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Articles

Effects of Hyperinsulinemia in the Primate Fetus

  1. John B Susa and
  2. Robert Schwartz
  1. Department of Pediatrics, Rhode Island Hospital and Brown University Providence, Rhode Island
  1. Address reprint requests to John B. Susa, Ph.D., Department of Pediatrics, Rhode Island Hospital, Providence, Rhode Island 02902
Diabetes 1985 Jun; 34(Supplement 2): 36-41. https://doi.org/10.2337/diab.34.2.S36
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Abstract

Nonhuman primate models of gestational diabetes have produced fetopathies most similar to those of the human infant of the mother with gestational diabetes (IGDM). Fetal hyperglycemia, hyperinsulinemia, macrosomia, selective organomegaly, intrauterine death, and placental hyperplasia are hallmarks of the fetopathy of the IGDM. The chronic infusion of insulin into the fetus of a normal pregnant rhesus monkey results in fetal hyperinsulinemia with normal to low plasma metabolic substrate concentrations. Under these conditions, fetal hyperinsulinemia is sufficient to cause fetal growth and hormone changes observed in the human IGDM. Our studies provide evidence that the soft tissue hyperplasia in the fetal macrosomia syndromes in humans and nonhuman primates in which fetal hyperinsulinemia is observed is the direct result of that chronic in utero hyperinsulinemia.

  • Copyright © 1985 by the American Diabetes Association

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June 1985, 34(Supplement 2)
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Effects of Hyperinsulinemia in the Primate Fetus
John B Susa, Robert Schwartz
Diabetes Jun 1985, 34 (Supplement 2) 36-41; DOI: 10.2337/diab.34.2.S36

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Effects of Hyperinsulinemia in the Primate Fetus
John B Susa, Robert Schwartz
Diabetes Jun 1985, 34 (Supplement 2) 36-41; DOI: 10.2337/diab.34.2.S36
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