Glucose interorgan exchange in chronic renal failure.

The mechanisms responsible for the altered glucose metabolism observed in chronic renal failure (CRF) were investigated in the postabsorptive state. In 11 patients with CRF and in 15 subjects with normal renal function, the hepato-splanchnic (HS), leg, and brain exchanges of glucose were measured; the HS exchange of gluconeogenic amino acids was also evaluated. Patients with CRF had normal glucose levels, whereas insulin levels and the ratio of insulin to glucose were significantly increased in comparison with controls. In CRF, HS glucose output was slightly lower in comparison with controls (0.46 +/- 0.04 vs. 0.57 +/- 0.04 mmoles/min X 1.73 m2 in controls; P less than 0.1). Arterial levels of alanine and glycine and their uptake by the HS bed were similar in both groups, but in CRF HS serine uptake disappeared, mainly as a consequence of a reduction of its fractional extraction. Conversely, a significant proline extraction became evident, primarily depending on the increased arterial levels of this amino acid. The total HS uptake of potential gluconeogenic amino acids was not different in the two groups, and its ratio to glucose output was increased in CRF (28.0 +/- 4.7 vs. 16.0 +/- 1.9 in controls). In CRF, the arterial-femoral venous differences of glucose were significantly reduced (0.11 +/- 0.04 vs. 0.25 +/- 0.04 mmoles/liter in controls), as was the fractional extraction of glucose in the leg. Finally, in CRF both glucose uptake and its fractional extraction by the brain were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)