Gut microbiota dysbiosis -associated obesity and its involvement in cardiovascular diseases and type 2 diabetes. A systematic review.

INTRODUCTION

Obesity is a complex, multifactorial disease caused by various factors. Recently, the role of the gut microbiota in the development of obesity and its complications has attracted increasing interest.

PURPOSE

This article focuses on the mechanisms by which gut microbiota dysbiosis induces insulin resistance, type 2 diabetes, and cardiovascular diseases linked to obesity, highlighting the mechanisms explaining the role of gut microbiota dysbiosis-associated inflammation in the onset of these pathologies.

METHODS

A systematic study was carried out to understand and summarize the published results on this topic. More than 150 articles were included in this search, including different types of studies, consulted by an online search in English using various electronic search databases and predefined keywords related to the objectives of our study.

RESULTS

We have summarized the data from the articles consulted in this search, and we have found a major gut microbiota alteration in obesity, characterized by a specific decrease in butyrate-producing bacteria and the production of metabolites and components that lead to metabolic impairments and affect the progression of various diseases associated with obesity through distinct signaling pathways, including insulin resistance, type 2 diabetes, and cardiovascular diseases (CVD). We have also focused on the major role of inflammation as a link between gut microbiota dysbiosis and obesity-associated metabolic complications by explaining the mechanisms involved.

CONCLUSION

Gut microbiota dysbiosis plays a crucial role in the development of various obesity-related metabolic abnormalities, among them type 2 diabetes and CVD, and represents a major challenge for chronic disease prevention and health. Indeed, the intestinal microbiota appears to be a promising target for the nutritional or therapeutic management of these diseases.