Pancreatic alpha cell response to alanine during and after normal and diabetic pregnancies

• Published in: Obstetrics and gynecology (New York. 1953) Vol. 56; no. 4; p. 440
• Main Authors: Kitzmiller, J L, Tanenberg, R J, Aoki, T T, Tabatabaii, A, Gleason, R, Jewett, J F, Hare, J W, Soeldner, J S
• Format: Journal Article
• Language: English
• Published: United States 01.10.1980
• Subjects: Administration, Oral; Adult; Alanine - administration & dosage; Alanine - pharmacology; Blood Glucose - metabolism; Female; Glucagon - metabolism; Humans; Insulin - metabolism; Insulin Secretion; Islets of Langerhans - cytology; Islets of Langerhans - drug effects; Islets of Langerhans - metabolism; Postpartum Period; Pregnancy; Pregnancy in Diabetics - metabolism; Pregnancy Trimester, Third; Stimulation, Chemical
• ISSN: 0029-7844

Pancreatic alpha cell response to oral alanine was assessed in the third trimester of pregnancy and in the puerperium in 16 insulin-dependent diabetic and 7 normal pegnant women. Insulin response was also measured in the nondiabetic subjects. The nondiabetic subjects had higher basal glucagon and insulin levels as well as a greater response to oral alanine stimulation at 34 weeks' gestation than at 6 weeks post partum. In addition, basal levels of both hormones remained low at a time remote from pregnancy (9 months post partum), indicating both hyperinsulinemia and hyperglucagonemia in the postabsorptive state in normal human pregnancy. The secretory response of glucagon and insulin or oral alanine was blunted at 6 weeks post partum in the nondiabetic subjects. This suggests that the late puerperium may not be an appropriate "nonpregnant control period" for metabolic studies. During pregnancy, basal and stimulated glucagon levels were not significantly different in diabetic and normal women. Despite higher concentrations of blood glucose in diabetic women, basal and stimulated glucagon secretion was equivalent in the 2 groups. No pegnancy-induced increment in glucagon secretion was evident in insulin-treated diabetic subjects. Thus hyperglucagonemia does not contribute to the increased requirements for insulin during pregnancy in these women.