| Generalized impairment of vasodilator reactivity during hyperinsulinemia in patients with obesity-related metabolic syndrome. | |
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MedLine Citation:
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PMID: 20923961 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Defective insulin-dependent vasodilation might contribute importantly to metabolic and vascular abnormalities of the metabolic syndrome (MetS). However, despite extensive investigation, the precise mechanisms involved in insulin's vasoactive effects have not been fully elucidated. Therefore, this study sought to better characterize insulin's physiological actions on vascular reactivity and their potential derangement in the MetS. Forearm blood flow responses to graded doses of acetylcholine, sodium nitroprusside, and verapamil were assessed by strain-gauge plethysmography in patients with obesity-related MetS (n = 20) and in matched controls (n = 18) before and after intra-arterial infusion of insulin (0.2 mU·kg(-1)·min(-1)). Possible involvement of increased oxidative stress in the impaired insulin-stimulated vasodilator responsiveness of patients with MetS (n = 12) was also investigated using vitamin C (25 mg/min). In control subjects, significant potentiation of the vasodilator responses to acetylcholine, nitroprusside, and verapamil was observed after insulin infusion (all P < 0.05). However, no significant change in vasodilator reactivity to either of these drugs was observed following hyperinsulinemia in patients with MetS (all P > 0.05). Interestingly, administration of vitamin C to patients with MetS during hyperinsulinemia significantly enhanced the vasodilator responsiveness to acetylcholine, nitroprusside, and verapamil (all P < 0.05 vs. hyperinsulinemia alone). In conclusion, insulin exerts a generalized facilitatory action on vasodilator reactivity, and this effect is impaired in patients with MetS likely because of increased oxidative stress. Given the importance of vasodilator reactivity in affecting glucose disposal and vascular homeostasis, this defect may then contribute to the development of metabolic and vascular complications in insulin-resistant states. |
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Authors:
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Francesca Schinzari; Manfredi Tesauro; Valentina Rovella; Angelica Galli; Nadia Mores; Ottavia Porzio; Davide Lauro; Carmine Cardillo |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-05 |
Journal Detail:
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Title: American journal of physiology. Endocrinology and metabolism Volume: 299 ISSN: 1522-1555 ISO Abbreviation: Am. J. Physiol. Endocrinol. Metab. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-30 Completed Date: 2010-12-28 Revised Date: 2011-08-12 |
Medline Journal Info:
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Nlm Unique ID: 100901226 Medline TA: Am J Physiol Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: E947-52 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Tor Vergata, Rome, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Analysis of Variance Ascorbic Acid / pharmacology Chromatography, High Pressure Liquid Dose-Response Relationship, Drug Enzyme-Linked Immunosorbent Assay Female Forearm / blood supply Glutathione / blood Humans Hyperinsulinism / complications, metabolism, physiopathology* Insulin / blood Interleukin-6 / blood Male Metabolic Syndrome X / complications, metabolism, physiopathology* Nitroprusside / pharmacology Obesity / complications, metabolism, physiopathology* Regional Blood Flow / physiology Tumor Necrosis Factor-alpha / blood Vasodilation / drug effects, physiology* Vasodilator Agents / pharmacology Verapamil / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-6; 0/Tumor Necrosis Factor-alpha; 0/Vasodilator Agents; 11061-68-0/Insulin; 15078-28-1/Nitroprusside; 50-81-7/Ascorbic Acid; 51-84-3/Acetylcholine; 52-53-9/Verapamil; 70-18-8/Glutathione |
| Comments/Corrections | |
Comment In:
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Am J Physiol Endocrinol Metab. 2011 Jul;301(1):E242-3; author reply E244
[PMID:
21705628
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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