Abstract

Decreased energy expenditure and chronically positive energy balance contribute to the prevalence of obesity and associated metabolic dysfunctions, such as dyslipidemia, hepatic fat accumulation, inflammation, and muscle mitochondrial defects. We investigated the effects of Chrysanthemum morifolium Ramat flower extract (CE) on obesity-induced inflammation and muscle mitochondria changes. Sprague–Dawley rats were randomly divided into four groups and fed either a normal diet, 45% high-fat diet (HF), HF containing 0.2% CE, or 0.4% CE for 13 weeks. CE alleviated HF-increased adipose tissue mass and size, dyslipidemia, hepatic fat deposition, and systematic inflammation, and increased energy expenditure. CE significantly decreased gene expression involved in adipogenesis, pro-inflammation, and the M1 macrophage phenotype, as well as glycerol-3-phosphate dehydrogenase (GPDH) and nuclear factor-kappa B (NF-kB) activities in epididymal adipose tissue. Moreover, CE supplementation improved hepatic fat accumulation and modulated gene expression related to fat synthesis and oxidation with an increase in adenosine monophosphate-activated protein kinase (AMPK) activity in the liver. Furthermore, CE increased muscle mitochondrial size, mitochondrial DNA (mtDNA) content, and gene expression related to mitochondrial biogenesis and function, including sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), and PGC-1α-target genes, along with AMPK-SIRT1 activities in the skeletal muscle. These results suggest that CE attenuates obesity-associated inflammation by modulating the muscle AMPK-SIRT1 pathway.

Highlights

  • Obesity results in a chronic energy imbalance between energy intake and energy expenditure

  • We investigated the molecular mechanism by which hot water extract of Chrysanthemum morifolium Ramat flower (CE) ameliorates high fat diet-induced obesity-related inflammation and skeletal muscle mitochondrial changes in obese rats

  • We demonstrate that CE supplementation reduces body fat adiposity and obesity-related inflammation in high-fat diet (HF)-fed obese rats

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Summary

Introduction

Obesity results in a chronic energy imbalance between energy intake and energy expenditure. Excess energy intake over energy expenditure results in fat accumulation in white adipose tissue, which is a main feature of obesity [1,2]. Reduced energy expenditure is a critical factor in metabolic regulation in the development of obesity [3,4]. Obesity-induced chronic inflammation contributes to the development of metabolic disorders, such as dyslipidemia, non-alcoholic fatty liver (NAFLD), type 2 diabetes, hypertension, and cardiovascular disease [8]. An understanding of the molecular mechanisms of adipose tissue during the development of obesity is critical for the prevention and treatment of obesity and related metabolic dysfunction

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