ABSTRACT
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.
KEYWORD
Insulin action - insulin resistance - capillary recruitment - muscle - skin