IDM have the propensity to hypoglycemia and hypoxia. Hypoxia can induce TNFα. Hyperglycemia increases GLUT1 in muscle, fatty tissue and cell lines. Therefore, IDM could have increased GLUT1 in the liver. TNFα increases glucose uptake in GLUT1 dominant cells. Thus, TNFα may increase liver glucose uptake, which leads to the decrease of gluconeogenesis. Since gluconeogenesis is necessary to maintain plasma glucose concentration in the newborn, the decreased gluconeogenesis would result ιυ hypoglycemia in IDM. Materials and Methods Pregnant SpragueDawley rats received an ip injection of streptozotocin (65 mg/kg) or an equivalent amount of saline on the 12th day of gestation. Rats on day 2 of life were used. Exp 1. Livers were harvested and sectioned at 50 μm thickness by cryostat. GLUT1 and GLUT2 were stained by an immunohistochemistry technique, using a floating method. Exp 2: Rats received an ip injection of TNFα (0.98 μg/kg) or an equivalent amount of saline. Plasma glucose concentration and liver PEPCK mRNA abundance were determined 0 or 6 hours after the injection. Results Exp 1: GLUT1 increased in IDM when compared to controls. Exp2: PEPCK mRNA abundance was decreased by TNFα. The decrease of PEPCK mRNA abundance was more significant (p<0.05) in IDM when compared to controls. Plasma glucose concentrations (mg/dl) are shown in the Table(mean±SEM, p<0.05 vs no TNFα in controls, **p<0.05 vs no TNFα in IDM) Conclusion IDM have a propensity to hypoglycemia and are more sensitive to hypoglycemic effects of TNFα.

Table 1
Full size table