In vitro hepatic gluconeogenesis and ketogenesis as affected by prolonged ketonemia-glucosuria and fasting in steers.
Both 1,3-butanediol, which causes ketonemia, and phlorizin, which causes glucosuria, were given to four steers for 28 days to determine effects of prolonged ketonemia and glucosuria on in vitro hepatic gluconeogenesis and ketogenesis. Treatments were: control ration; control with butanediol plus phlorizin; and fasting for 9 days. Liver slices, obtained by biopsy, were incubated with carbon-14 substrates. Substrate converted to glucose [mumol/(h X g liver)] during control, butanediol plus phlorizin, and fasting averaged 2.34, 7.21, and 12.00 for propionate; .99, 3.80, and 12.26 for lactate; .30, .76, and 2.20 for alanine; and 2.06, 5.37, and 5.78 for glycerol. Omission of calcium++ eliminated increases of gluconeogenesis caused by butanediol plus phlorizin and by fasting. Ketone bodies, octanoate, and bovine serum albumin did not affect glucose production markedly. Stearate inhibited gluconeogenesis during all periods except fasting. Production of beta-hydroxybutyrate [mumol/(h X g liver)] during control, butanediol plus phlorizin, and fasting averaged 2.07, 4.27, and 3.25 from butyrate and .06, .27, and .02 from palmitate. Results demonstrate that the gluconeogenic capacity of bovine liver is responsive to physiological and nutritional status.[1]References
- In vitro hepatic gluconeogenesis and ketogenesis as affected by prolonged ketonemia-glucosuria and fasting in steers. Lyle, R.R., Birkmeyer, K.D., Young, J.W. J. Dairy Sci. (1984) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
