Glucose metabolism in rat kidney: influence of insulin and adrenaline

Abstract

In previous investigations it was revealed that following the administration of toxic amounts of Salyrgan the renal glycogen concentration rises (Dziurik, Brixov'a & Kolesar, 1961). Pytasz, Zarzycki & Taborska (1960) drew attention to the fact that adrenaline does not reduce the renal glycogen concentration. Their method for the estimation of glycogen is not very specific. When repeating their experiments in our laboratory, using a more specific method, we found that adrenaline actually does not reduce the renal glycogen concentration. In some of our experiments we even found an increased renal glycogen concentration after the administration of adrenaline, despite the fact that its concentration in liver and muscle fell at the same time (Krajci-Lazairy, Dz(urik & Niederland, 1962). The explanation of these paradoxical findings is difficult. In any case they suggest a different glycogen metabolism in kidney compared with that in liver and muscle.It may be assumed that the glycogen metabolism in kidneys is related to glucose metabolism. Teng (1954) demonstrated that in kidney slices there is a direct relation between the glucose and glycogen concentrations. In the present paper we describe experiments on effects of insulin and adrenaline on renal glucose metabolism. METHODSAnimals. Male Wistar rats, weighing 150-200 g, were used. The rats were given food and water ad libitum.Adrenaline (Spofa) (50 ,ug/100 g body wt.) was administered subcutaneously, 1 hr before the withdrawal of blood samples, and insulin (Novo) (0 5 u./100 g body wt.) subcutaneously at the same time.Estimation of renal blood flow. 60 min before the withdrawal of blood samples water (5 ml./100 g body wt.) was given intraperitoneally. 25 min before the blood samples were collected para-amino-hippurate (PAH) (0-75 ml. 1-2 %/100 g) was injected subcutaneously.Urine was collected for 10-15 min. Blood was subsequently withdrawn from the renal vein and aorta under light ether anaesthesia. To prevent the development of ischaemia only 1 ml. blood was withdrawn. In order to reduce the volume of renal dead 3pace, one week before the experiment sub-total cystectomy was performed in the experimental animals.

[14C]bicarbonate fixation into glucose and other metabolites in the liver of the starved rat under halothane anaesthesia. Metabolic channelling of mitochondrial oxaloacetate

“…Two types of experiment have led to irreconcilable values. Dzurik et al (1963) and Churchill et al (1973) measured the dependence of renal uptake and output on the concentrations of circulating glucose, which in our rats were close to or above those at which there was net renal output. According to those authors, renal gluconeogenesis could be ignored.…”

Renal gluconeogenesis in acidosis, alkalosis, and potassium deficiency: its possible role in regulation of renal ammonia production.

“…Renal gluconeogenesis may be a significant factor in over-all metabolism of carbohydrate in the body, for in vivo production of glucose by the kidneys is considerable (21,22). The observation that acidosis and potassium depletion enhance the capacity of kidney cortex to produce glucose in vitro suggests that in these states the renal production of glucose in vivo may be increased.…”

Effect of Hippurate on Glucose Utilization in Rat Kidney Cortex Slices

“…On the other hand, no insulin effect could be detected in the case of kidney cortex slices incubated in medi um containing insulin probably because of its rapid breakdown [17]. However, insulin ap plied to fasting rats 15-30 min before sacrifice stimulates glucose utilization as shown previ ously in vivo [15] and in the presented experi ments.…”

“…Insulin increases the uptake and epine phrine the release of glucose [15]. Insulin also increases glucose utilization and oxidation in isolated rat perfused kidney [16].…”