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

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.

Human exposure to bisphenol A through dietary sources and development of diabetes mellitus: a cross-sectional study in Pakistani population.

Bisphenol A (BPA) is considered as xenoestrogen, a crucial component utilized for the manufacturing of plastic products. It has a potential to disrupt the endocrine system and induces endocrine-related metabolic disorders. We aimed to investigate the exposure of BPA in Pakistani population and its association with sociodemographic features, dietary habits, and risk factors of diabetes mellitus (DM). This cross-sectional study was conducted on 400 participants among which 61.75% participants were diabetic and 38.25% were non-diabetic. We developed a structured questionnaire, gathered sociodemographic data, and collected their urine and blood samples for the estimation of BPA and various biomarkers as risk factors of DM, respectively. Pearson correlation coefficient was determined for urinary BPA levels and DM risk factors. Urinary BPA values were adjusted for confounders. Sociodemographic data shown that urinary BPA level was significantly higher (p < 0.05) in obese people (BMI > 27) living in semi-urban and industrial areas. BPA was detectable in 75% of study participants. Urinary BPA level was found to be higher in diabetic participants compared with that of non-diabetics. A significant correlation is observed between BPA exposure and DM risk factors. We found that urinary BPA level was correlated with elevated levels of HbA1c (r = 0.6028), HOMA-IR (r = 0.5356), CRP (r = 0.6946), BUN (r = 0.6077), AST (r = 0.5151), FFA (r = 0.5759), TGs (r = 0.5608), and MDA (r = 0.6908). Hence, our study adds to the growing body of evidence supporting the role of BPA exposure as a risk factor for DM and may be associated with higher glycemic index, increased pro-inflammatory and oxidative stress biomarkers, dyslipidemia, and impaired functioning of the liver and kidney. Heating food in plastic containers and consumption of packed food items are the main sources of BPA exposure which are positively associated with DM.

Chronic exposure of bisphenol A impairs carbohydrate and lipid metabolism by altering corresponding enzymatic and metabolic pathways.

Bisphenol-A (BPA), a widespread endocrine-disrupting chemical, has been recognized as a risk factor for metabolic disorders. BPA is considered to be involved in the impairment of carbohydrate and lipid metabolism but the underlying mechanisms still need to be elucidated. Present study was aimed to investigate the impact of BPA exposure on enzymatic and metabolic pathways that are responsible to regulate the carbohydrate and lipid metabolism. Experimental rats were exposed to different doses of BPA (50, 500, 2500 and 5000 µg/kg/day orally) dissolved in 1.5% dimethyl sulfoxide for a period of 3 months. Serum level of key metabolic enzymes (α-amylase, α-glucosidase, hexokinase, glucose-6-phosphatase and HMG-CoA-reductase) was measured by ELISA method. BPA-exposure suppressed the mRNA expression of gene encoding insulin resulting in poor insulin production. While hexokinase, acetyl-CoA carboxylase and squalene epoxide were up-regulated upon BPA exposure that justified the increased lipid profile. Moreover, BPA exposure showed considerably decreased glucose uptake through insulin signaling via Akt/GLUT4 pathways. There was a significant (p < 0.001) reduction in tissue level of glucose transporters. BPA significantly (p < 0.001) decreased the serum levels of oxidative stress biomarkers (GSH, CAT, and SOD). Serum levels of leptin, TNF-α, and IL-6 were rapidly increased upon exposure to BPA (p < 0.001). It was clearly evident from this study that BPA disturbed the carbohydrate and lipid metabolism after chronic exposure. It also accelerated the inflammatory processes by increasing the oxidative stress which ultimately lead towards the insulin resistance and impaired carbohydrate and lipid metabolism.