Observations on sodium retention related to insulin treatment of experimental diabetes.
Streptozotocin (STZ)-diabetic rats regularly retained sodium (Na+), and tended to retain potassium (K+) as well, in response to insulin. Diabetic patients have also been reported to exhibit antinatriuresis and antikaliuresis early in the course of insulin therapy. Insulin-related Na+ retention can occur without a marked reduction in blood glucose level and does not appear to be attributable to preexisting Na+ depletion, mineralocorticoid effect, or suppression of glucosuria. The decrease in urinary Na+ excretion (UNaV) in the rats incident to insulin administration was appreciably greater than the decrease in chloride (Cl-) or water excretion. The significance of this observation is uncertain. It may be, in part, a consequence of the nephrotoxicity of STZ. Insulin-related Na+ retention may be closely related pathogenetically to the Na+ retention of refeeding and may reflect a direct renal action of insulin or, less likely, an alteration of renal tubular metabolism in response to insulin-mediated changes in sytemic metabolism.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002712:Chlorides / Q000652:urine; D003920:Diabetes Mellitus / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D006029:Glycosuria; D007328:Insulin / Q000627:therapeutic use; D007668:Kidney / Q000187:drug effects; D008297:Male; D009318:Natriuresis; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D013311:Streptozocin
D001786:Blood Glucose; D002712:Chlorides; D007328:Insulin; D013311:Streptozocin; D012964:Sodium; D011188:Potassium