1975 Volume 17 Issue 1 Pages 31-46
Since the early of this century many hypotheses have been reported about the cause of glucose intolerance of chronic renal failure. But any precise conclusion is not established yet. Therefore, studies concerning on the abnormal glucose and lipid metabolism of chronic renal failure have been carried out, The results are as follows. 1. The glucose decay constant (K-value) of decompensated renal failure was significantly deprssed but improved by undergoing regular hemodialysis, though not (improved) to the value of controls. From the points of improvement of K-value and normalization of insulin secretion in short-term hemodilysis, the existence of insulin antagoinstic substance in uremic patients are hypothesized. On the other hand, through the clinical results insulin/glucose ratio was high in the patients with decompensated renal failure but showed the tendency to be lowered in long-term hemodialysis (approximately over 12 months), and moreover, K-value and insulin sensitivity were improved, it is suggested that long-term hemodialysis may contribute to the improvement of peripheral tissue metabolism. 2. In patients with chronic renal failure hypertriglyceridemia was often observed and LPL activity was suppressed. It is suggested that the existence of LPL inhibitor is to be in the uremic serum and peritoneal dialysate. The inhibiotry effect was lowered by peritoneal dialysis, while it was increased in short-term hemodialysis and decreased in long-term hemodialysis. Decreased C 18 value was found in FFA and triglyceride by gas liquid chromatographic analysis. It seems highly probable that not the abnormal carbohydrate metabolism but the metabolic disturbances in chronic renal failure has the primary important relation, with the abnormality of lipid metabolism in chronic renal failure.