Hepatic glucose uptake and disposition during short-term high-fat vs. high-fructose feeding

dc.contributor.authorCoate, Katie C.
dc.contributor.authorKraft, Guillaume
dc.contributor.authorMoore, Mary Courtney
dc.contributor.authorSmith, Marta S.
dc.contributor.authorRamnanan, Christopher
dc.contributor.authorIrimia, Jose M.
dc.contributor.authorRoach, Peter J.
dc.contributor.authorFarmer, Ben
dc.contributor.authorNeal, Doss W.
dc.contributor.authorWilliams, Phil
dc.contributor.authorCherrington, Alan D.
dc.contributor.departmentDepartment of Biochemistry & Molecular Biology, IU School of Medicineen_US
dc.date.accessioned2016-03-24T14:42:23Z
dc.date.available2016-03-24T14:42:23Z
dc.date.issued2014-07-15
dc.description.abstractIn dogs consuming a high-fat and -fructose diet (52 and 17% of total energy, respectively) for 4 wk, hepatic glucose uptake (HGU) in response to hyperinsulinemia, hyperglycemia, and portal glucose delivery is markedly blunted with reduction in glucokinase (GK) protein and glycogen synthase (GS) activity. The present study compared the impact of selective increases in dietary fat and fructose on liver glucose metabolism. Dogs consumed weight-maintaining chow (CTR) or hypercaloric high-fat (HFA) or high-fructose (HFR) diets diet for 4 wk before undergoing clamp studies with infusion of somatostatin and intraportal insulin (3–4 times basal) and glucagon (basal). The hepatic glucose load (HGL) was doubled during the clamp using peripheral vein (Pe) glucose infusion in the first 90 min (P1) and portal vein (4 mg·kg−1·min−1) plus Pe glucose infusion during the final 90 min (P2). During P2, HGU was 2.8 ± 0.2, 1.0 ± 0.2, and 0.8 ± 0.2 mg·kg−1·min−1 in CTR, HFA, and HFR, respectively (P < 0.05 for HFA and HFR vs. CTR). Compared with CTR, hepatic GK protein and catalytic activity were reduced (P < 0.05) 35 and 56%, respectively, in HFA, and 53 and 74%, respectively, in HFR. Liver glycogen concentrations were 20 and 38% lower in HFA and HFR than CTR (P < 0.05). Hepatic Akt phosphorylation was decreased (P < 0.05) in HFA (21%) but not HFR. Thus, HFR impaired hepatic GK and glycogen more than HFA, whereas HFA reduced insulin signaling more than HFR. HFA and HFR effects were not additive, suggesting that they act via the same mechanism or their effects converge at a saturable step.en_US
dc.identifier.citationCoate, K. C., Kraft, G., Moore, M. C., Smith, M. S., Ramnanan, C., Irimia, J. M., … Cherrington, A. D. (2014). Hepatic glucose uptake and disposition during short-term high-fat vs. high-fructose feeding. American Journal of Physiology - Endocrinology and Metabolism, 307(2), E151–E160. http://doi.org/10.1152/ajpendo.00083.2014en_US
dc.identifier.urihttps://hdl.handle.net/1805/9013
dc.language.isoen_USen_US
dc.publisherAmerican Physiological Society (APS)en_US
dc.relation.isversionof10.1152/ajpendo.00083.2014en_US
dc.relation.journalAmerican Journal of Physiology - Endocrinology and Metabolismen_US
dc.rightsPublisher Policyen_US
dc.sourcePMCen_US
dc.subjectGlucokinaseen_US
dc.subjectglycogenen_US
dc.subjectglycogen synthaseen_US
dc.subjectglycogen phosphorylaseen_US
dc.subjectinsulin signalingen_US
dc.titleHepatic glucose uptake and disposition during short-term high-fat vs. high-fructose feedingen_US
dc.typeArticleen_US
ul.alternative.fulltexthttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4101635/en_US
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