Phosphodiesterase 5 inhibition improves beta-cell function in metabolic syndrome.

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2009-05

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Abstract

OBJECTIVE: This study tested the hypothesis that phosphodiesterase 5 inhibition alone or in combination with ACE inhibition improves glucose homeostasis and fibrinolysis in individuals with metabolic syndrome. RESEARCH DESIGN AND METHODS: Insulin sensitivity, beta-cell function, and fibrinolytic parameters were measured in 18 adults with metabolic syndrome on 4 separate days after a randomized, crossover, double-blind, 3-week treatment with placebo, ramipril (10 mg/day), tadalafil (10 mg o.d.), and ramipril plus tadalafil. RESULTS: Ramipril decreased systolic and diastolic blood pressure, ACE activity, and angiotensin II and increased plasma renin activity. Ramipril did not affect insulin sensitivity or beta-cell function. In contrast, tadalafil improved beta-cell function (P = 0.01). This effect was observed in women (331.9 +/- 209.3 vs. 154.4 +/- 48.0 32 micro x mmol(-1) x l(-1), respectively, for tadalafil treatment vs. placebo; P = 0.01) but not in men. There was no effect of any treatment on fibrinolysis. CONCLUSIONS Phosphodiesterase 5 inhibition may represent a novel strategy for improving beta-cell function in metabolic syndrome.

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10.2337/dc08-1862

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Hill, Kevin D, Aaron W Eckhauser, Annis Marney and Nancy J Brown (2009). Phosphodiesterase 5 inhibition improves beta-cell function in metabolic syndrome. Diabetes Care, 32(5). pp. 857–859. 10.2337/dc08-1862 Retrieved from https://hdl.handle.net/10161/13549.

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Hill

Kevin Dennis Hill

Professor of Pediatrics

Clinical research including outcomes, drug and device trials, short and long term safety and efficacy of interventions and hemodynamic effects of interventions.


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