Abstract
Abstract Cortisol stimulated the synthesis of glycogen in fetal rat liver explants. The increase was proportional to the amount of glucose present in the incubation medium and occurred slowly over a 44-hour period. The ability of cortisol to stimulate glycogen synthesis was accelerated after prior incubation of explants for 42 hours with no steroid. Glucose alone led to the synthesis of very little glycogen. [U-14C]-glucose added to the incubation medium was incorporated into glycogen. The specific activities of [U-14C]glucose in the medium and in glycogen synthesized over a 44-hour period were approximately the same whether or not cortisol was present, indicating that glycogen was derived mainly from glucose. Fetal livers synthesized glucose and glycogen from l-[U-14C]alanine to a limited degree. The incorporation of label ranged from 0.2% to 1.6% of the dose; the extent was determined by the conditions of incubation. Cortisol did not affect the over-all gluconeogenic process, but it increased the proportion of label incorporated into glycogen and decreased the incorporation into glucose. Gluconeogenesis from l-[U-14C]alanine did not take place in the absence of glucose. Cortisol did not induce any changes which could be correlated with glycogen synthesis in the activities of phosphoenolpyruvate carboxykinase, glycogen phosphorylase, glucose 6-phosphatase, fructose 1,6-diphosphatase, pyruvate kinase, alanine aminotransferase, or aspartate aminotransferase. Accumulation of glycogen under all conditions studied was directly proportional to changes in glycogen synthetase b. The a form of the enzyme was not affected by cortisol. It is concluded that (a) the major source of glycogen in fetal rat liver is glucose; (b) synthesis of glycogen from glucose is stimulated by cortisol; (c) gluconeogenesis takes place in fetal liver to a measureable extent; (d) cortisol does not influence gluconeogenesis; (e) cortisol directs a common six-carbon intermediate towards glycogen synthesis and away from glucose formation; (f) the effect of cortisol on glycogen synthesis depends on its ability to increase glycogen synthetase b activity.
Highlights
Xtimulation of GlycogenSynthesisby Co&sol-We have confirmed the observations of many investigators who reported that the glycogen content of fetal rat liver increases rapidly several days before birth and drops quickly thereafter [3, 14]
In order to evaluate the stability of fetal liver glycogen, liver
Glycogen Xynthetase-Since the fetal rat liver synthesizes glycogen mainly by glycogenesis, and only to a small extent by glyconeogenesis, we examined the effects of cortisol on glycogen synthetase, the enzyme generally considered to be rate-limiting in the transformation of glucose B-phosphate to glycogen
Summary
Pregnant CFE rats (Carworth Farms, Inc., New City, New York) were received at approximately 18 days after conception. When the fetuses were 20 f 1 days old, they were removed under sterile conditions after killing the mother with ether. The ages of the fetuses were determined from their crown-rump length and weight, utilizing published tables [22]. Livers were removed and established in culture as described by Wicks [19]. In experiments in which glucose content of the incubations was varied, the initial medium was specially formulated by the manufacturer (Microbiological Associates, Inc., Bethesda, Md.) to contain no glucose. Cortisol when added was dissolved in ethanol and introduced into the incubation medium in a volume of 0.1 ml to give a final concentration of 2 X 10m6 M steroid. An equal volume of ethanol was added to control dishes
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