Abstract:

Objective To investigate the effects of gestational diabetes mellitus (GDM) on the cardiac function of female offspring rats and underlying mechanisms by the rat model. Methods Wild type female SD rats were injected with streptozotocin (35 mg/kg) in the second trimester of pregnancy to establish the GDM model (GDM group). The control group was also established. Female F1 offspring rats were fed for 24 weeks after they were born. During this period, random blood glucose level, blood pressure, and heart rate were measured and glucose tolerance test and insulin tolerance test were conducted. The in vitro myocardial ischemia/reperfusion (I/R) model was established. The signaling pathways of protein kinase B (Akt), adenine monophosphate activated protein kinase (AMPK), and acetyl-coenzyme A carboxylase (ACC) in cardiac tissues were detected by Western blotting. Results The in vitro cardiac contractile function of female F1 offspring of the GDM group after I/R was significantly weaker than that of the control group (P=0.048 6). The results of Western blotting showed that the phosphorylation of AMPK and ACC in cardiac tissues of female F1 offspring of the GDM group after in vitro I/R was significantly lower than that of the control group (P=0.005 6). Conclusion GDM results in cardiac I/R intolerance of female offspring rats, which may be relevant to the blunt response to I/R stimulation caused by the phosphorylation of AMPK.

Key words: gestational diabetes mellitus, offspring, cardiac ischemia and reperfusion