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1980, 198613). , 1986). However, the defective central insulin action may be restricted to the food intake regulatory pathways, since S. J. Holt and D. A. York (unpublished observations) have recently observed a normal suppression of sympathetic firing rate after intracerebroventricular insulin injections into the falfa rat. It is also possible that the described defects in the brain insulin system are a secondary reflection of the developing obesity and insulin insensitivity that are characteristic of peripheral tissues at this stage.
D. CONTROLLED SYSTEM There are functional changes in several components of the controlled system following a VMH lesion. , 1983). Insulin secretion by isolated islets or perfused pancreas rises by 2-fold or more within 7 days after VMH lesions (Smith and Campfield, 1986; Rohner-Jeanrenaud and Jeanrenaud, 1980). The neurotransmitter acetylcholine is less effective in stimulating insulin from islets of VMH-lesioned rats than from control rats and there is a shift in the log dose response curve. This is the effect one might expect from a tissue exposed to increased tonic stimulation.
Since the various peripheral responses to central 2-DG are thought to reflect the effects of glucoprivation at multiple central sites, the consistent suppression of these effects by corticosterone suggest that glucocorticoids must also act at multiple central loci, possibly through a common mechanism. 4. Peptides A wide range of effects of glucocorticoids on the central nervous system have been described (Meyer, 1985). While the evidence to date implicates an interaction between glucocorticoids and glucose-initiated responses, it is not clear whether this a direct interaction.