Effect of human insulin administration on urinary acidification in patients with insulin-dependent diabetes.
A previous study has shown that oral glucose administration results in a transient fall in urinary acid excretion in humans. The present study was undertaken to determine the effect of physiologic doses of insulin on urinary acidification while maintaining serum glucose concentration constant. This was accomplished by using a euglycemic insulin clamp method. Eight patients with insulin-dependent diabetes and no clinical or laboratory evidence of detectable renal disease were studied. Data obtained during two 2-hour periods of steady state insulin infusion rates of 0.2 and 0.5 mU/kg/min were compared. This resulted in steady state serum free insulin levels of 15 +/- 0.1 and 39 +/- 0.6 uU/ml respectively. Urinary pH and bicarbonate excretion rate rose while the excretion rates of titratable acid, ammonium and net acid fell significantly with increased insulin administration. These changes occurred in the absence of any significant changes in serum glucose, potassium, Ca2+ or phosphorus concentrations or urinary excretion rates of Na+, K+, phosphorus or Ca2+. These data suggest that increased insulin levels within the physiological range can result in a transient fall in the rate of urinary acid excretion. These findings confirm previous observations in animals and suggest that insulin may be the cause of post prandial urinary "alkaline tide".
Vaziri
N D
ND
Byrne
C
C
Staten
M
M
Charles
A
A
D000328:Adult; D001639:Bicarbonates / Q000652:urine; D001786:Blood Glucose / Q000032:analysis; D003922:Diabetes Mellitus, Type 1 / Q000652:urine*; D004573:Electrolytes / Q000652:urine; D005260:Female; D005947:Glucose / Q000494:pharmacology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007328:Insulin / Q000494:pharmacology*; D008297:Male
D001639:Bicarbonates; D001786:Blood Glucose; D004573:Electrolytes; D007328:Insulin; D005947:Glucose