Pesticides exposure induced obesity and its associated diseases: recent progress and challenges

Abstract

The potential influence of pesticide residue exposure on glucose and lipid metabolism dysregulation has received extensive attention in recent years due to its great threat to food safety and human health. To understand the most recent research progress, we reviewed the publications about the influence and mechanisms of different pesticides’ exposure on the development of obesity, type 2 diabetes, and the associated diseases from 2015 to 2021 in this paper. Pesticides from several different classes were observed to significantly promote 3T3-L1 adipocytes adipogenesis and fat accumulation. Several key adipogenic regulators, including CCAAT/enhancer-binding proteinα (C/EBPα), peroxisome proliferators-activated receptors (PPARγ), fatty acid synthase increased (FAS), and glucose transporter 4 (GLUT4) were suggested to be responsible for the enhanced adipogenesis induced by pesticides. Besides, these pesticides may inhibit the phosphorylation of adenosine 5′-monophosphate-activated protein kinase (AMPK) to promote the expression of these key adipogenic regulators. Moreover, apolipoprotein E3 (apoE3) expressing mice or mice with high-fat diet are more vulnerable to pesticide-induced obesity. Besides, pesticides may also alter the gut microbiota, destroy the gut barrier integrity, enabling the lipopolysaccharide to enter the gut, thereby causing inflammation, eventually leading to lipogenesis. Although emerging evidences are linking pesticides exposure to impaired glucose, lipid metabolism, and altered gut microbiota, more mechanism and epidemiology studies, as well as the determination of physiological levels of pesticides, are needed to better understand the role of pesticide exposure in the development of these chronic diseases.