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Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance

OBJECTIVE: The study investigated the effect of angiotensin receptor blockers (ARB) on glucose homeostasis and inflammatory parameters in patients with impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: We prospectively studied the insulin sensitivity index (ISI) and homeostasis model as...

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Autores principales: Pscherer, Stefan, Heemann, Uwe, Frank, Helga
Formato: Texto
Lenguaje:English
Publicado: American Diabetes Association 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845051/
https://www.ncbi.nlm.nih.gov/pubmed/20086255
http://dx.doi.org/10.2337/dc09-1381
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author Pscherer, Stefan
Heemann, Uwe
Frank, Helga
author_facet Pscherer, Stefan
Heemann, Uwe
Frank, Helga
author_sort Pscherer, Stefan
collection PubMed
description OBJECTIVE: The study investigated the effect of angiotensin receptor blockers (ARB) on glucose homeostasis and inflammatory parameters in patients with impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: We prospectively studied the insulin sensitivity index (ISI) and homeostasis model assessment–insulin resistance (HOMA-IR) in 13 obese males with IGT and in 13 matched control subjects with normal glucose tolerance (NGT) during hyperglycemic testing over 90 min. Adiponectin, retinol-binding protein 4 (RBP4), and high-sensitive C-reactive protein (hsCRP) were analyzed. Measurements were performed at baseline and after a 4-week treatment with 160 mg/day valsartan. The results of the IGT and NGT groups were compared. RESULTS: At baseline, HOMA-IR (IGT 4.1 ± 3 vs. NGT 2.3 ± 1.0, P < 0.01), hsCRP (IGT 3.9 ± 1.9 vs. NGT 1.8 ± 1 mg/l, P < 0.05), and RBP4 (IGT 27.1 ± 2.1 vs. NGT 24.0 ± 2.0 ng/ml, P < 0.05) were significantly higher, whereas ISI (IGT 1.5 ± 0.9 vs. NGT 1.8 ± 1.2, P < 0.05) and plasma adiponectin (IGT 3.2 ± 0.9, NGT 5.2 ± 2.4 μg/ml, P < 0.05) were significantly lower in the IGT group compared with the NGT group. Under ARB, there was an increase in both groups of adiponectin (IGT 4.1 ± 1.9 μg/ml, NGT 6.3 ± 2.9 μg/ml, P < 0.05) and an increase in ISI (IGT 1.5 ± 0.9 to 2.3 ± 1 μg/ml, NGT 1.8 ± 1 to 2.5 ± 2 μg/ml, P < 0.05). HOMA-IR (4.1 ± 3 to 2.6 ± 2; P < 0.01), hsCRP (3.9 ± 1.9 to 1.8 ± 1 mg/l, P < 0.05), and RBP4 (27.1 ± 2.1 to 22.1 ± 1.8 ng/ml, P < 0.01) decreased significantly in the IGT group. CONCLUSIONS: Insulin sensitivity and associated inflammatory factors improve under ARB in IGT patients.
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spelling pubmed-28450512011-04-01 Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance Pscherer, Stefan Heemann, Uwe Frank, Helga Diabetes Care Original Research OBJECTIVE: The study investigated the effect of angiotensin receptor blockers (ARB) on glucose homeostasis and inflammatory parameters in patients with impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: We prospectively studied the insulin sensitivity index (ISI) and homeostasis model assessment–insulin resistance (HOMA-IR) in 13 obese males with IGT and in 13 matched control subjects with normal glucose tolerance (NGT) during hyperglycemic testing over 90 min. Adiponectin, retinol-binding protein 4 (RBP4), and high-sensitive C-reactive protein (hsCRP) were analyzed. Measurements were performed at baseline and after a 4-week treatment with 160 mg/day valsartan. The results of the IGT and NGT groups were compared. RESULTS: At baseline, HOMA-IR (IGT 4.1 ± 3 vs. NGT 2.3 ± 1.0, P < 0.01), hsCRP (IGT 3.9 ± 1.9 vs. NGT 1.8 ± 1 mg/l, P < 0.05), and RBP4 (IGT 27.1 ± 2.1 vs. NGT 24.0 ± 2.0 ng/ml, P < 0.05) were significantly higher, whereas ISI (IGT 1.5 ± 0.9 vs. NGT 1.8 ± 1.2, P < 0.05) and plasma adiponectin (IGT 3.2 ± 0.9, NGT 5.2 ± 2.4 μg/ml, P < 0.05) were significantly lower in the IGT group compared with the NGT group. Under ARB, there was an increase in both groups of adiponectin (IGT 4.1 ± 1.9 μg/ml, NGT 6.3 ± 2.9 μg/ml, P < 0.05) and an increase in ISI (IGT 1.5 ± 0.9 to 2.3 ± 1 μg/ml, NGT 1.8 ± 1 to 2.5 ± 2 μg/ml, P < 0.05). HOMA-IR (4.1 ± 3 to 2.6 ± 2; P < 0.01), hsCRP (3.9 ± 1.9 to 1.8 ± 1 mg/l, P < 0.05), and RBP4 (27.1 ± 2.1 to 22.1 ± 1.8 ng/ml, P < 0.01) decreased significantly in the IGT group. CONCLUSIONS: Insulin sensitivity and associated inflammatory factors improve under ARB in IGT patients. American Diabetes Association 2010-04 2010-01-19 /pmc/articles/PMC2845051/ /pubmed/20086255 http://dx.doi.org/10.2337/dc09-1381 Text en © 2010 by the American Diabetes Association. https://creativecommons.org/licenses/by-nc-nd/3.0/Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ (https://creativecommons.org/licenses/by-nc-nd/3.0/) for details.
spellingShingle Original Research
Pscherer, Stefan
Heemann, Uwe
Frank, Helga
Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance
title Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance
title_full Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance
title_fullStr Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance
title_full_unstemmed Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance
title_short Effect of Renin-Angiotensin System Blockade on Insulin Resistance and Inflammatory Parameters in Patients With Impaired Glucose Tolerance
title_sort effect of renin-angiotensin system blockade on insulin resistance and inflammatory parameters in patients with impaired glucose tolerance
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845051/
https://www.ncbi.nlm.nih.gov/pubmed/20086255
http://dx.doi.org/10.2337/dc09-1381
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