Effect of pioglitazone on endothelial function in impaired glucose tolerance

Quinn, Cathy E.; Lockhart, Christopher; Hamilton, Paul; Loughrey, Clodagh; McVeigh, Gary E.

doi:10.1111/j.1463-1326.2010.01224.x

Cited by 17 publications

(19 citation statements)

References 40 publications

(47 reference statements)

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“…The results indicated that, in patients with impaired glucose tolerance, pioglitazone may stimulate adiponectin secretion, improve endothelial function and hence inhibit the progression of coronary atherosclerosis. The present study was in accordance with several other investigations [17,18]. Adiponectin, an adipocyte-derived peptide, has important roles in increasing the availability of nitric oxide, reducing oxidative stress and ⁄ or directly enhancing relaxation of vascular smooth muscle, as well as anti-inflammatory actions [19].…”

Section: Discussionsupporting

confidence: 93%

“…The results of this study indicated that increasing serum adiponectin level might contribute to the effects of pioglitazone in improving endothelial function. With respect to whether improving endothelial function has a role in the mechanism of the beneficial effects of pioglitazone on atherosclerosis, consistent results were reported by different groups [17,18]. The present study also indicated that pioglitazone could increase adponectin secretion, which was correlated with improvement in endothelial function and regression of coronary plaques.…”

Section: Discussionsupporting

confidence: 91%

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Pioglitazone induces regression and stabilization of coronary atherosclerotic plaques in patients with impaired glucose tolerance

Zhang

et al. 2012

Diabetic Medicine

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 91%

Pioglitazone induces regression and stabilization of coronary atherosclerotic plaques in patients with impaired glucose tolerance

Zhang

et al. 2012

Diabetic Medicine

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“…Recent studies have demonstrated that pioglitazone treatment improves plaque stability and endothelial function [5]–[7] in IGT patients, suggesting that its beneficial effects may also occur in pre-diabetic conditions. Experiments conducted in cultured EPCs supported a positive action of pioglitazone on key regulators of atherosclerosis independently of its metabolic action [31], [32].…”

Section: Discussionmentioning

confidence: 99%

“…Impaired glucose tolerance (IGT) is a prediabetic condition characterized by insulin-resistance, predisposing to increased cardiovascular disease (CVD) risk [3]. Recent studies have demonstrated that pioglitazone reduces atherosclerotic plaque inflammation [4] and development [5], [6], and improves endothelial function [7] in subjects with IGT, pointing towards potential beneficial CV properties in pre-diabetic conditions. Experimental studies support the hypothesis that putative pioglitazone CV protective effects extend beyond its metabolic action [8], [9], although the precise molecular mechanisms remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Pioglitazone Improves In Vitro Viability and Function of Endothelial Progenitor Cells from Individuals with Impaired Glucose Tolerance

et al. 2012

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BackgroundEvidence suggests that the PPARγ-agonist insulin sensitizer pioglitazone, may provide potential beneficial cardiovascular (CV) effects beyond its anti-hyperglycaemic function. A reduced endothelial progenitor cell (EPC) number is associated with impaired glucose tolerance (IGT) or diabetes, conditions characterised by increased CV risk.AimTo evaluate whether pioglitazone can provide benefit in vitro in EPCs obtained from IGT subjects.Materials and MethodsEarly and late-outgrowth EPCs were obtained from peripheral blood mononuclear cells of 14 IGT subjects. The in vitro effect of pioglitazone (10 µM) with/without PPARγ-antagonist GW9662 (1 µM) was assessed on EPC viability, apoptosis, ability to form tubular-like structures and pro-inflammatory molecule expression.ResultsPioglitazone increased early and late-outgrowth EPC viability, with negligible effects on apoptosis. The capacity of EPCs to form tubular-like structures was improved by pioglitazone in early (mean increase 28%; p = 0.005) and late-outgrowth (mean increase 30%; p = 0.037) EPCs. Pioglitazone reduced ICAM-1 and VCAM-1 adhesion molecule expression in both early (p = 0.001 and p = 0.012 respectively) and late-outgrowth (p = 0.047 and p = 0.048, respectively) EPCs. Similarly, pioglitazone reduced TNFα gene and protein expression in both early (p = 0.034;p = 0.022) and late-outgrowth (p = 0.026;p = 0.017) EPCs compared to control. These effects were prevented by incubation with the PPARγ-antagonist GW9662.ConclusionPioglitazone exerts beneficial effects in vitro on EPCs isolated from IGT subjects, supporting the potential implication of pioglitazone as a CV protective agents.

