Maternal mild hyperglycemia led to obese offspring developing insulin resistance, hyperglycemia, hyperinsulinemia, and qualitative abnormalities of lipoproteins by 3 months of age.
Does maternal mild diabetes alter lipoprotein metabolism in obese offspring over time?
Fetal hyperinsulinemia in a rat model is associated with the development of insulin resistance and dyslipoproteinemia by 3 months of age, suggesting it is a risk factor for later metabolic diseases.
The time course of changes in lipoprotein metabolism of obese offspring of mildly diabetic rats was studied with respect to serum lipoprotein composition as well as LCAT and tissue lipoprotein lipase (LPL) activities. Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin on day 5 of gestation. Control pregnant rats were injected with citrate buffer. At birth, obese pups had higher serum glucose, insulin, and lipoprotein (VLDL, LDL-HDL1, HDL(2-3)) levels than control pups. After 1 mon of life, all of these parameters in obese rats became similar to those of controls. However, LCAT, adipose tissue LPL, and hepatic triacylglycerol lipase activities were high. At 2 mon of age, VLDL-TAG levels were higher in obese females than in controls. By the age of 3 mon, obese offspring had developed insulin resistance with hyperglycemia, hyperinsulinemia, and higher serum lipoprotein concentrations. Indeed, qualitative abnormalities of lipoproteins were seen and were typical of obese and diabetic human beings. Fetal hyperinsulinemia should be considered as a risk factor for later metabolic diseases, including dyslipoproteinemia.
Merzouk et al. (Thu,) conducted a other in Obese offspring of mildly diabetic rats. Maternal mild hyperglycemia (streptozotocin-induced) vs. Control pregnant rats injected with citrate buffer was evaluated on Lipoprotein metabolism (serum lipoprotein composition, LCAT, and tissue LPL activities). Maternal mild hyperglycemia led to obese offspring developing insulin resistance, hyperglycemia, hyperinsulinemia, and qualitative abnormalities of lipoproteins by 3 months of age.