Glucocorticoids and insulin both modulate caloric intake through actions on the brain

Authors


  • This report was presented at The Journal of Physiology Symposium on Obesity and the central nervous system, Washington, DC, USA, 1 September 2007. It was commissioned by the Editorial Board and reflects the views of the author.

Corresponding author M. Dallman: Department of Physiology, Box 0444, University of California San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0444, USA. Email: mary.dallman@ucsf.edu

Abstract

Glucocorticoids act primarily in a feed-forward fashion on brain to activate CNS pathways that implement wanting appropriate to physiological needs. Thus, depending on the available conditions, elevated glucocorticoids may augment the behavioural want to run, fight or feed. Although glucocorticoids stimulate intake of chow, fat and sucrose, insulin appears to sculpt calorie-associated desires toward foods high in fat, acting through hepatic branch afferents of the vagus nerve. Both conditions of reduced food allowance and chronic stress excite glucocorticoid-augmented central neural networks that may lead toward ultimate abdominal obesity.

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