Exposure to certain environmental factors during the early stages of development was found to affect health in adulthood. Among factors, oxidative stress has been suggested to be involved in fetal programming, leading to elevated risk for metabolic disorders, including type 2 diabetes; however, the possibility that antioxidant consumption during early life may affect the development of diabetes has scarcely been studied.
The aim of this study was to investigate the effect of N-acetyl-L-cysteine (NAC) given during pregnancy and lactation on the susceptibility of offspring to develop glucose intolerance and type 2 diabetes induced by high fat diet (HFD) feeding at adulthood. C57bl6 mice were given NAC during pregnancy and lactation. Isolated pancreatic islets of NAC-treated offspring (6 weeks old) had an increased efficacy of glucose stimulated insulin secretion (GSIS) and a higher resistance to H2O2-induced damage. HFD was given to control and NAC-offspring at an age of 6 weeks for additional 9 weeks. Results of glucose and insulin tolerance tests were improved, fasting insulin level was reduced, and islets diameter was lower in male offspring of NAC-treated mice compared to their HFD-fed littermates. Insulin sensitivity in skeletal muscle was increased, as determined by elevated phosphorylation of Akt, GSK3b and PRAS40 in offspring of NAC-treated mice.
Conclution: NAC consumption during early life improves glucose tolerance in adulthood in mice. The mechanisms underlying the observed effects should be investigated further.