title: Gluconeogenesis in hepatocytes of immature rainbow trout (Oncorhynchus mykiss): control by estradiol.
abstract: Estradiol treatment of starving immature rainbow trout dramatically alters the metabolic performance of isolated hepatocytes. One and two weeks postimplantation with estradiol, the rate of de novo glucose synthesis from [14C]alanine is reduced fourfold from 0.4 mumol/g/hr to 0.1 mumol/g/hr, compared with vehicle-injected control fish. After 6 weeks, the rate of glucose production on a gram wet weight basis is identical in both treatment groups, but significantly larger (by 80%) in the estradiol-treated group than in the controls, if expressed normalized to the hepatosomatic index (HSI). Estradiol treatment caused preferential partitioning of alanine carbon into oxidative pathways away from gluconeogenesis, indicated by a significantly lower ratio of glucose production over CO2 production in hepatocytes isolated from estradiol-treated animals. Incorporation of [14C]alanine into acid-precipitable protein is significantly larger in the estradiol-treated group after 2 weeks, and also after 6 weeks, when normalized to the HSI, indicating that part of the protein synthesized in the estradiol-treated groups is vitellogenin. No differences were detected between estradiol-treated animals and control animals in the activities of enzymes associated with gluconeogenesis [phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase (FBPase)] and amino acid metabolism (alanine and aspartate aminotransferases) in the time course investigated (expressed on a wet weight basis). Activities normalized to the HSI are higher in fish implanted with estradiol compared with controls at 2 and 6 weeks. In keeping with the increased potential of hepatocytes for CO2 production from alanine, estradiol treatment doubled and tripled the maximum activity of pyruvate kinase 1 and 2 weeks postimplantation, respectively. Fish were fasted to avoid erratic feeding due to treatments. Superimposed on estradiol actions are effects of starvation: a fourfold increase in the rate of gluconeogenesis, a threefold increase in oxidative flux, and a fivefold increase in the activity of FBPase--all normalized to hepatocyte weight.
authors.affiliation: Department of Biochemistry and Microbiology, University of Victoria, British Columbia, Canada.
authors.forename: B
authors.initials: B
authors.lastname: Korsgaard
authors.forename: T P
authors.initials: TP
authors.lastname: Mommsen
mesh_terms: D000409:Alanine / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology*; D005943:Gluconeogenesis / Q000187:drug effects*; D006019:Glycolysis; D007700:Kinetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D011770:Pyruvate Kinase / Q000378:metabolism; D012313:RNA / Q000378:metabolism; D013217:Starvation; D014337:Trout / Q000254:growth & development / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D002245:Carbon Dioxide; D004958:Estradiol; D012313:RNA; D004247:DNA; D011770:Pyruvate Kinase; D000409:Alanine