Abstract

The gut microbiota, often viewed as a “digestive organ,” can influence the development of obesity and related metabolic disorders. Diet is significantly important in shaping the structure and modulating the function of the gut microbiota. Apigenin (Api) widely exists in fruits and vegetables as a naturally occurring flavonoid and has anti-obesogenic, anti-inflammatory, and anti-carcinogenic properties. Its low bioavailability means it has enough time to interact with the intestine thus becomes a potential substrate for the gut intestine; thus, contributing to gut health. Here, we show that Api reduces whole-body weight, low-grade inflammation, and insulin resistance in high-fat diet (HFD)-induced obese mice. Our results reflect that Api supplementation can substantially improve intestinal dysbiosis triggered by HFD and restores gut barrier damage by alleviating metabolic endotoxemia. Augmentation of Akkermansia and Incertae_Sedis along with reduction of Faecalibaculum and Dubosiella at the genus level potentially mediated the protective effects of Api on metabolic syndrome. Furthermore, we show that the impact of Api on the reduction of body weight and the modification of gut microbiota could be transferred from Api-administered mice to HFD-feeding mice via horizontal fecal microbiota transplantation. Taken together, our data highlight the prebiotic role of Api and show its contribution to the restraint of gut dysbiosis and metabolic deterioration associated with obesity in mice.

Highlights

  • Obesity, a metabolic disturbance, is featured by excessive accumulation of body fat due to the imbalance between energy intake and consumption

  • N, the administration of Api markedly improved glucose intolerance and enhanced insulin sensitivity after high-fat diet (HFD) feeding. These findings indicate that Api may offer a metabolic protective function in HFD-fed mice by alleviating obesity and insulin resistance

  • Intensive investigations have proved that gut microbiota dysbiosis is closely associated with dietary habits and can lead to the development of a metabolic syndrome caused by obesity (Miele et al, 2009; Marchesi et al, 2016)

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Summary

Introduction

A metabolic disturbance, is featured by excessive accumulation of body fat due to the imbalance between energy intake and consumption (where energy intake exceeds energy expenditure; Must et al, 1999). Excessive abdominal fat increases the risk of metabolic syndrome, which is closely associated with numerous chronic diseases, such as cardiovascular disease, hypertension, dyslipidemia, non-alcoholic fatty liver disease (NAFLD), diabetes, and cancer (Despres and Lemieux, 2006). It is self-evident that obesity can pose adverse effects on human health. Previous studies have suggested that gut microbiota dysbiosis contributes to the obesity pathophysiology and is related to chronic metabolic diseases, such as NAFLD and diabetes (Canfora et al, 2019). Improving the condition of the gut microbiota is a potential treatment for obesity

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