The increasing incidence and prevalence of insulin resistance and its
associated co-morbidities represents a growing concern to public health policy
across developed economies world wide. While the economic and psycho-social
implications of insulin resistance and the ultimate development of type II diabetes
mellitus are profound, much of this is associated with the increased probability of
afflicted individuals for the development of peripheral vascular disease; with the
hallmark characteristics of impaired matching of skeletal muscle perfusion with
elevated metabolic demand. Two models of insulin resistance are highlighted in
this chapter: the fructose-fed rodent model (which develops insulin resistance in
the absence of obesity) and the obese Zucker rat (which develops insulin
resistance subsequent to a chronic hyperphagia). While this chapter provides an
overview of some of the skeletal muscle perfusion impairments associated with
insulin resistance and its satellite co-morbidities, it also provides a discussion of
key contributing elements to this relative ischemic condition. Specifically, this
chapter will discuss the contributions of altered vascular reactivity from the
perspective of both dilator and constrictor responses, the impact of insulin
resistance on potassium channel function, structural alterations to microvascular
networks (microvascular rarefaction), and the impact of insulin resistance on
patterns of capillary recruitment. What rapidly becomes apparent is that the
profound impact of pathological states such as insulin resistance on skeletal
muscle perfusion represents a spatially and temporally distributed outcome with
many contributors resulting in an integrated negative outcome.
Keywords: Vascular reactivity, vasculopathy, impaired glycemic control, skeletal muscle perfusion.
