Effect of Pesticides on Peroxisome Proliferator-Activated Receptors (PPARs) and Their Association with Obesity and Diabetes

Figure 2

Effects of pesticides on carbohydrate and fat metabolism involving diabetes and obesity through activation of PPARs. Activation of PPARs by pesticides and their effects have been linked to the development of obesity and diabetes in many tissues: adipocytes (a) show mainly PPARα and PPARγ activation to lipid metabolism; in hepatocytes (b) PPARγ is involved in lipid metabolism, PPARα is associated with peroxisome proliferation to cancer and PPAR β/δ in the carbohydrate metabolism; in pancreatic beta cells (c) the role of PPAR affected by pesticides and the function of these cells is not clear; in myocytes (d) PPAR β/δ activation is essential for the regulation of energy metabolism, but the effects of pesticide exposure are unclear; finally, (e) the disruption of the gut microbiota in the development of obesity and diabetes about PPAR activation is unknown. Abbreviations: ACC, acetyl Co-A carboxylase; ACO, acyl-CoA oxidase; AMPKa, AMP-activated protein kinase alpha; ATP, adenosine triphosphate; C/EBP-α, CCAAT enhancer binding protein alpha; C/EBP-δ, CCAAT enhancer binding protein delta; C/EBP-β, CCAAT enhancer binding protein beta; CPT-1, carnitine palmitoyltransferase I; ER, endoplasmic reticulum, FABP4, fatty acid-binding protein 4; FAS, fatty acid synthase; GLUT-2, glucose transporter type 2; GLUT-4, glucose transporter type 4; LPL, lipoprotein lipase; PPARα, peroxisome proliferator-activated receptor alpha; PPARβ/δ, peroxisome proliferator-activated receptor beta/delta; PPARγ, peroxisome proliferator-activated receptor gamma; ROS, reactive oxygen species; RXR, retinoid X receptor; SREBP-1C, sterol regulatory element-binding protein 1, TG, triglycerides.