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Impaired microvascular perfusion: a consequence of vascular dysfunction and a potential cause of insulin resistance in muscle

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Clark, MG (2008) Impaired microvascular perfusion: a consequence of vascular dysfunction and a potential cause of insulin resistance in muscle. American Journal of Physiology: Endocrinology and Metabolism, 295 (4). E732-E750. ISSN 0193-1849

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Abstract

Insulin has an exercise-like action to increase microvascular perfusion of skeletal muscle and thereby enhance delivery of hormone and nutrient to the myocytes. With insulin resistance, insulin's action to increase microvascular perfusion is markedly impaired. This review examines the present status of these observations and techniques available to measure such changes as well as the possible underpinning mechanisms. Low physiological doses of insulin and light exercise have been shown to increase microvascular perfusion without increasing bulk blood flow. In these circumstances, blood flow is proposed to be redirected from the nonnutritive route to the nutritive route with flow becoming dominant in the nonnutritive route when insulin resistance has developed. Increased vasomotion controlled by vascular smooth muscle may be part of the explanation by which insulin mediates an increase in microvascular perfusion, as seen from the effects of insulin on both muscle and skin microvascular blood flow. In addition, vascular dysfunction appears to be an early development in the onset of insulin resistance, with the consequence that impaired glucose delivery, more so than insulin delivery, accounts for the diminished glucose uptake by insulin-resistant muscle. Regular exercise may prevent and ameliorate insulin resistance by increasing "vascular fitness" and thereby recovering insulin-mediated capillary recruitment.

Item Type: Article
Journal or Publication Title: American Journal of Physiology: Endocrinology and Metabolism
Page Range: E732-E750
ISSN: 0193-1849
Identification Number - DOI: 10.1152/ajpendo.90477.2008
Additional Information: Copyright © 2008 by the American Physiological Society.
Date Deposited: 02 Mar 2009 22:52
Last Modified: 18 Nov 2014 03:56
URI: http://eprints.utas.edu.au/id/eprint/8424
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