Glucose, an essential substrate for fetal myocardial oxidative metabolism, is transported into cardiomyocytes by facilitative glucose transporter (Glut) proteins, isoforms Glut 1 (basal) and Glut 4 (insulin-responsive). Previous studies in the adult and fetal rat revealed changes in myocardial Glut concentrations due to perturbations in circulating glucose & insulin levels. To investigate the time-dependent effect of fetal hyperglycemia with initial hyperinsulinemia (up to 48 hr) followed by normoinsulinemia (>48 hr to 41d) (HYPER) and hypoglycemia with consistent hypoinsulinemia (HYPO) upon fetal myocardial Glut 1 and Glut 4 levels, we used the late gestation chronically catheterized pregnant sheep. Maternal continuous 50% glucose infusions created the HYPER state (+80% in mother & fetus) (n=14), while 2 mU/kg/min of continuous maternal insulin infusions caused the HYPO state(<50% of normal) (n=13). Fetal myocardial Glut 1 and Glut 4 levels were assessed at 0 hr (n=5 [HYPER]; 6 [HYPO]), 2-3 hr (n=2 [HYPER]), 24-48 hr (n=2[HYPO]), 10-13d, (n=4 [HYPER]), 15-20d (n=3 [HYPER]), 25-41 d (n=5 [HYPO]) by quantitative Western blot analysis using the rabbit anti-rat Glut 1 and Glut 4 COOH peptide IgGs. HYPER did not alter fetal myocardial Glut 1 and Glut 4 concentrations at all times studied. In contrast, HYPO failed to alter Glut 1 but caused a two-fold increase in Glut 4 levels at all times investigated(p<0.02). These myocardial changes are unique and unlike our previous results in fetal ovine insulin responsive tissues (skeletal muscle and fat - Ped Res 37:347&1817;1995). We conclude that 1] HYPER & HYPO states associated with changes in fetal glucose & insulin levels do not alter fetal myocardial Glut 1 levels, 2] HYPER with transient hyperinsulinemia followed by normoinsulinemia does not affect myocardial GLUT 4, and 3] HYPO characterized by persistent fetal hypoinsulinemia increases myocardial Glut 4 concentrations. We speculate that the fetal hypoinsulinemia induced Glut 4 elevation may preempt the development of in-utero & postnatal insulin hyperresponsiveness.