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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

In vitro hepatic gluconeogenesis during experimental ketosis produced in steers by 1,3-butanediol and phlorizin.

Adaptations of in vitro incorporation of gluconeogenic substrates into glucose and adaptations of metabolite concentrations of liver to subcutaneous phlorizin and dietary 1,3-butanediol were examined for liver samples from dairy steers. Later, the same adaptations were examined after 6 days of feed restriction. Feeding 1,3-butanediol significantly decreased conversion of carbon-14 of lactate and propionate to glucose and to carbon dioxide. There were no changes of concentrations of hepatic glycogen or triglyceride, and increases were only minor for beta-hydroxybutyrate concentration. Both phlorizin, with or without 1,3-butanediol, and feed restriction significantly increased rates of carbon incorporation into glucose from aspartate, lactate, and propionate but did not change rates of oxidation to carbon dioxide. Phlorizin had no effect on hepatic glycogen or triglyceride concentrations, but feed restriction decreased liver glycogen and increased triglyceride concentrations. Changes associated with either phlorizin treatment or feed restriction are consistent with a decreased ratio of insulin to glucagon of blood plasma. When combined, phlorizin and 1,3-butanediol seem to have some utility for developing a ketosis model.[1]

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