Maternal dietary chromium restriction programs muscle development and function in the rat offspring

Abstract

Intrauterine growth retardation programs the fetus to manipulated metabolic changes that lead to adult diseases. Considering that chromium (Cr) supplements influence lean body mass (LBM) in both humans and experimental animals, we have studied the effect of maternal Cr restriction on muscle development and function in the rat offspring. Female weanling Wistar/NIN rats received, for 12 weeks, a control or 65% Cr-restricted diet ad libitum and mated with control males. While control mothers/offspring received control diet throughout (CrC), some restricted mothers were switched to control diet from conception (CrRC) and parturition (CrRP) and their offspring were weaned on to control diet. Half of the remaining restricted pups were weaned on to control diet (CrRW) and the other half continued on restricted diet throughout (CrR). Maternal CrR significantly decreased the percent of LBM (LBM %) and fat-free mass (FFM %) in the offspring and this was associated with decreased expression of the myogenic genes: MyoD, Myf5 and MyoG. Surprisingly, expression of the muscle atrophy genes, Atrogin and MuRF 1, was also decreased in CrR offspring. Although basal glucose uptake by muscle was higher in CrR than in CrC offspring, the stimulation with insulin was comparable, implying no change in its insulin sensitivity. Rehabilitation partly corrected myogenic and atrophic gene expression but had no effect on LBM % or FFM % or glucose uptake by muscle. The results show that maternal Cr restriction in rats may irreversibly impair muscle development and glucose uptake by muscle. Modulation of muscle atrophy appears to be an adaptive mechanism to preserve muscle mass in CrR offspring.