In both developed and emerging countries, sedentary life style and over exposition to high energy dense foods has led to a thermodynamic imbalance and consequently obesity. Obesity often involves a behavioural component in which, similar to drugs abuse, compulsive consumption of palatable food rich in lipids and sugar drives energy intake far beyond metabolic demands. The hypothalamus is one of the primary integration sites of circulating energy-related signals like leptin or ghrelin and is therefore considered as one of the main central regulators of energy balance. However, food intake is also modulated by sensory inputs, such as tastes and odours, as well as by affective or emotional states. The mesolimbic pathway is well established as a key actor of the rewarding aspect of feeding. Particularly, the hedonic and motivational aspects of food are closely tied to the release of the neurotransmitter dopamine (DA) in striatal structure such as the Nucleus Accumbens (Nacc). In both rodent and humans several studies shows an attenuated activity of dopaminergic signal associated with obesity and there is evidence that consumption of palatable food per se leads to DA signalling alterations. Furthermore impaired cognition in obese mice is improved by selectively lowering triglycerides (TG) and intracerebroventricular administration of TG induces by itself acquisition impairment in several cognitive paradigms in normal body weight mice. Together, these observations raise the possibility that nutritional lipids, particularly TG, directly affect cognitive and reward processes by modulating the mesolimbic pathway and might contribute to the downward spiral of compulsive consumption of palatable food and obesity. This review is an attempt to capture recent evolution in the field that might point toward a direct action of nutritional lipid in the reward circuitry.
Bibliographical noteCopyright © 2015 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.
Ideas discussed here are based in part on a presentation of the author at the 12th Euro Fed Lipid Congress. This work as supported by ATIP grant from the “Centre National de la Recherche Scientifique” (CNRS) and by the “Agence Nationale de la Recherche” (ANR-09-BLAN-0267-02 and ANR 11 BSV1 021 01). CC received a PhD fellowship from the CNRS, a research fellowship from the “Societe Francophone du Diabete-Roche” (SFD) and an award from the “Groupe d'Etude et de Recherche en Lipidomique” (GERLI). We acknowledge Mr Kenneth Jackson for his precious inputs in manuscript editing.
- feeding behaviour
- lipoprotein lipase