Key result
Insulin acts to recruit muscle capillary flow to enhance microvascular perfusion, an effect that correlates with muscle glucose uptake and is impaired in obese insulin-resistant patients.
Impaired microvascular perfusion and blunted hemodynamic responses to insulin contribute to the pathophysiology of insulin resistance in obesity and type 2 diabetes.
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Impaired hemodynamics may contribute to muscle insulin resistance; hypothesis-generating and should not yet change practice.
Insulin resistance of muscle has been attributed to impairment of elements of insulin signaling, glucose transport, and/or metabolism within the muscle cells. This article explores the notion that a component of insulin resistance in vivo may result from impaired hemodynamic effects of this hormone to facilitate access to the muscle cells for itself and other nutrients, including glucose. In chronic situations this may manifest as a decreased capillary density of muscle, but in the acute, there may be impaired mechanisms for increasing total limb blood flow or for achieving optimal microvascular perfusion. Newly developed techniques show that insulin acts to recruit muscle capillary flow to enhance microvascular perfusion in animals and humans. This microvascular effect of insulin correlates closely with muscle glucose uptake, is independent of increases in bulk blood flow, and is impaired in obese insulin-resistant patients. Similarly, there are impaired vasodilatory responses in the skin of diabetic subjects.
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Clark et al. (2002) conducted a review in Insulin resistance and Type 2 Diabetes. Insulin was evaluated. Insulin acts to recruit muscle capillary flow to enhance microvascular perfusion, an effect that correlates with muscle glucose uptake and is impaired in obese insulin-resistant patients.
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