The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses.
Despite the effects of insulinopenia in type 1 diabetes and evidence that insulin stimulates multiple renal sodium transporters, it is not known whether normal variation in plasma insulin regulates sodium homeostasis physiologically. This study tested whether the normal postprandial increase in plasma insulin significantly attenuates renal sodium and volume losses. Rats were instrumented with chronic artery and vein catheters, housed in metabolic cages, and connected to hydraulic swivels. Measurements of urine volume and sodium excretion (UNaV) over 24 h and the 4-h postprandial period were made in control (C) rats and insulin-clamped (IC) rats in which the postprandial increase in insulin was prevented. Twenty-four-hour urine volume (36 ± 3 vs. 15 ± 2 ml/day) and UNaV (3.0 ± 0.2 vs. 2.5 ± 0.2 mmol/day) were greater in the IC compared with C rats, respectively. Four hours after rats were given a gel meal, blood glucose and urine volume were greater in IC rats, but UNaV decreased. To simulate a meal while controlling blood glucose, C and IC rats received a glucose bolus that yielded peak increases in blood glucose that were not different between groups. Urine volume (9.7 ± 0.7 vs. 6.0 ± 0.8 ml/4 h) and UNaV (0.50 ± 0.08 vs. 0.20 ± 0.06 mmol/4 h) were greater in the IC vs. C rats, respectively, over the 4-h test. These data demonstrate that the normal increase in circulating insulin in response to hyperglycemia may be required to prevent excessive renal sodium and volume losses and suggest that insulin may be a physiological regulator of sodium balance.
Department of Physiology, Medical College of Georgia, Augusta, Georgia.
Debra L
DL
Irsik
Department of Biology, Indiana University-Purdue University Indianapolis, Indianapolis, Indiana; and.
Bonnie L
BL
Blazer-Yost
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Alexander
0000-0002-5190-8356
A
Staruschenko
Department of Physiology, Medical College of Georgia, Augusta, Georgia; mbrands@augusta.edu.
Michael W
MW
Brands
D000818:Animals; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D015309:Glucose Clamp Technique; D006943:Hyperglycemia / Q000097:blood* / Q000503:physiopathology / Q000652:urine; D007328:Insulin / Q000097:blood*; D007668:Kidney / Q000378:metabolism*; D008297:Male; D023421:Models, Animal; D009318:Natriuresis; D019518:Postprandial Period; D017207:Rats, Sprague-Dawley; D065667:Renal Elimination; D012964:Sodium / Q000652:urine*; D013997:Time Factors; D015854:Up-Regulation; D014554:Urination
D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D012964:Sodium
insulin; postprandial; sodium excretion; urine volume