Abstract
Green tea (GT) has various health effects, including anti-obesity properties. However, the multiple molecular mechanisms of the effects have not been fully determined. The aim of this study was to elucidate the anti-obesity effects of GT via the analysis of its metabolic and transcriptional responses based on RNA-seq profiles. C57BL/6J mice were fed a normal, high-fat (60% energy as fat), or high-fat + 0.25% (w/w) GT diet for 12 weeks. The GT extract ameliorated obesity, hepatic steatosis, dyslipidemia, and insulin resistance in diet-induced obesity (DIO) mice. GT supplementation resulted in body weight gain reduction than mice fed high-fat through enhanced energy expenditure, and reduced adiposity. The transcriptome profiles of epididymal white adipose tissue (eWAT) suggested that GT augments transcriptional responses to the degradation of branched chain amino acids (BCAAs), as well as AMP-activated protein kinase (AMPK) signaling, which suggests enhanced energy homeostasis. Our findings provide some significant insights into the effects of GT for the prevention of obesity and its comorbidities. We demonstrated that the GT extract contributed to the regulation of systemic metabolic homeostasis via transcriptional responses to not only lipid and glucose metabolism, but also amino acid metabolism via BCAA degradation in the adipose tissue of DIO mice.
Highlights
Obesity is a metabolic disorder characterized by excess fat accumulation in the body
These adipokines may contribute to the whole-body homeostasis in normal conditions; in an obese state, enlarged adipose tissue leads to the dysregulated secretion of adipokines
At 5 weeks of age, they were randomly divided into 3 groups of 10 mice per group, and fed either a normal diet (ND), high-fat diet (HFD), or HFD + 0.25% (w/w) Green tea (GT) extract for 12 weeks
Summary
Obesity is a metabolic disorder characterized by excess fat accumulation in the body It is associated with the development of hyperlipidemia, insulin resistance, type 2 diabetes mellitus, hypertension, and non-alcoholic fatty liver disease [1]. Adipose tissue is considered as a regulator of energy homeostasis and a key endocrine organ secreting multiple adipokines. These adipokines may contribute to the whole-body homeostasis in normal conditions; in an obese state, enlarged adipose tissue leads to the dysregulated secretion of adipokines. The dysregulated production of adipokines in obesity may contribute to inflammation, and to the development of various metabolic diseases via altered lipid and glucose homeostasis [4,5].
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