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Hepatic insulin extraction in human pregnancy
The hepatic degradation of insulin in late pregnancy has been estimated by determination of the molar C-peptide: Insulin (C/l) ratio under fasting conditions in 20 normal women in late pregnancy and again 4--8 weeks post-partum. Fasting plasma C-peptide and insulin concentrations were both significantly enhanced in pregnancy. However, since the relative gestational increments in plasma C-peptide and insulin concentrations were of almost the same magnitude, the C/l ratio remained unaffected by pregnancy (7.3 +/- 0.07 (mean +/- S.E.M) (pregnancy) vs. 7.4 +/- 0.8 (post-partum), N.S.). The results suggest that, in pregnancy, peripheral hyperinsulinaemia is due, in general, to pancreatic hypersecretion rather than to diminished hepatic extraction of insulin.
The hepatic degradation of insulin in late pregnancy has been estimated by determination of the molar C-peptide: Insulin (C/l) ratio under fasting conditions in 20 normal women in late pregnancy and again 4--8 weeks post-partum. Fasting plasma C-peptide and insulin concentrations were both significantly enhanced in pregnancy. However, since the relative gestational increments in plasma C-peptide and insulin concentrations were of almost the same magnitude, the C/l ratio remained unaffected by pregnancy (7.3 +/- 0.07 (mean +/- S.E.M) (pregnancy) vs. 7.4 +/- 0.8 (post-partum), N.S.). The results suggest that, in pregnancy, peripheral hyperinsulinaemia is due, in general, to pancreatic hypersecretion rather than to diminished hepatic extraction of insulin.