Influence of lactation on morphometric and secretory variables in pancreatic beta-cell of mildly diabetic rats.
In nondiabetic rats, lactation accelerates the restoration of pancreatic beta-cell function after the period of increased secretory activity associated with pregnancy. To investigate whether a comparable situation prevails in mildly diabetic animals, streptozocin (22.5 mg/kg body wt) was administered to female rats at the onset of pregnancy. Plasma glucose and insulin concentrations, content and release of insulin in isolated islets, total mass and volume density of both the endocrine pancreas and granulated beta-cells, and ultrastructural prevalence of light and dark secretory granules were measured on the 20th day of pregnancy and in lactating and nonlactating animals 20 days after delivery. In the mildly diabetic animals, the changes in endocrine pancreatic function normally associated with pregnancy and lactation were greatly attenuated, albeit not completely eliminated. We propose that the increased biosynthetic and secretory activity imposed on surviving beta-cells after streptozocin administration tends to mask the adaptative changes in beta-cell function otherwise seen during the postpartum and lactation period.
Marynissen
G
G
Malaisse
W J
WJ
Van Assche
F A
FA
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology*; D005260:Female; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D007774:Lactation / Q000378:metabolism / Q000502:physiology*; D009929:Organ Size; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D007328:Insulin