels and adipose tissue macrophage M1 polarization gene markers, such as iNOS, CD11c, and Arg1, and pro-inflammatory gene expression, including TNF-α, IL-6, and MCP-1, were remarkably downregulated in the TB-L and TB-H groups. Moreover, TB supplementation increased gene expression of PGC-1α and SIRT1, involved in muscle biogenesis and function. These results suggested that TB might attenuate obesity-induced inflammation and mitochondrial dysfunction by modulating adipose tissue inflammation and the muscle PGC-1α/SIRT1 pathway.

Highlights

  • Obesity refers to excessive fat accumulation in adipose tissue due to chronic positive energy balance [1]

  • Obesity refers to an abnormal adipose-hypertrophy state, which is often accompanied by a chronic inflammatory state [3,21]

  • Obesity refers to an abnormal adipose-hypertrophy state, which is often accompanied by a with macrophage polarization [6]

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Summary

Introduction

Obesity refers to excessive fat accumulation in adipose tissue due to chronic positive energy balance [1]. Cytokines are secreted from adipose tissue macrophage (ATM), which classically comprise two different forms: pro-inflammatory macrophage M1 and anti-inflammatory macrophage M2. Nutrients 2019, 11, 654 tend to change from M2 to M1 during the progression of adipose hypertrophy, and subsequently release pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and monocyte chemoattractant protein 1 (MCP-1) [5,6]. Such transformation of adipose tissue-resident macrophages is referred as macrophage polarization

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