Induction of rat kidney gluconeogenic ability after impairment of liver gluconeogenesis.
The renal gluconeogenic response to the inhibition of liver gluconeogenesis was studied in rats treated with CCl4. This treatment resulted in a generalized fall of hepatic gluconeogenic enzyme activities and a complete impairment of liver gluconeogenesis. On the contrary, an enhancement of renal phosphoenolpyruvate carboxykinase activity and gluconeogenic ability was found. This stimulation seemed to be not related to metabolic acidosis but mediated by glucocorticoids. On the other hand, the pattern of intermediate metabolites in kidney suggested that renal gluconeogenesis was operative in these conditions, probably playing a key role in glucose homeostasis.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000201:enzymology*; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D005260:Female; D006597:Fructose-Bisphosphatase / Q000378:metabolism; D005943:Gluconeogenesis; D005952:Glucose-6-Phosphatase / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000201:enzymology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000201:enzymology*; D008297:Male; D009928:Organ Specificity; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000378:metabolism; D051381:Rats; D014221:Triamcinolone / Q000494:pharmacology
D003609:Dactinomycin; D014221:Triamcinolone; D003513:Cycloheximide; D007770:L-Lactate Dehydrogenase; D006597:Fructose-Bisphosphatase; D005952:Glucose-6-Phosphatase; D010729:Phosphoenolpyruvate Carboxykinase (GTP)