Background/ObjectiveThe prevalence of type 2 diabetes is increasing rapidly around the world. Work-related stress is thought to be a major risk factor for type 2 diabetes; however, this association has not been widely studied, and the findings that have been reported are inconsistent. Therefore, we conducted a meta-analysis of prospective cohort studies to explore the association between work-related stress and risk for type 2 diabetes.MethodsA systematic literature search and manual search limited to articles published in English were performed to select the prospective cohort studies evaluated the association between work-related stress and risk for type 2 diabetes up to September 2014 from four electronic databases including PubMed, EMBASE, the Cochrane Library and Web of Science. A random-effects model was used to estimate the overall risk.ResultsNo significant association was found between work-related stress and risk for type 2 diabetes based on meta-analysis of seven prospective cohort studies involving 214,086 participants and 5,511 cases (job demands: relative risk 0.94 [95% confidence interval 0.72–1.23]; decision latitude: relative risk 1.16 [0.85–1.58]; job strain: relative risk 1.12 [.0.95–1.32]). However, an association between work-related stress and risk for type 2 diabetes was observed in women (job strain: relative risk 1.22 [1.01–1.46]) (P = 0.04). A sensitivity analysis conducted by excluding one study in each turn yielded similar results. No publication bias was detected with a funnel plot despite the limited number of studies included in the analysis.ConclusionsThe results of this meta-analysis did not confirm a direct association between work-related stress and risk for type 2 diabetes. In subgroup analyses we found job strain was a risk factor for type 2 diabetes in women.

Diabetes-associated cognitive decline (DACD) is a brain injury induced by diabetes mellitus, with cognitive impairment as the major symptom. Growing evidence has revealed that DACD is correlated with disruptions in synapses involved in cognition. Within synapses, more specifically in areas of postsynaptic density (PSD), there is a high concentration of proteins that receive and transduce synaptic information. In the present study, to identify the differentially expressed PSD proteins among DACD mice, ZiBuPiYin recipe (ZBPYR)-treated DACD mice and control mice, we applied isobaric tags for relative and absolute quantitation (iTRAQ) with LC-MS/MS technology, by which three biological replicates and three technical replicates were examined. A total of 24 and 23 differentially expressed proteins were observed in control versus DACD mice and in DACD versus ZBPYR-treated DACD mice, respectively. Notably, we found 'Protein processing in endoplasmic reticulum' and 'PI3K-Akt signaling pathway' might be impaired in DACD pathogenesis, while Growth factor receptor-bound protein 2 might be a crucial protein as a molecular target of the neuroprotective effects of ZBPYR. To our knowledge, this is the first study to provide a reference proteome map for DACD and ZBPYR-treated DACD mouse forebrain PSD to aid understanding the underlying mechanisms of DACD and ZBPYR.