Stimulation of gluconeogenesis by cortisol in fetal rat liver in organ culture.
Fetal rat liver explants (gestational day 20) depleted of glycogen converted L-[14C]alanine into labeled glucose and glycogen. Cortisol 1) stimulated net glyconeogenesis about 2-fold at 22 h of incubation after a 7-h lag; 2) increased the total amount of glycogen in the explant 2-fold; 3) stimulated the net incorporation of label from [14C]alanine into both glucose and glycogen. Both [3H]glucose added to the medium and glucose generated by gluconeogenesis from [14C]alanine contributed to the glycogen formed. Cortisol led to greater 14C uptake than 3H uptake into glycogen. During gluconeogenesis, [14C]glycogen was first formed and subsequently broke down to [14C]glucose. In the absence of cortisol, glucose and glycogen reached equilibrium with each other. In the presence of cortisol, preferential uptake of alanine into glycogen persisted throughout the 22 h of incubation, and equilibrium was not reached. Gluconeogenesis from [14C]glycerol was greater than from [14C]alanine. Cortisol stimulated its conversion to glycogen but not to glucose. It was concluded that gluconeogenesis in fetal rat liver occurs under organ culture conditions, that its stimulation by cortisol is direct and is localized in two regions: conversion of L-alanine to triose phosphates and of glucose-6-phosphate to glycogen.
D000409:Alanine / Q000378:metabolism; D000818:Animals; D005260:Female; D005333:Fetus; D005943:Gluconeogenesis / Q000187:drug effects*; D006854:Hydrocortisone / Q000494:pharmacology*; D007700:Kinetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008112:Liver Glycogen / Q000096:biosynthesis; D009924:Organ Culture Techniques; D011247:Pregnancy; D051381:Rats
D008112:Liver Glycogen; D000409:Alanine; D006854:Hydrocortisone