The effect of long-term magnesium treatment on changes in hepatic autophagic and apoptotic ability of type 2 diabetic female rats and their offspring

Abstract

AimWe investigated the role of magnesium sulfate (MgSO4) and insulin administration on improved autophagy and apoptosis to prevent diabetes in high-fat diet (HFD)-diabetic parents and their offspring. MethodsA HFD and a low dose of streptozotocin (STZ) were used to induce diabetes. Animals were assigned to four groups: non-diabetic control (NDC), diabetic control (DC), the diabetic group received insulin (INS), and the diabetic group received magnesium (MG). The duration of the research was 6 months, and offspring were fed a normal diet for 4 months. Blood glucose was determined weekly in rats (parents and offspring). The gene expression of adenosine monophosphate-activated protein kinase (AMPKα1), Bcl-2-interacting myosin-like coiled-coil protein (Becline-1), P62, Microtubule-associated protein 1 light chain 3 (LC3-II), and caspase-9 of liver tissues were assessed using Real-time PCR. ResultThe analysis of maternal gene expression data showed that treatment with MG and INS considerably augmented the AMPKα1 and LC3-II genes expression and diminished P62 and caspase-9 expression. Also, a significant decrease in the expression of AMPKα1, LC3-II, P62, and Becline-1 was observed in the female offspring in the MG and INS groups. Significant alterations in levels of AMPKα1, Beclin-1, P62, and caspase-9 mRNA were not observed between groups in male offspring, but the expression of LC3-II considerably diminished in the groups compared with the DC group. DiscussionOur data demonstrated that MG supplementation strengthened the mother's autophagy and reduced the transmission of damage to the female offspring. In the male offspring, the transmission of damage was generally less, and MG improved the autophagy condition in the male offspring. Our findings support the presence of a link between autophagy induction and MG-modified biomaterials and determine a potential mechanism of MG-mediated diabetes and autophagy.