Fermín Aranda

Selective changes in the protein-turnover rates and nature of growth induced in trout liver by long-term starvation followed by re-feeding

We report upon the effects of a cycle of long-term starvation followed by re-feeding on the liver-protein turnover rates and nature of protein growth in the rainbow trout (Oncorhynchus mykiss). We determined the protein-turnover rate and its relationship with the nucleic-acid concentrations in the livers of juvenile trout starved for 70 days and then re-fed for 9 days. During starvation the total hepatic-protein and RNA contents decreased significantly and the absolute protein-synthesis rate (AS) also fell, whilst the fractional protein-synthesis rate (KS) remained unchanged and the fractional protein-degradation rate (KD) increased significantly. Total DNA content, an indicator of hyperplasia, and the protein:DNA ratio, an indicator of hypertrophy, both fell considerably. After re-feeding for 9 days the protein-accumulation rates (KG, AG) rose sharply, as did KS, AS, KD, protein-synthesis efficiency (KRNA) and the protein-synthesis rate/DNA unit (KDNA). The total hepatic protein and RNA contents increased but still remained below the control values. The protein:DNA and RNA:DNA ratios increased significantly compared to starved fish. These changes demonstrate the high response capacity of the protein-turnover rates in trout liver upon re-feeding after long-term starvation. Upon re-feeding hypertrophic growth increased considerably whilst hyperplasia remained at starvation levels.

Influence of experimental diabetes on the kinetic behaviour of renal cortex hexose monophosphate dehydrogenases

1. Short term (1-2 hr) and long-term (2 days) effects of experimental alloxan induced diabetes on the kinetics of the renal hexose monophosphate shunt dehydrogenases are reported. 2. Alloxan diabetes for 2 days significantly increased kidney weight (16%) adding about 80 mg/day per g of kidney. No significant changes were found in renal growth 1-2 hr after alloxan injection. 3. Under these experimental conditions, the activities of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase significantly increased (103 and 33% respectively) at all substrate concentrations, without affecting the KmS of either enzyme. 4. There was no effect of alloxan on the activity of these enzymes at 1-2 hr. Saturation curves show that all enzymes exhibited a M-M kinetic without evidence of sigmoidicity. 5. The results suggest that increased renal hexose monophosphate dehydrogenases activities are due to increased concentrations of the rate limiting proteins. 6. The relationship between these changes and renal hypertrophy is also discussed.

The influence of lipogenic and lipolytic conditions on the pentose phosphate pathway dehydrogenases in rat-kidney-cortex

The effects of various lipogenic and antilipogenic states on the activities of rat-kidney cortex glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase have been studied. These conditions are related to the long-term administration of different diets, such as high-carbohydrate (80%) and high-fat (23%), and also to a state of fast. Contrary to what happens in liver cells and kidney cortex during a high protein diet administration, none of these nutritional conditions produced significant changes in the kinetics of either kidney hexose monophosphate dehydrogenases.

Metabolic adaptation of renal carbohydrate metabolism. IV. The use of site-specific liver gluconeogenesis inhibitors to ascertain the role of renal gluconeogenesis (1)

The in vitro and in vivo effects of several different inhibitors of carbohydrate metabolism have been studied. The in vitro addition of 5-methoxyindole-2-carboxylic acid (MICA), pent-4-enoic acid, and quinolinic acid to the perfusion medium significantly inhibited liver gluconeogenesis in 48-hour-starved rats (100% inhibition when MICA and quinolinic acid were added at 0.8 and 2.4 mM, respectively). In vivo the level of inhibition varied greatly depending upon whether MICA was administered by intragastric tube or intraperitoneal injection. In all cases the inhibitory capacity of MICA on liver gluconeogenesis was significantly higher when injected intraperitoneally. On the other hand, the administration of MICA produced a significant, dose-dependent, increase in renal gluconeogenesis in both fed and 48-hour-starved rats, more so when the inhibitor was administered by intraperitoneal injection.