Alterations in basal glucose metabolism during late pregnancy in the conscious dog

We assessed basal glucose metabolism in 16 female nonpregnant (NP) and 16 l ate-pregnant (P) conscious, 18-h-fasted dogs that had catheters inserted in to the hepatic and portal veins and femoral artery similar to 17 days befor e the experiment. Pregnancy resulted in lower arterial plasma insulin (11 /- 1 and 4 +/- 1 muU/ml in NP and P, respectively, P < 0.06), but plasma gl ucose (5.9 +/- 0.1 and 5.6 +/- 0.1 mg/dl in NP and P, respectively) and glu cagon (39 +/- 3 and 36 +/- 2 pg/ml in NP and P, respectively) were not diff erent. Net hepatic glucose output was greater in pregnancy (42.1 +/- 3.1 an d 56.7 +/- 4.0 <mu>mol . 100 g liver(-1) . min(-1) in NP and P, respectivel y, P < 0.06). Total net hepatic gluconeogenic substrate uptake (lactate, al anine, glycerol, and amino acids), a close estimate of the gluconeogenic ra te, was not different between the groups (20.6 +/- 2.8 and 21.2 +/- 1.8 <mu >mol 100 g liver(-1) . min(-1) in NP and P, respectively), indicating that the increment in net hepatic glucose output resulted from an increase in th e contribution of glycogenolytically derived glucose. However, total glycog enolysis was not altered in pregnancy. Ketogenesis was enhanced nearly thre efold by pregnancy (6.9 +/- 1.2 and 18.2 +/- 3.4 mu mol . 100 g liver(-1) . min(-1) in NP and P, respectively), despite equivalent net hepatic noneste rified fatty acid uptake. Thus late pregnancy in the dog is not accompanied by changes in the absolute rates of gluconeogenesis or glycogenolysis. Rat her, repartitioning of the glucose released from glycogen is responsible fo r the increase in hepatic glucose production.