The effect of insulin on carbohydrate formation in the liver

Abstract

Slices of liver of starved rats were shaken in Ringer solution at 38[degree]. Estimations of fermentable cbhy. and urea N were carried out both at the beginning and at the end of the exp. period. An increase both of cbhy. and urea N could be obtained amounting to 2.28 mg and 0.248 mg respectively per g fresh liver. Both the syntheses of cbhy. and urea N were reduced by 43% and 56% respectively in presence of insulin. The former reduction was considered a proof that carbohydrate synthesis was from more than one source, part of which was affected by insulin; the latter gave a hint of protein being one of the gluconeogenetic sources, the amount of reduction being in agreement with the general conception that 58% of the protein is capable of forming sugar. Addition of alanine, glutamic acid, aspartic acid and arginine gave rise to extra cbhy. synthesis. In the case of alanine an increase of extra urea was demonstrated. Insulin inhibited extra cbhy. formation by alanine almost completely, and urea formation partially. Quantitative agreements between the effects of insulin on cbhy. formation and urea-N formation were demonstrated when the exp. was carried out on the same liver. As there was no insulin effect on the extra cbhy. formation in presence of both pyruvic and lactic acid, it was concluded that insulin exerts its inhibitory effect on the deamination of amino acids. No increase in cbhy. and urea formation was obtained in presence of glycine. Resp. exps. showed a slight lowering effect of O2 consumption in presence of insulin and in absence of added substrate, and no effect in the resp. metabolism in the presence of lactate. Alanine and glycine, as well as pyruvate and lactate, give rise to increased O2 consumption. Insulin lowers the R.Q. in presence of added alanine.