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“…These results suggest that insulin resistance is associated with short-term, but not long-term, attenuation of vascular endothelial function both after test meal ingestion and after oral glucose loading. Oral antidiabetic agents, such as pioglitazone, that decrease insulin resistance also improve endothelial function in patients with diabetes [22] or impaired glucose tolerance [23]. Improvement of fasting FMD is correlated with improvement of insulin resistance [24].…”

Section: Discussionmentioning

confidence: 99%

The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

Suzuki

Watanabe

Futami-Suda

et al. 2012

Cardiovasc Diabetol

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BackgroundPrevious studies have demonstrated that postprandial hyperglycemia attenuates brachial artery flow-mediated dilation (FMD) in prediabetic patients, in diabetic patients, and even in normal subjects. We have previously reported that postprandial hyperinsulinemia also attenuates FMD. In the present study we evaluated the relationship between different degrees of postprandial attenuation of FMD induced by postprandial hyperglycemia and hyperinsulinemia and differences in ingested carbohydrate content in non-diabetic individuals.MethodsThirty-seven healthy subjects with no family history of diabetes were divided into 3 groups: a 75-g oral glucose loading group (OG group) (n = 14), a test meal group (TM group) (n = 12; 400 kcal, carbohydrate content 40.7 g), and a control group (n = 11). The FMD was measured at preload (FMD0) and at 60 minutes (FMD60) and 120 (FMD120) minutes after loading. Plasma glucose (PG) and immunoreactive insulin (IRI) levels were determined at preload (PG0, IRI0) and at 30 (PG30, IRI30), 60 (PG60, IRI60), and 120 (PG120, IRI120) minutes after loading.ResultPercentage decreases from FMD0 to FMD60 were significantly greater in the TM group (−21.19% ± 17.90%; P < 0.001) and the OG group (−17.59% ± 26.64%) than in the control group (6.46% ± 9.17%; P < 0.01), whereas no significant difference was observed between the TM and OG groups. In contrast, the percentage decrease from FMD0 to FMD120 was significantly greater in the OG group (−18.91% ± 16.58%) than in the control group (6.78% ± 11.43%; P < 0.001) or the TM group (5.22% ± 37.22%; P < 0.05), but no significant difference was observed between the control and TM groups. The FMD60 was significantly correlated with HOMA-IR (r = −0.389; P < 0.05). In contrast, FMD120 was significantly correlated with IRI60 (r = −0.462; P < 0.05) and the AUC of IRI (r = −0.468; P < 0.05). Furthermore, the percentage change from FMD0 to FMD120 was significantly correlated with the CV of PG (r = 0.404; P < 0.05), IRI60 (r = 0.401; p < 0.05) and the AUC of IRI (r = 0.427; P < 0.05). No significant correlation was observed between any other FMDs and glucose metabolic variables.ConclusionDifferences in the attenuation of postprandial FMD induced by different postprandial insulin levels may occur a long time postprandially but not shortly after a meal.

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Effect of pioglitazone on endothelial function in impaired glucose tolerance

Abstract: Pioglitazone improved endothelial function in IGT. Treatment with pioglitazone may reduce the risk of cardiovascular disease in this patient group.

Cited by 17 publications

References 40 publications

Pioglitazone induces regression and stabilization of coronary atherosclerotic plaques in patients with impaired glucose tolerance

Pioglitazone induces regression and stabilization of coronary atherosclerotic plaques in patients with impaired glucose tolerance

Pioglitazone Improves In Vitro Viability and Function of Endothelial Progenitor Cells from Individuals with Impaired Glucose Tolerance

The effects of postprandial glucose and insulin levels on postprandial endothelial function in subjects with normal glucose tolerance

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