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Diabetes Metab J. 2012 Apr;36(2):83-89. English. Review. https://doi.org/10.4093/dmj.2012.36.2.83
Liu Z , Ko SH , Chai W , Cao W .
Division of Endocrinology & Metabolism, Department of Internal Medicine, University of Virginia Health System, Charlottesville, VA, USA. zl3e@virginia.edu
Division of Endocrinology & Metabolism, Department of Internal Medicine, The Catholic University of Korea College of Medicine, Suwon, Korea.
Department of Nutrition, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Abstract

Insulin increases microvascular perfusion and substrate exchange surface area in muscle, which is pivotal for hormone action and substrate exchange, by activating insulin signaling cascade in the endothelial cells to produce nitric oxide. This action of insulin is closely coupled with its metabolic action and type 2 diabetes is associated with both metabolic and microvascular insulin resistance. Muscle microvascular perfusion/volume can be assessed by 1-methylxanthine metabolism, contrast-enhanced ultrasound and positron emission tomography. In addition to insulin, several factors have been shown to recruit muscle microvasculature, including exercise or muscle contraction, mixed meals, glucagon-like peptide 1 and angiotensin II type 1 receptor (AT1R) blocker. On the other hand, factors that cause metabolic insulin resistance, such as inflammatory cytokines, free fatty acids, and selective activation of the AT1R, are capable of causing microvascular insulin resistance. Therapies targeting microvascular insulin resistance may help prevent or control diabetes and decrease the associated cardiovascular morbidity and mortality.

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