Prior exercise increases net hepatic glucose uptake during a glucose load.
The aim of these studies was to determine whether prior exercise enhances net hepatic glucose uptake (NHGU) during a glucose load. Sampling catheters (carotid artery, portal, hepatic, and iliac veins), infusion catheters (portal vein and vena cava), and Doppler flow probes (portal vein, hepatic and iliac arteries) were implanted. Exercise (150 min; n = 6) or rest (n = 6) was followed by a 30-min control period and a 100-min experimental period (3.5 mg. kg-1. min-1 of glucose in portal vein and as needed in vena cava to clamp arterial blood glucose at approximately 130 mg/dl). Somatostatin was infused, and insulin and glucagon were replaced intraportally at fourfold basal and basal rates, respectively. During experimental period the arterial-portal venous (a-pv) glucose gradient (mg/dl) was -18 +/- 1 in sedentary and -19 +/- 1 in exercised dogs. Arterial insulin and glucagon were similar in the two groups. Net hepatic glucose balance (mg. kg-1. min-1) shifted from 1.9 +/- 0.2 in control period to -1.8 +/- 0.2 (negative rates represent net uptake) during experimental period in sedentary dogs (Delta3.7 +/- 0.5); with prior exercise it shifted from 4.1 +/- 0.3 (P < 0.01 vs. sedentary) in control period to -3.2 +/- 0.4 (P < 0.05 vs. sedentary) during experimental period (Delta7.3 +/- 0.7, P < 0.01 vs. sedentary). Net hindlimb glucose uptake (mg/min) was 4 +/- 1 in sedentary animals in control period and 13 +/- 2 during experimental period; in exercised animals it was 7 +/- 1 in control period (P < 0. 01 vs. sedentary) and 32 +/- 4 (P < 0.01 vs. sedentary) during experimental period. As the total glucose infusion rate (mg. kg-1. min-1) was 7 +/- 1 in sedentary and 11 +/- 1 in exercised dogs, approximately 30% of the added glucose infusion due to prior exercise could be accounted for by the greater NHGU. In conclusion, when determinants of hepatic glucose uptake (insulin, glucagon, a-pv glucose gradient, glycemia) are controlled, prior exercise increases NHGU during a glucose load due to an effect that is intrinsic to the liver. Increased glucose disposal in the postexercise state is therefore due to an improved ability of both liver and muscle to take up glucose.
Galassetti
P
P
Department of Molecular Physiology and Biophysics, and Diabetes Research and Training Center, Vanderbilt University, Nashville, Tennessee 37232-0615, USA.
Coker
R H
RH
Lacy
D B
DB
Cherrington
A D
AD
Wasserman
D H
DH
D000818:Animals; D001158:Arteries; D001775:Blood Circulation / Q000502:physiology; D001786:Blood Glucose / Q000032:analysis; D004285:Dogs; D005260:Female; D005943:Gluconeogenesis / Q000502:physiology; D005947:Glucose / Q000493:pharmacokinetics*; D006614:Hindlimb / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D009043:Motor Activity / Q000502:physiology*; D010187:Pancreatic Hormones / Q000097:blood; D011169:Portal Vein; D011355:Prodrugs / Q000378:metabolism
D001786:Blood Glucose; D010187:Pancreatic Hormones; D011355:Prodrugs; D005947:Glucose