Brain Capillary Endothelial Transport of Insulin

Abstract

The most immediate short-term action of insulin on cells is the increase in plasma membrane glucose transporter activity in such tissues as fat, skeletal muscle, and heart.1 Although insulin does not cause a short-term increase in glucose transport into brain,2,3 it does have important long-term actions on brain at the physiologic concentrations occurring in plasma, i.e., 1–10 ng/ml (25–250 μU/ml). For example, physiologic concentrations of insulin increase the glutamate-induced firing rate of cholinergic retinal neurons in tissue culture,4 and increase the coupling across nascent synapses of superior cervical ganglion cells or sympathetic neurons in primary tissue culture.5,6 In vivo studies have shown that the hypothalamic injection of picomolar quantities of insulin increases the firing rate of rat sympathetic nerves innervating brown fat,7 and that the chronic intraventricular infusion of insulin in baboons enhances the suppressive effect of intravenous cholecystokinin-8 on meal size.8