Fetal pancreatic glucagon responses in glucose-intolerant nonhuman primate pregnancy.
Rhesus monkey pancreatic alpha-cell function in streptozotoc-induced glucose-intolerant pregnancy is similar to that in normal primate pregnancy. Specifically, basal maternal and fetal plasma glucagon levels equate, and the fetal alpha cell does not respond to the glucagonogenic stimulus of either intravenous alanine or insulin-induced hypoglycemia. This contrasts with the accelerated maturation of the fetal beta cell in glucose-intolerant pregnancy, and does not support the concept of functional coupling of the pancreatic islet by a common glucose-based process. Fetal plasma glucagon levels do increase after L-dopa injection to the fetus. These data indicate that alpha cell unresponsiveness is a function of the glucagon-releasing mechanism rather than inadequate hormonal synthesis.
D000409:Alanine / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000139:chemically induced; D005260:Female; D005934:Glucagon / Q000097:blood*; D000882:Haplorhini; D007980:Levodopa / Q000494:pharmacology; D008253:Macaca mulatta; D010179:Pancreas / Q000166:cytology / Q000378:metabolism*; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000378:metabolism*; D013311:Streptozocin
D001786:Blood Glucose; D007980:Levodopa; D013311:Streptozocin; D005934:Glucagon; D000409:Alanine