title: Direct effects of catecholamines on hepatic glucose production in conscious dog are due to glycogenolysis.
abstract: The effects of catecholamines (CATS) infused into the hepatic portal vein were studied in ten 18-h-fasted conscious dogs. Glucose production (GP) and gluconeogenesis (GNG) were assessed using tracer ([3H]glucose, [14C]alanine) and arteriovenous difference techniques. Each experiment consisted of a 100-min equilibration, a 40-min basal, and two 90-min test periods. A pancreatic clamp (somatostatin + basal portal insulin and glucagon) was used to fix insulin and glucagon at basal levels. Propranolol (1 microgram.kg-1.min-1) and phentolamine (2 micrograms.kg-1.min-1) were infused intraportally during both test periods of the blockade group while a carrier solution was infused in the control group. Norepinephrine (NE; 100 ng.kg-1.min-1) and epinephrine (Epi; 40 ng.kg-1.min-1) were infused intraportally during the second test period of both protocols. Portal NE (70 +/- 46 to 8,404 +/- 674 and 162 +/- 57 to 6,530 +/- 624 pg/ml, respectively) and portal Epi (21 +/- 11 to 3,587 +/- 309 and 29 +/- 6 to 2,989 +/- 406 pg/ml, respectively) rose in the control and adrenergic blockade groups, respectively. The increases in arterial NE and Epi were modest in both groups. Intraportal infusion of CATS increased GP from 2.1 +/- 0.2 to 6.2 +/- 1.0 mg.kg-1.min-1 in the control group but did not change it (2.7 +/- 0.4 to 2.7 +/- 0.3 mg.kg-1.min-1) in the blockade group. Portal CATS had no effect on GNG in the presence or absence of adrenergic blockade (GNG rose from 0.7 +/- 0.2 to 0.9 +/- 0.2 and 0.8 +/- 0.2 to 1.0 +/- 0.2 mg.kg-1.min-1 in the control and blockade groups, respectively). In conclusion, portal infusion of catecholamines significantly augmented GP by selectively stimulating glycogenolysis. The increase in hepatic GP could be completely inhibited by intraportal adrenergic blockade.
authors: Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615, USA.
authors: C A
authors: CA
authors: Chu
authors: D K
authors: DK
authors: Sindelar
authors: D W
authors: DW
authors: Neal
authors: A D
authors: AD
authors: Cherrington
mesh_terms: D020155:3-Hydroxybutyric Acid; D018674:Adrenergic Antagonists / Q000494:pharmacology; D000409:Alanine / Q000097:blood / Q000378:metabolism; D000818:Animals; D001158:Arteries; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism; D005260:Female; D005943:Gluconeogenesis; D005947:Glucose / Q000096:biosynthesis*; D005990:Glycerol / Q000097:blood / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D006728:Hormones / Q000097:blood; D006885:Hydroxybutyrates / Q000097:blood / Q000378:metabolism; D007773:Lactates / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*
chemical_list: D018674:Adrenergic Antagonists; D005230:Fatty Acids, Nonesterified; D006728:Hormones; D006885:Hydroxybutyrates; D007773:Lactates; D006003:Glycogen; D005947:Glucose; D000409:Alanine; D005990:Glycerol; D020155:3-Hydroxybutyric Acid; D009638:Norepinephrine; D004837:Epinephrine