In idiopathic recurrent
calcium urolithiasis (RCU) the state of
insulin and carbohydrate metabolism, and relationships to minerals such as
phosphate, are insufficiently understood. Therefore, in two groups of males with RCU (
n = 30) and healthy controls (n = 8) the response to an oral
carbohydrate- and
calcium-rich test meal was studied with respect to
glucose,
insulin, and
C-peptide in peripheral venous blood (taken before and up to 180 min post-load), and
phosphate and
glucose in fasting and post-load urine. In one RCU group (n = 16) the meal was supplemented with
ascorbic acid (ASC; 5 mg/kg
body weight). The mean age (RCU 29, RCU + ASC 30, controls 27 years) and mean body mass index [RCU 24.4, RCU + ASC 25.0, controls 24.0 kg/m2] were similar.
Insulin resistance (synonymous sensitivity of peripheral organs to
insulin) was calculated from
insulin serum concentration, as was also integrated
insulin,
C-peptide, and
glucose. Untreated stone patients (RCU) developed hyperinsulinaemia between 60 and 120 min post-load, increased integrated
insulin, and
insulin resistance (P < or = 0.05 vs controls), whereas the rise of
C-peptide and glycaemia (absolute and integrated values) was only of borderline significance. Fasting
phosphaturia was low in both RCU subgroups vs controls; however,
phosphaturia in untreated RCU rose in response to the meal, contrasting sharply with a decrease in controls. ASC supplementation of the meal (in the RCU + ASC subgroup) normalized
insulin, failed to normalize post-load
phosphaturia, but reduced post-load glucosuria and urinary pH significantly (mean pH values 5.55 vs 5.93 in untreated RCU, controls 5.50). Postprandial urinary
oxalate, calcium,
protein, and supersaturation products were not changed. The postprandial changes in
phosphaturia and
insulin sensitivity were inversely correlated (n = 38, r = -0.44, P = 0.007). It was concluded that in younger RCU males: (1) postprandial hyperinsulinaemia, the failure to reduce
phosphaturia and - within limits - glucosuria, appropriately, as well as poor urine acidification are important features of the metabolism; (2) these phenomena are probably caused by
insulin resistance of organs, the kidney included; and (3) the addition of a supraphysiological dose of ASC to a meal, the subsequent abolition of hyperinsulinaemia, and the restoration of normal urine acidification suggest that this
antioxidant is capable of counteracting some pre-existing basic abnormality of cell metabolism in RCU.