Background: There has been increased recognition that prenatal or perinatal nutrition has an effect on the development of type 2 diabetes (T2D) in ad

In previously published articles, we evaluated the toxicity of four organophosphate (OP) pesticides (dichlorvos, dimethoate, acephate, and phorate) in rats using metabonomic technology at their corresponding no observed adverse effect levels (NOAELs). The results show that a single pesticide did not elicit a toxic response. The joint toxic action of four pesticides (at their corresponding NOAELs) was evaluated by metabolomic analysis of rat plasma under experimental conditions similar to those of the four single OP pesticides. The pesticides were administered daily to rats through drinking water for 24 weeks. The mixture of four pesticides showed a joint toxic action at the NOAELs of each pesticide. The 19 metabolites were statistically significantly changed in all the treated groups compared with those in the control group (p < 0.05 or p < 0.01). Exposure to OP pesticides resulted in increased lysoPC (15 : 0/0 : 0), lysoPC (16 : 0/0 : 0), lysoPC (O-18 : 0/0 : 0), lysoPC (P-19 : 1(12Z)/0 : 0), lysoPC (18 : 1(9Z)/0 : 0), lysoPC (18 : 0/0 : 0), lysoPC (20 : 4(5Z, 8Z, 11Z, 14Z)/0 : 0), lysoPE (16 : 0/0 : 0), lysoPC (17 : 0/0 : 0), 4-pyridoxic acid, glutamic acid, glycocholic acid, and arachidonic acid, as well as decreased C16 sphinganine, C17 sphinganine, phytosphingosine, indoleacrylic acid, tryptophan, and iodotyrosine in rat plasma. The results indicate that the mixture of OP pesticides induced oxidative stress, liver and renal dysfunction, disturbed the metabolism of lipids and amino acids, and interfered with the function of the thyroid gland. The present plasma results provided complementarities with our previous metabolomic analysis of the rat urine profile exposed to a mixture of four OP pesticides, and also contributed to the understanding of the mechanism of joint toxic action.

The relationship between selenium (Se) and type 2 diabetes (T2D) remains controversial. In previous animal and cell studies, Se was found to be insulin mimic and antidiabetic, whereas recent epidemiological and interventional trials have shown an unexpected association between high Se intake and increased risk of T2D. The present study aimed to investigate the significance of dietary Se and T2D in North Chinese adults. A large sample of the population was enrolled through cluster sampling in Northern China (N = 8824). Information on basic characteristics, anthropometric measures, and dietary Se intake was collected from each subject for analysis. Multivariable logistic regression was used to investigate the association between dietary Se and T2D through adjusted odds ratio (OR) and the corresponding 95% confidence interval (CI). The average nutritional Se intake was 52.43 μg/day, and the prevalence of T2D was 20.4% in the studied population. The OR for developing T2D was 1.66 (95% CI: 1.38, 1.99; P for linear trend <0.005), comparing the highest to the lowest quintile of energy‐adjusted Se intake in multivariate logistic regression analysis. The mediation analysis discovered that glucose metabolism (indicated by FBG and HbA1c) mediated this association. In conclusion, our research adds further support to the role of high dietary Se in the incidence of T2D. The results also suggested that this association was mediated by glucose metabolism.