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1 Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and 2 Department of Medicine, Research Center, Hotel-Dieu de Montreal, Montreal, Quebec, Canada H2W 1T8
We assessed basal glucose metabolism in 16 female nonpregnant (NP) and 16 late-pregnant (P) conscious, 18-h-fasted
dogs that had catheters inserted into the hepatic and portal veins and
femoral artery ~17 days before the experiment. Pregnancy resulted in
lower arterial plasma insulin (11 ± 1 and 4 ± 1 µU/ml in
NP and P, respectively, P < 0.05), but plasma glucose
(5.9 ± 0.1 and 5.6 ± 0.1 mg/dl in NP and P, respectively)
and glucagon (39 ± 3 and 36 ± 2 pg/ml in NP and P,
respectively) were not different. Net hepatic glucose output was
greater in pregnancy (42.1 ± 3.1 and 56.7 ± 4.0 µmol · 100 g
liver
1 · min1 in NP and P,
respectively, P < 0.05). Total net hepatic
gluconeogenic substrate uptake (lactate, alanine, glycerol, and amino
acids), a close estimate of the gluconeogenic rate, was not different between the groups (20.6 ± 2.8 and 21.2 ± 1.8 µmol · 100 g
liver1 · min1 in NP and P,
respectively), indicating that the increment in net hepatic glucose
output resulted from an increase in the contribution of
glycogenolytically derived glucose. However, total glycogenolysis was
not altered in pregnancy. Ketogenesis was enhanced nearly threefold by
pregnancy (6.9 ± 1.2 and 18.2 ± 3.4 µmol · 100 g liver1 · min1 in NP and P,
respectively), despite equivalent net hepatic nonesterified fatty acid
uptake. Thus late pregnancy in the dog is not accompanied by changes in
the absolute rates of gluconeogenesis or glycogenolysis. Rather,
repartitioning of the glucose released from glycogen is responsible for
the increase in hepatic glucose production.
hepatic glucose production; gluconeogenesis; glycogenolysis; lipolysis; ketogenesis
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