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Physiol Behav. 2007 Aug 15;91(5):486-98. Epub 2007 Jan 12.

Interactions between the "cognitive" and "metabolic" brain in the control of food intake.

Author information

1
Neurobiology of Nutrition Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. berthohr@pbrc.edu

Abstract

If the new environment and modern lifestyle cause obesity in individuals with thrifty genes by increasing energy intake, it is important to know by what mechanisms hyperphagia occurs and why energy balance is not kept in check by the homeostatic regulator. The argument is developed that procuring and ingesting food is an evolutionarily conserved survival mechanism that occupies large parts of the brain's computing capacity including not only the hypothalamus but also a number of cortico-limbic structures. These forebrain systems evolved to engage powerful emotions for guaranteed supply and ingestion of beneficial foods from a sparse and often hostile environment. They are now simply overwhelmed with an abundance of food and food cues that is no longer interrupted by frequent famines. After briefly reviewing structure and functions of the relevant cortico-limbic structures and the better-known hypothalamic homeostatic regulator, the review focuses mainly on interactions between the two systems. Although several cortico-limbic processes are sensitive to metabolic depletion and repletion signals, it appears that they are underlying the same reversible leptin resistance that renders hypothalamic circuits insensible to continuously high leptin levels during periods of feast. It is hypothesized that this naturally occurring leptin resistance allowed temporary neutralization of satiety mechanisms and evolved as a response to survive subsequent periods of famine. With today's continuous and abundant food availability for a segment of the population, the powerful cognitive processes to eat and the resulting overweight can partially escape negative feedback control in prone individuals most strongly expressing such thrifty genes.

PMID:
17307205
DOI:
10.1016/j.physbeh.2006.12.016
[Indexed for MEDLINE]

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