Summary: Supplementary Figures
Transendothelial transport of insulin and glucose to muscle interstitium. (A) In the normal state,
insulin (blue) and glucose (green) must travel from the blood stream across endothelial cells (red) and
potentially pericytes (yellow) to reach the muscle interstitium and activate insulin signaling in myocytes.
The basal flow rate is depicted by the horizontal arrow. (B) Insulin induces vasodilation of muscle
vasculature, which is thought to increase nutritive blood flow, which increases transport of insulin and
glucose to the muscle interstitium. (C) In insulin resistant situations, insulin exerts only vasoconstriction
signals, which decreases nutritive flow, leading to reduced glucose and insulin transendothelial transport.
(D) Loss of pericytes is thought to increase muscle vessel permeability and transendothelial transport.
Insulin-induced vasodilation and vasoconstriction signaling in endothelial cells and pericytes. (A)
Insulin signaling in endothelial cells results in increased NO production and secretion, which stimulates in
dephosphorylation of myosin in pericytes and vSMCs and results in vasorelaxation. Note that signaling
events that increase vasodilation are shown in green and those that increase vasoconstriction are shown in
red. (B) Conversely, insulin also stimulates endothelin-1 production, which stimulates myosin
phosphorylation and results in vasoconstriction.
Increased pericyte hypertrophy with obesity. (A-B) Islet -smooth muscle actin staining (red)
increases from lean (+/+) (A) to ob/ob mice (B), suggesting that islet pericytes are acquiring more