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1 Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA; Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, TN, USA
* To whom correspondence should be addressed. E-mail: genie.moore{at}vanderbilt.edu.
Our aim was to assess the magnitude of peripheral insulin resistance and whether changes in hepatic insulin action were evident in a canine model of late (3rd trimester) pregnancy. A 3h hyperinsulinemic (5 mU.kg-1.min-1)-euglycemic clamp was conducted using conscious, 18h-fasted pregnant (P; n=6) and nonpregnant (NP; n=6) female dogs in which catheters for intraportal insulin infusion and assessment of hepatic substrate balances were implanted ~17 days prior to experimentation. Arterial plasma insulin rose from 11±2 to 192±24 and 4±2 to 178±5 µU/ml in the third hr in NP and P, respectively. Glucagon fell equivalently in both groups. Basal net hepatic glucose output was lower in NP (1.9±0.1 vs. 2.4±0.2 mg.kg-1.min-1, P < 0.05). Hyperinsulinemia completely suppressed hepatic glucose release in both groups (-0.4±0.2 and -0.1±0.2 mg.kg-1.min-1 in NP and P, respectively). More exogenous glucose was required to maintain euglycemia in NP (15.2±1.3 vs. 11.5±1.1 mg.kg-1.min-1, P < 0.05). Non-esterified fatty acids fell similarly in both groups. Net hepatic gluconeogenic amino acid uptake with high insulin did not differ in NP and P. Peripheral insulin action is markedly impaired in this canine model of pregnancy, whereas hepatic glucose production is completely suppressed by high circulating insulin levels.
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