Insulin Sensitivity during Late Gestation in Ewes Affected by Pregnancy Toxemia and in Ewes with High and Low Susceptibility to this Disorder

Abstract

Insulin resistance during late gestation might act as 1 etiologic factor causing pregnancy toxemia in ewes. Evaluation of pancreatic insulin secretion and peripheral insulin sensitivity in ewes with differing susceptibility to pregnancy toxemia and in ketotic ewes. Pregnant ewes suffering from (PT, n=5) and ewes with high (HR, n=7) and low risk (LR, n=5) of being affected by pregnancy toxemia. In a case-control study, the pancreatic insulin release and the peripheral insulin sensitivity were assessed by means of the intravenous glucose tolerance test with subsequent measurement of the plasma concentrations of glucose, insulin, nonesterified fatty acids (NEFA), and β-hydroxybutyrate (β-HB). The ewes were tested during late pregnancy within 5 and 15days antepartum. The insulin secretion after glucose administration was significantly lower in the HR and PT than in the LR ewes. The baseline rate of lipolysis was significantly increased in the HR ewes, but the NEFA clearance was similar in both risk groups, albeit delayed in the PT ewes. The baseline β-HB concentration was significantly higher in the PT than in the HR and LR ewes. In the HR and in the PT ewes, the plasma β-HB concentrations did not decrease after glucose administration. There is reduced pancreatic first-phase insulin response and impaired insulin-dependent inhibition of the ketone body formation during late pregnancy in the HR and PT ewes. This insulin resistance might represent 1 causative factor in the pathogenesis of ovine pregnancy toxemia.