| Perivascular fatty tissue at the brachial artery is linked to insulin resistance but not to local endothelial dysfunction. | |
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MedLine Citation:
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PMID: 18712517 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIMS/HYPOTHESIS: Different ectopic fat depots, such as visceral or hepatic fat, are known to affect whole body insulin sensitivity. It has recently been hypothesised that differences in perivascular adipose tissue (PVAT) mass around resistance vessels may also contribute to insulin resistance, possibly via direct vascular effects leading to reduced capillary cross-sectional area in the muscle, which in turn affects muscular blood flow and glucose uptake. Based on this, the aim of the present study was to test whether PVAT around conduit arteries (i.e. the brachial artery) influences NO bioavailability, expressed as flow-mediated dilation (FMD), or insulin sensitivity in humans in vivo. METHODS: Insulin sensitivity was measured by OGTT in all 95 participants (59 women, 36 men; median age 47 years, range 19-66 years) and by the gold standard, a euglycaemic-hyperinsulinaemic clamp, in a randomly selected subgroup of 33 participants. Quantification of the different fat compartments, including PVAT around the brachial artery, was achieved by high-resolution magnetic resonance imaging (1.5 T). Blood flow and FMD were measured at the brachial artery using high-resolution (13 MHz) ultrasound, after 5 min of forearm occlusion. RESULTS: PVAT was negatively correlated with insulin sensitivity and the post-ischaemic increase in blood flow. The association between PVAT and insulin sensitivity (r = -0.54, beta = -0.37, p = 0.009) was independent of age, sex, visceral adipose tissue, liver fat, BMI and further cardiovascular risk factors. No correlation could be detected between PVAT and local endothelial function. However, we observed an independent association between PVAT and post-ischaemic increase in blood flow (r = -0.241; beta = -1.69; p = 0.02). CONCLUSIONS/INTERPRETATION: PVAT seems to play an independent role in the pathogenesis of insulin resistance. This may be due to direct vascular effects influencing muscular blood flow. |
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Authors:
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K Rittig; K Staib; J Machann; M Böttcher; A Peter; F Schick; C Claussen; N Stefan; A Fritsche; H-U Häring; B Balletshofer |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-08-20 |
Journal Detail:
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Title: Diabetologia Volume: 51 ISSN: 0012-186X ISO Abbreviation: Diabetologia Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-10-07 Completed Date: 2008-11-18 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0006777 Medline TA: Diabetologia Country: Germany |
Other Details:
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Languages: eng Pagination: 2093-9 Citation Subset: IM |
Affiliation:
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Department of Endocrinology, University of Tübingen, Otfried-Müller Strasse 10, 72076, Tübingen, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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physiology*,
physiopathology Adult Aged Arm Blood Flow Velocity Blood Glucose / metabolism Brachial Artery / anatomy & histology, physiology, physiopathology* Diabetes Mellitus, Type 2 / epidemiology Female Glucose Clamp Technique Glucose Tolerance Test Humans Hyperinsulinism / physiopathology* Ischemia / physiopathology Liver / anatomy & histology Magnetic Resonance Imaging Male Middle Aged Vasodilation |
| Chemical | |
Reg. No./Substance:
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0/Blood Glucose |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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