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AIM: To compare the acute effects of l-carnitine (LCT) and dl-carnitine (DLC) on hepatic catabolism of l-alanine and l-glutamine in rats. METHODS: Livers from 24 h fasted and fed rats were perfused in situ. The substrates l-alanine (5 mmol/L) and l-glutamine (5 mmol/L) were employed. The gluconeogenic and ureogenic activity was measured as the difference between the rates of glucose and urea released during and before the infusion of l-glutamine or l-alanine. RESULTS: LCT (60 umol/L) but not DLC (60 umol/L and 120 umol/L) increased the production of glucose and urea from l-glutamine. However, neither LCT (60 umol/L and 120 umol/L) nor DLC (60 umol/L and 240 μmol/L) showed any significant effect on hepatic glucose and urea production from l-alanine. CONCLUSION: The results showed a different acute effect of LCT and DLC on the activation of hepatic gluco-neogenesis and ureagenesis promoted by l-glutamine, reinforcing the idea that DLC could not replace LCT.
AIM: To compare the acute effects of l-carnitine (LCT) and dl-carnitine (DLC) on hepatic catabolism of l-alanine and l-glutamine in rats. METHODS: Livers from 24 h fasted and fed rats were perfused in situ. The substrates l-alanine (5 mmol / L) and l-glutamine (5 mmol / L) were employed. The gluconeogenic and ureogenic activity was measured as the difference between the rates of glucose and urea released during and before the infusion of l- glutamate or l-alanine. RESULTS: LCT (60 umol / L) but not DLC (60 umol / L and 120 umol / L) increased the production of glucose and urea from 1- and 120 umol / L) nor DLC (60 umol / L and 240 μmol / L) showed any significant effect on hepatic glucose and urea production from l-alanine. CONCLUSION: The results showed a different acute effect of LCT and DLC on the activation of hepatic gluco-neogenesis and ureagenesis promoted by l-glutamine, reinforcing the idea that DLC could not replace LCT.