Glucose Metabolism In Offspring Research Articles

Neonatal glucose metabolism in offspring of mothers with varying degrees of hyperglycemia during pregnancy

The definition of neonatal hypoglycemia is controversial. Operational thresholds of blood glucose values at which intervention should be considered have been proposed. IDM and GDM infants frequently exhibit a pronounced drop of plasma glucose immediately after birth. This exaggerated physiological decline of glucose is transient and is seldom accompanied by suppressed lipolysis or clinical symptoms. It is generally attributed to hyperinsulinism elicited by maternal hyperglycemia. Alternative substrates for CNS i.e. lactate and astrocyte glycogen may explain lack of symptoms. Similarly low glucose values later on may cause clinical symptoms. Glucose production rates vary from attenuated to normal likely reflecting differences in maternal glycemic control. The HAPO study of around 25,000 non-diabetic pregnancies revealed strong associations between glucose values (75g OGTT) and increased fetal size and hyperinsulinemia at birth - findings adding strong support to the maternal hyperglycemia - fetal hypinsulinism theory. Mothers with the highest fasting glucose had infants with the highest frequency of clinical neonatal hypoglycaemia (4,6%).

P2-41 Effects of ewe size and nutrition during pregnancy on glucose metabolism in offspring

P2-41 Effects of ewe size and nutrition during pregnancy on glucose metabolism in offspring

Diabetic pregnancy in rats leads to impaired glucose metabolism in offspring involving tissue-specific dysregulation of 11β-hydroxysteroid dehydrogenase type 1 expression

Population-based studies have shown that the offspring of diabetic mothers have an increased risk of developing obesity, insulin resistance, type 2 diabetes and hypertension in later life. To investigate mechanism for the high incidence of metabolic diseases in the offspring of diabetic mothers, we focused on the tissue-specific glucocorticoid regulation by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and studied offspring born to streptozotocin-induced diabetic rats. The body weights of newborn rats from diabetic mothers were heavier than those from control mothers. Offspring born to diabetic mothers demonstrated insulin resistance and mild glucose intolerance after glucose loading at 10 weeks and showed significantly increased 11β-HSD1 mRNA and enzyme activity in adipose tissue at 12 weeks of age without obvious obesity. Hepatic 11β-HSD1 mRNA was also elevated. We propose that the 11β-HSD1 in adipose tissue and liver may play a key role in the development of metabolic syndrome in the offspring of diabetic mothers. Tissue-specific glucocorticoid dysregulation provides a candidate mechanism for the high incidence of metabolic diseases in the offspring of diabetic mothers. Therefore early analyses before apparent obesity are needed to elucidate the molecular mechanisms that may be programmed during the fetal period.