Serum selenium level and gestational diabetes mellitus: a systematic review and meta-analysis.

BACKGROUND: The association between serum selenium level and gestational diabetes mellitus (GDM) is controversial. The aim of our study was to systematically review available literature linking selenium to GDM for a comprehensive understanding of the relationship between serum selenium level and GDM in human. METHODS: PubMed, The Cochrane Library and Medline were searched for studies published up to August 2016. Manual searches of references of the relevant original studies were carried out. Pooled estimates were measured using the fixed or random effect model. Overall effect was reported in a standard mean difference (SMD). All data were analyzed with Review Manager 5.3 and Stata 12.0. RESULTS: Of 44 references reviewed, seven studies involving 569 patients met our inclusion criteria and contributed to meta-analysis. All the studies were used to evaluate the relationship between serum selenium level and GDM. Selenium level was significantly lower in women with GDM than those without GDM (SMD = -1.17; 95 % CI: -1.98 to -0.35, P = 0.005). Subgroup analysis showed that such trend was consistent within the non-Caucasian population (Asia: SMD = -2.82; 95 % CI: -5.21 to -0.43, P = 0.02; Africa: SMD = -0.56; 95 % CI: -1.07 to -0.05, P = 0.03) and in the third trimester (SMD = -1.78; 95 % CI: -3.04 to -0.52, P = 0.006), but not within the Caucasian population (Europe: SMD = -0.6; 95 % CI: -1.98 to 0.78, P = 0.39) or in the second trimester (SMD = -0.68; 95 % CI: -1.6 to 0.25, P = 0.15). CONCLUSIONS: The available evidences suggested that serum selenium level was lower in women with GDM than those with normal glucose tolerance, especially within the non-Caucasian population and in the third trimester. However, well-designed prospective studies are needed to understand dynamic associations between selenium status and GDM risk.

Ventricular hypertrophy abrogates intralipid-induced cardioprotection by alteration of reperfusion injury salvage kinase/glycogen synthase kinase 3ß signal.

Recent studies have demonstrated that intralipid (ILP) conferred myocardial protection against ischemia-reperfusion (IR) injury through activation of reperfusion injury salvage kinase (RISK) pathway. As RISK signal has been shown to be impaired in hypertrophied myocardium, we investigated whether ILP-induced cardiac protection was maintained in hypertrophied rat hearts. Transverse aortic constriction was performed on male Sprague-Dawley rats to induce left ventricular hypertrophy, then sham-operated or hypertrophied rat hearts were isolated and perfused retrogradely by the Langendorff for 30 min (equilibration) followed by 40 min of ischemia and then 120 min of reperfusion. The isolated hearts received 15-min episode of 1% ILP separated by 15 min of washout or three episodes of 5-min ischemia followed by 5-min reperfusion before ischemia. The hemodynamics, infarct size, apoptosis, phosphorylated protein kinase B (p-Akt), phosphorylated extracellular regulated protein kinase 1/2 (ERK1/2), phosphorylated glycogen synthase kinase 3ß (GSK3ß), Bcl-2, phosphorylated Bad, and Bax were determined. We found that ILP significantly improved left ventricular hemodynamics and reduced infarct size and the number of TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling)-positive cells in the sham-operated rat hearts exposed to IR. However, such myocardial infarct-sparing effect of ILP was completely blocked by phosphatidylinositol-3-kinase inhibitor wortmannin, but only partially by mitogen-activated protein kinase kinase inhibitor PD98059 in sham-operated hearts. Intralipd upregulated the phosphorylation of Akt, extracellular regulated protein kinase 1/2 (ERK1/2), and their downstream target of GSK3ß and antiapoptotic Bcl-2 expression in healthy rat hearts. Nonetheless, ILP failed to improve left ventricular hemodynamics and reduced infarct size and apoptosis and increase the phosphorylated Akt, ERK1/2, GSK3ß, and antiapoptotic Bcl-2 in hypertrophied myocardium. In contrast, ischemic preconditioning increased the phosphorylation of Akt, ERK1/2 and GSK3ß, improved heart pump function, and reduced myocardial necrosis in sham-operated hearts, a phenomenon partially attenuated by ventricular hypertrophy. Interestingly, GSK inhibitor SB216763 conferred cardioprotection against IR injury in sham-operated hearts, but failed to exert cardioprotection in hypertrophied myocardium. Our results indicated that ventricular hypertrophy abrogated ILP-induced cardioprotection against IR injury by alteration of RISK/GSK3ß signal.