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Hepatic Sulfur Amino Acid Metabolism in Rats with Chronic Renal Failure¹

Division of Clinical Nutrition, Research Institute, Hospital for Sick Children, and Departments of Paediatrics and Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada M5G 1X8

We recently demonstrated elevated plasma amino acid concentrations and abnormal responses to amino acid supplementation (e.g., elevated methionine and phenylalanine) in children with chronic renal failure (CRF). We also recently developed an improved model of CRF in which animals manifest abnormal tissue amino acid levels, marked anorexia and growth failure. The objective of the current study was to determine the etiology of elevations of sulfur amino acids in animals with chronic renal failure. Chronic renal failure, defined as creatinine clearance < 30% of control values, was induced in male rats in a two-stage surgical procedure. Four groups were studied over 2, 4 and 6 wk: control (non-operated) control (sham-operated), pair-fed (sham-operated and pair-fed with uremics) and CRF. Animals with CRF were anorexic and growth-retarded. Although plasma sulfur amino acid levels tended to be lower in the uremic animals than in controls, hepatic tissue concentrations were higher. Methionine adenosyltransferase was higher, but cystathione synthase and cystathionase activities were not significantly different in rats with CRF compared to pair-fed controls. We conclude that uremia, not malnutrition, affected sulfur amino acid metabolism and that with CRF, a normal adaptive response to elevated methionine levels was occurring, sufficient to normalize sulfur amino acid pool size. Alternative causes of elevated sulfur amino acids must be sought.

KEY WORDS: • rats • sulfur amino acids • chronic renal failure • adenosyltransferase • cystathione ß-synthase

¹ This research was funded by a grant from the Kidney Foundation of Canada. M. A. Bocock was supported as a graduate student (M.S.) by a fellowship from the Research Institute of the Hospital for Sick Children.

² To whom reprint requests should be sent.

Manuscript received 12 June 1989. Revision accepted 29 January 1990.