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


Clark, MG, 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) pp. E732-E750. (2008) [Substantial Review]

DOI: doi:10.1152/ajpendo.90477.2008


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. Copyright © 2008 the American Physiological Society.

Item Details

Item Type:Substantial Review
Research Division:Biomedical and Clinical Sciences
Research Group:Medical physiology
Research Field:Systems physiology
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Clark, MG (Professor Michael Clark)
ID Code:54856
Year Published:2008
Web of Science® Times Cited:134
Deposited By:Menzies Institute for Medical Research
Deposited On:2009-03-02
Last Modified:2009-03-02

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