Mechanisms of cellular insulin resistance in human pregnancy

Theodore P. Ciaraldi*, Michael Kettel, Albert El-Roiey, Zecharia Madar, Donna Reichart, Samuel S.C. Yen, Jerrold M. Olefsky

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

Abstract

OBJECTIVE: The cellular mechanism(s) of insulin resistance developed during pregnancy were studied by investigating the functionality of insulin receptors and glucose transport. STUDY DESIGN: Abdominal adipose tissue was obtained from eight lean pregnant and nine control subjects, matched for insulin resistance by intravenous glucose tolerance testing. Insulin receptor binding and glucose transport were measured in freshly isolated adipocytes. Receptor kinase activity was measured on partially purified receptors. Data were analyzed by Student t test. RESULTS: High-affinity insulin receptors were reduced in cells from pregnant compared with normal controls (2.0 ± 0.4 vs 5.8 ± 1.3 × 104 sites per cell, p < 0.05). Kinase activity of insulin receptors was unaltered in pregnancy. Adipocytes from pregnant subjects displayed a threefold decrease in insulin sensitivity for glucose transport (median effective concentration 324 ± 93 vs 93 ± 14 pmol/L, p < 0.025) and a reduction in maximal insulin-stimulated glucose transport (1.58 ± 0.15 vs 2.33 ± 0.24 pmol/105 cells/10 seconds, p < 0.025). CONCLUSION:These results show that adipocytes from pregnant subjects exhibit decreased insulin receptor number and an impaired insulin sensitivity in the absence of functional alterations of receptor kinase activity. (AM J OBSTET GYNECOL 1994;170:635-41.)

Original languageEnglish
Pages (from-to)635-641
Number of pages7
JournalAmerican Journal of Obstetrics and Gynecology
Volume170
Issue number2
DOIs
StatePublished - 1994

Keywords

  • adipocytes
  • insulin receptor kinase
  • insulin resistance
  • Pregnancy

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