Hepatic insulin and glucagon receptors in pregnancy: Their role in the enhanced catabolism during fasting

Gerhard Baumann*, Gobchai Puavilai, Norbert Freinkel, Lawrence A. Domont, Boyd E Metzger, Harold B. Levene

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


The response to dietary deprivation in late pregnancy, as compared to the non-pregnant condition, is more rapid and profound in terms of mobilization of fuels from peripheral tissues as well as hepatic ketogenesis and gluconeogenesis ("accelerated starvation"). We examined the potential role of hepatic insulin and glucagon receptors in mediating these changes by comparing 48-h fasted 18-day pregnant and age-matched nongravid rats. Molar ratios for insulin:glucagon in peripheral and portal blood were significantly higher in the pregnant rats. Insulin binding to purified liver plasma membrane receptors, when appropriately corrected for differences in insulin degradation by the membrane system, was marginally diminished in the pregnant animals. Glucagon binding and adenylate cyclase activation by glucagon was indistinguishable in the two groups of animals. On the basis of portal vein hormone concentrations and the values for receptor binding, liver insulinization relative to glucagonization appears to be unchanged or slightly increased in the fasted pregnant rat compared to the fasted nongravid rat. Thus, it seems unlikely that much of the “accelerated starvation” response in late pregnancy can be ascribed to diminished insulin and/or increased glucagon availability at the hepatocellular level. Instead, it is hypothesized that postreceptor events play the major role in sustaining the intrahepatic realignments of established fasting in late pregnancy.

Original languageEnglish (US)
Pages (from-to)1979-1986
Number of pages8
Issue number5
StatePublished - Jan 1 1981

ASJC Scopus subject areas

  • Endocrinology

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