POSTPRANDIAL HYPERINSULINEMIA, INSULIN-RESISTANCE AND INAPPROPRIATELYHIGH PHOSPHATURIA ARE FEATURES OF YOUNGER MALES WITH IDIOPATHIC CALCIUM UROLITHIASIS - ATTENUATION BY ASCORBIC-ACID SUPPLEMENTATION OF A TEST MEAL

In idiopathic recurrent calcium urolithiasis (RCU) the state of insuli n and carbohydrate metabolism, and relationships to minerals such as p hosphate, are insufficiently understood. Therefore, in two groups of m ales with RCU (n = 30) and healthy controls (n = 8) the response to an oral carbohydrate- and calcium-rich test meal was studied with respec t to glucose, insulin, and C-peptide in peripheral venous blood (taken before and up to 180 min post-load), and phosphate and glucose in fas ting and post-load urine. In one RCU group (n = 16) the meal was suppl emented with ascorbic acid (ASC; 5 mg/kg body weight). The mean age (R CU 29, RCU + ASC 30, controls 27 years) and mean body mass index [RCU 24.4, RCU + ASC 25.0, controls 24.0 kg/m(2)] were similar. Insulin res istance (synonymous sensitivity of peripheral organs to insulin) was c alculated from insulin serum concentration, as was also integrated ins ulin, C-peptide, and glucose. Untreated stone patients (RCU) developed hyperinsulinaemia between 60 and 120 min post-load, increased integra ted insulin, and insulin resistance (P less than or equal to 0.05 vs c ontrols), whereas the rise of C-peptide and glycaemia (absolute and in tegrated values) was only of borderline significance. Fasting phosphat uria was low in both RCU subgroups vs controls; however, phosphaturia in untreated RCU rose in response to the meal, contrasting sharply wit h a decrease in controls. ASC supplementation of the meal (in the RCU + ASC subgroup) normalized insulin, failed to normalize post-load phos phaturia, but reduced post-load glucosuria and urinary pH significantl y (mean pH values 5.55 vs 5.93 in untreated RCU, controls 5.50). Postp randial urinary oxalate, calcium, protein, and supersaturation product s were not changed. The postprandial changes in phosphaturia and insul in sensitivity were inversely correlated (n = 38, r = -0.44, P = 0.007 ). It was concluded that in younger RCU males: (1) postprandial hyperi nsulinaemia, the failure to reduce phosphaturia and - within limits - glucosuria, appropriately, as well as poor urine acidification are imp ortant features of the metabolism; (2) these phenomena are probably ca used by insulin resistance of organs, the kidney included; and (3) the addition of a supraphysiological dose of ASC to a meal, the subsequen t abolition of hyperinsulinaemia, and the restoration of normal urine acidification suggest that this antioxidant is capable of counteractin g some pre-existing basic abnormality of cell metabolism in RCU.