The effect of losartan on insulin resistance and beta cell function in chronic hemodialysis patients

Citation
S. Fishman et al., The effect of losartan on insulin resistance and beta cell function in chronic hemodialysis patients, RENAL FAIL, 23(5), 2001, pp. 685-692
Citations number
20
Categorie Soggetti
Urology & Nephrology
Journal title
RENAL FAILURE
ISSN journal
0886022X → ACNP
Volume
23
Issue
5
Year of publication
2001
Pages
685 - 692
Database
ISI
SICI code
0886-022X(2001)23:5<685:TEOLOI>2.0.ZU;2-H
Abstract
Insulin resistance (IR) is prevalent in hemodialysis patients. IR and hyper insulinemia have an important role in the development of atherosclerosis, w hich is the most common cause of morbidity and mortality in hemodialysis pa tients. Thus, antihypertensive drugs that lower IR, may have an additional beneficial effect in the treatment of cardiovascular diseases in these pati ents. In this preliminary study we examined the effect of Losartan (an angi otensin II receptor antagonist) treatment on IR and beta cell function in f ive hypertensive non-diabetic chronic hemodialysis patients. All other know n causes of IR in end stage renal failure were excluded. After a washout pe riod of two weeks, Losartan 50 mg, was administered for 6 weeks. Fasting bl ood glucose (FBG) and insulin levels were measured before and after the tre atment IR and beta cell function were calculated using the "homeostasis mod el assessment"-HOMA. Systolic and diastolic blood pressure (BP) have not ch anged significantly throughout the study. FBG increased significantly from 76 mg/dL +/- 1 to 89 mg/dL +/- 4 (p < 0.01), however, insulin levels have n ot changed significantly. Calculated IR values did not show a difference, b ut calculated beta cell function decreased significantly after Losartan tre atment from 291% +/- 50 to 146% +/- 10, (p < 0.016). These preliminary resu lts suggest that in chronic hemodialysis hypertensive non-diabetic patients short treatment with Losartan has deleterious effect on glucose homeostasi s mediated via a decrease in beta cell function.