title: Prior exercise and the response to insulin-induced hypoglycemia in the dog.
abstract: To test whether hepatic insulin action and the response to an insulin-induced decrement in blood glucose are enhanced in the immediate postexercise state as they are during exercise, dogs had sampling (artery, portal vein, and hepatic vein) catheters and flow probes (portal vein and hepatic artery) implanted 16 days before a study. After 150 min of moderate treadmill exercise or rest, dogs were studied during a 150-min hyperinsulinemic (1 mU.kg(-1).min(-1)) euglycemic (n = 5 exercised and n = 9 sedentary) or hypoglycemic (65 mg/dl; n = 8 exercised and n = 9 sedentary) clamp. Net hepatic glucose output (NHGO) and endogenous glucose appearance (R(a)) and utilization (R(d)) were assessed with arteriovenous and isotopic ([3-(3)H]glucose) methods. Results show that, immediately after prolonged, moderate exercise, in relation to sedentary controls: 1) the glucose infusion rate required to maintain euglycemia, but not hypoglycemia, was higher; 2) R(d) was greater under euglycemic, but not hypoglycemic conditions; 3) NHGO, but not R(a), was suppressed more by a hyperinsulinemic euglycemic clamp, suggesting that hepatic glucose uptake was increased; 4) a decrement in glucose completely reversed the enhanced suppression of NHGO by insulin that followed exercise; and 5) arterial glucagon and cortisol were transiently higher in the presence of a decrement in glucose. In summary, an increase in insulin action that was readily evident under euglycemic conditions after exercise was abolished by moderate hypoglycemia. The means by which the glucoregulatory system is able to overcome the increase in insulin action during moderate hypoglycemia is related not to an increase in R(a) but to a reduction in insulin-stimulated R(d). The primary site of this reduction is the liver.
authors.affiliation: Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615, USA.
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Koyama
authors.forename: Pietro
authors.initials: P
authors.lastname: Galassetti
authors.forename: Robert H
authors.initials: RH
authors.lastname: Coker
authors.forename: R Richard
authors.initials: RR
authors.lastname: Pencek
authors.forename: D Brooks
authors.initials: DB
authors.lastname: Lacy
authors.forename: Stephen N
authors.initials: SN
authors.lastname: Davis
authors.forename: David H
authors.initials: DH
authors.lastname: Wasserman
mesh_terms: D000818:Animals; D001786:Blood Glucose; D002250:Carbon Radioisotopes; D002395:Catecholamines / Q000097:blood; D004285:Dogs; D004734:Energy Metabolism / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000493:pharmacokinetics; D005990:Glycerol / Q000097:blood; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000139:chemically induced / Q000378:metabolism*; D007004:Hypoglycemic Agents / Q000097:blood / Q000494:pharmacology*; D007083:Iliac Artery / Q000502:physiology; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D019344:Lactic Acid / Q000378:metabolism; D008099:Liver / Q000098:blood supply / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D010084:Oxidation-Reduction; D005082:Physical Exertion / Q000502:physiology*; D012039:Regional Blood Flow; D014316:Tritium
chemical_list: D001786:Blood Glucose; D002250:Carbon Radioisotopes; D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D007004:Hypoglycemic Agents; D007328:Insulin; D014316:Tritium; D019344:Lactic Acid; D005934:Glucagon; D005947:Glucose; D005990:Glycerol; D006854:Hydrocortisone