-transparent.png){kind=logo}
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.
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
July 2015,
Radiology,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
January 1976,
Perspectives in nephrology and hypertension,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
July 2020,
Toxicology and applied pharmacology,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
April 2015,
Current opinion in pediatrics,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
April 1993,
Transplantation,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
January 1981,
Journal of medical primatology,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
June 1999,
Transplantation proceedings,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
August 1994,
Laboratory investigation; a journal of technical methods and pathology,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
July 2010,
Biological psychiatry,
M Epstein, and
R A Chez, and
G K Oakes, and
D H Mintz
January 1974,
Drug metabolism and disposition: the biological fate of chemicals,
