Intracellular Metabolism in Diabetic Embryopathy

Zhiyong Zhao

doi:10.34297/ajbsr.2021.13.001891

Abstract

Diabetes mellitus in early pregnancy can cause congenital birth defects in infants, a complication known as diabetic embryopathy. Formation of structural abnormalities, commonly seen in the central nervous and cardiovascular systems, is associated with increased programmed cell death (apoptosis) and decreased cell proliferation in the developing organs. Under maternal hyperglycemic conditions, influx of glucose into cells of the embryos disturbs intracellular metabolic homeostasis. Disturbed glycolysis generates factors through side pathways to perturb cell signaling and organelle functions. Perturbed phospholipid metabolism produces signaling metabolites and peroxidation products to suppress cell survival and induce apoptosis. Targeting the key processes and factors in the metabolism of glucose and phospholipids is a potential intervention strategy to prevent birth defects in diabetic pregnancies.

Highlights

Diabetes mellitus in early pregnancy imposes a risk of birth defects in infants [1,2,3,4]
It is urgent to understand the mechanism of diabetic embryopathy to develop interventions to prevent birth defects in diabetic pregnancies
These findings indicate that a potential strategy to use certain species of phospholipids, such as fish oil to replenish cardiolipin, to reduce embryonic malformations in diabetic pregnancies

Summary

Introduction

Diabetes mellitus in early pregnancy imposes a risk of birth defects in infants [1,2,3,4]. In the embryos cultured in high glucose [122], or the embryos in diabetic pregnant animals [131,132,133], treatment with arachidonic acid decreases malformation rates. These findings indicate that a potential strategy to use certain species of phospholipids, such as fish oil to replenish cardiolipin, to reduce embryonic malformations in diabetic pregnancies. In the cells of embryos from diabetic animals, decreases in arachidonic acid levels have been observed, indicating an active metabolism of the phospholipid [90,114]. These suggest that PGE2 may protect embryos from hyperglycemic insult

Concluding Remarks

Conflict of interest