Biochemical investigation of human exposure to aflatoxin M1 and its association with risk factors of diabetes mellitus.

Abstract

Recently, aflatoxin M1 (AFM1) has emerged as a major health concern owing to its exposure to human being via consumption of milk, dairy products, and food commodities, and this has a strong association with risk factors that may lead to the onset of type 2 diabetes mellitus (T2DM) and various other associated metabolic disorders. This study was conducted to investigate the exposure to AFM1 and its association with sociodemographic features and risk factors of T2DM. Urine and blood samples from 672 participants were collected to investigate the concentration of AFM1 in urine and glucose, glycosylated hemoglobin (HbA1c), insulin, α-amylase, dipeptidyl peptidase-IV (DPP-IV), free fatty acids (FFAs), triglycerides (TGs), high-density lipoprotein cholesterol (HDL-chol), interleukine-6 (IL-6), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), creatinine, uric acid, blood urea nitrogen (BUN), aspartate aminotransferase (AST), and alanine transaminase (ALT) from the blood of study participants. Association of exposure to AFM1 with sociodemographic features and risk factors of T2DM was determined using person correlation coefficient (r), coefficient of determination (R2), and 95% confidence interval, and the level of significance (P<0.05) was measured by Student's unpaired t-test. Among the participants in which AFM1 was detected, 62.91% of participants were found to be diabetic and 37.09% of participants were found to be non-diabetic. Further to this, it was also found that concentration of AFM1 in the urine of diabetic participants was found to be higher (P<0.05) as compared to that in non-diabetic participants. Association of AFM1 exposure with risk factors of T2MD exhibits that exposure to AFM1 was responsible for the induction of inflammatory responses and oxidative stress that may lead to the onset of impaired insulin secretion and metabolism of carbohydrates and ultimately the onset of T2DM and associated metabolic disorders. Hence, it can be summarized that exposure to AFM1 is one of the causative factors that may lead to potentiate the several risk factors notably inflammatory responses and oxidative stress that ultimately induce the pathogenesis of T2DM and associated metabolic disorders. The key findings of this study suggest that human population who are at greater risk of AFM1 exposure can develop T2DM and other associated metabolic risk factors.