Send to

Choose Destination
Eur J Pharmacol. 2004 Apr 19;490(1-3):59-70.

Brain insulin and feeding: a bi-directional communication.

Author information

Chercheur INSERM, UMR 7059 CNRS, University Paris 7, 2 place Jussieu, case 7126, 75251 Paris Cedex 05, France.


Insulin and specific insulin receptors are found widely distributed in the central nervous system (CNS) networks related in particular to energy homeostasis. This review highlights the complex regulatory loop between dietary nutrients, brain insulin and feeding. It is well documented that brain insulin has a negative, anorexigenic effect on food intake. At present, a specific role for brain insulin on cognitive functions related to feeding is emerging. The balance between orexigenic and anorexigenic pathways in the hypothalamus is crucial for the maintenance of energy homeostasis in animals and humans. The ingestion of nutrients triggers neurochemical events that signal nutrient and energy availability in the CNS, down regulate stimulators, activate anorexigenic factors, including brain insulin, and result in reduced eating. The effects of insulin in the CNS are under a multilevel control of food-intake peripherally and in the CNS, via the metabolic, endocrine and neural modifications induced by nutrients. Single meals as well as glucose and serotonin are able to regulate insulin release directly in the hypothalamus and may be of importance for its biological effects. Central mechanisms operating in glucose-induced insulin release show some analogy with the mechanisms operating in the pancreas. Leptin and melanocortins, peptides that down regulate food intake and are largely affected by nutrients, are highly interactive with insulin in the CNS probably via the neurotransmitter serotonin. In the hypothalamus, insulin and leptin share a common signaling pathway involved in food intake, namely the insulin receptor substrate, phosphatidylinositol 3-kinase pathway. Over or under-feeding, unbalanced single meals or diets, in particular diets enriched in fat, modify the amount of insulin actively transported into the brain, the release of brain insulin, the expression of insulin messenger RNA and potentially disrupt insulin signaling in the CNS. This impairment may result in disorders related to feeding behavior and energy homeostasis leading to profound dysregulations, obesity or diabetes.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center