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This Article Full Text Full Text (PDF) All Versions of this Article: 289/2/E225    most recent 00614.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Moore, M. C. Articles by Cherrington, A. D. Search for Related Content PubMed PubMed Citation Articles by Moore, M. C. Articles by Cherrington, A. D.

Portal 5-hydroxytryptophan infusion enhances glucose disposal in conscious dogs

¹Department of Molecular Physiology and Biophysics, ²Diabetes Research and Training Center, Vanderbilt University School of Medicine, Nashville, Tennessee; ³Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Japan; and ⁴Morinaga Institute of Biological Science, Tsurumi, Yokohama, Japan

Submitted 29 December 2004 ; accepted in final form 3 March 2005

Intraportal serotonin infusion enhances net hepatic glucose uptake (NHGU) during glucose infusion but blunts nonhepatic glucose uptake and can cause gastrointestinal discomfort and diarrhea at high doses. Whether the serotonin precursor 5-hydroxytryptophan (5-HTP) could enhance NHGU without gastrointestinal side effects during glucose infusion was examined in conscious 42-h-fasted dogs, using arteriovenous difference and tracer ([3-³H]glucose) techniques. Experiments consisted of equilibration (–120 to –30 min), basal (–30 to 0 min), and experimental (EXP; 0–270 min) periods. During EXP, somatostatin, fourfold basal intraportal insulin, basal intraportal glucagon, and peripheral glucose (to double the hepatic glucose load) were infused. In one group of dogs (HTP, n = 6), saline was infused intraportally from 0 to 90 min (P1), and 5-HTP was infused intraportally at 10, 20, and 40 µg·kg^–1·min^–1 from 90 to 150 (P2), 150 to 210 (P3), and 210 to 270 (P4) min, respectively. In the other group (SAL, n = 7), saline was infused intraportally from 0 to 270 min. NHGU in SAL was 14.8 ± 1.9, 18.5 ± 2.3, 16.3 ± 1.4, and 19.7 ± 1.6 µmol·kg^–1·min^–1 in P1–P4, whereas NHGU in 5-HTP averaged 16.4 ± 2.6, 18.5 ± 1.4, 20.8 ± 2.0, and 27.6 ± 2.6 µmol·kg^–1·min^–1 (P < 0.05 vs. SAL). Nonhepatic glucose uptake (µmol·kg^–1·min^–1) in SAL was 30.2 ± 4.3, 36.8 ± 5.8, 44.3 ± 5.8, and 54.6 ± 11.8 during P1–P4, respectively, whereas in HTP the corresponding values were 26.3 ± 6.8, 44.9 ± 10.1, 47.5 ± 11.7, and 51.4 ± 13.2 (not significant between groups). Intraportal 5-HTP enhances NHGU without significantly altering nonhepatic glucose uptake or causing gastrointestinal side effects, raising the possibility that a related agent might have a role in reducing postprandial hyperglycemia.

glycemia; liver; portal vein; leptin; adiponectin

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