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Influence of PPARγ agonists and polymorphism Pro12 Ala on blood pressure values in patients with type 2 diabetes. Initial coverage
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Abstract
Background PPARγ is a transcriptor factor with wide spectrum activity. Its expression disorders, connected with polymorphic variants, are responsible for obesity, insulin resitance and also hypertension. The aim of this study was to assess the influence of PPARγ agonist (roziglitazon) and polymorphism Pro12Ala of this receptor on blood pressure values in type 2 diabetes
Material and methods In 45 patients, who were treated sulfonylurea and metformin with inadequate metabolic control and insulin resitance, rosiglitazone 4 mg per day was administered. Polymorphism Pro12Ala was estimated [SnaPshot; ABI PRISM310]. In 45 patients with type 2 diabetes before and following 22 weeks of rosiglitazone therapy blood pressure valuses were estimated (mean of three measurments). Other tests were conducted using routine lab tests.
Results A heterozygous genotyp Pro12Ala was found in 12 patients and and a homozygous genotyp Pro12Pro in 33 patients. Following rosiglitazone therapy a statistically significant downward tendency of systolic blood pressure valuses was noted (before: 145.35 ± 20.25 mm Hg vs. after: 139.40 ± 15.39 mm Hg; p < 0.045 ). A downward tendency of diastolic blood pressure valuses was observed as well, but it did not achieve significance level (before: 86.37 ± 10.77 vs. after: 83.73 ± 10.19 [mm Hg]; p = 0.170). Blood pressure reduction was noted only in patients with genotype Pro12Ala PPARγ (p < 0.023). A statistically significant downward tendency of blood pressure was not noted in patients with Pro12Pro genotype (p = 0.307).
Conclusions 1. Exogenous stimulation of PPARγ receptor is connected with statistically significant downward tendency of systolic blood pressure values. 2. Hypotensive effect of rosiglitazone appears first in all patients with Pro12Ala genotype.
Abstract
Background PPARγ is a transcriptor factor with wide spectrum activity. Its expression disorders, connected with polymorphic variants, are responsible for obesity, insulin resitance and also hypertension. The aim of this study was to assess the influence of PPARγ agonist (roziglitazon) and polymorphism Pro12Ala of this receptor on blood pressure values in type 2 diabetes
Material and methods In 45 patients, who were treated sulfonylurea and metformin with inadequate metabolic control and insulin resitance, rosiglitazone 4 mg per day was administered. Polymorphism Pro12Ala was estimated [SnaPshot; ABI PRISM310]. In 45 patients with type 2 diabetes before and following 22 weeks of rosiglitazone therapy blood pressure valuses were estimated (mean of three measurments). Other tests were conducted using routine lab tests.
Results A heterozygous genotyp Pro12Ala was found in 12 patients and and a homozygous genotyp Pro12Pro in 33 patients. Following rosiglitazone therapy a statistically significant downward tendency of systolic blood pressure valuses was noted (before: 145.35 ± 20.25 mm Hg vs. after: 139.40 ± 15.39 mm Hg; p < 0.045 ). A downward tendency of diastolic blood pressure valuses was observed as well, but it did not achieve significance level (before: 86.37 ± 10.77 vs. after: 83.73 ± 10.19 [mm Hg]; p = 0.170). Blood pressure reduction was noted only in patients with genotype Pro12Ala PPARγ (p < 0.023). A statistically significant downward tendency of blood pressure was not noted in patients with Pro12Pro genotype (p = 0.307).
Conclusions 1. Exogenous stimulation of PPARγ receptor is connected with statistically significant downward tendency of systolic blood pressure values. 2. Hypotensive effect of rosiglitazone appears first in all patients with Pro12Ala genotype.
Keywords
Pro12Ala polymorphism; PPARγ; hypertension; type 2 diabetes; rosiglitazone
About this articleTitle
Influence of PPARγ agonists and polymorphism Pro12 Ala on blood pressure values in patients with type 2 diabetes. Initial coverage
Journal
Issue
Article type
Original paper
Pages
215-222
Published online
2007-05-31
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663
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1720
Bibliographic record
Nadciśnienie tętnicze 2007;11(3):215-222.
Keywords
Pro12Ala polymorphism
PPARγ
hypertension
type 2 diabetes
rosiglitazone
Authors
Małgorzata Gacka
Tadeusz Dobosz
Stanisław Szymaniec
Dorota Bednarska-Chabowska
Arleta Lebioda
Rajmund Adamiec