Abstract

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. Despite genetic predisposition, obesity often involves a behavioral component in which, similar to drugs of abuse, compulsive consumption of palatable food rich in lipids and sugar drives energy intake far beyond metabolic demands. Food intake is 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 main 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 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 mesolimbic pathway.

Highlights

  • Between 1980 and 2008 the mean BMI of the world’s population has increased dramatically

  • The central regulator of food intake and energy expenditure is the brain and the hypothalamus which is the primary site of circulating energy-related signals integration like leptin, ghrelin, or lipids and glucose (Schwartz and Porte, 2005)

  • Alteration of hypothalamic lipid sensing appears to be involved in several brain response to nutrient oversupply that leads to obesity (Velloso and Schwartz, 2011)

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Summary

Introduction

Between 1980 and 2008 the mean BMI of the world’s population has increased dramatically. The central regulator of food intake and energy expenditure is the brain and the hypothalamus which is the primary site of circulating energy-related signals integration like leptin, ghrelin, or lipids and glucose (Schwartz and Porte, 2005) Imbalance in this regulatory process invariably leads to metabolic diseases such as obesity and diabetes in both humans and rodent models (Denis et al, 2014; Schwartz and Porte, 2005). Obesityassociated cognitive impairment can be improved by selective lowering of circulating triglyceride (TG) (Farr et al, 2008) Those observations raise the possibility that nutritional lipids, and triglycerides, directly act on brain structure-through mechanism similar as hypothalamic lipid sensing to affect cognitive and reward processes and contribute to the downward spiral of compulsive food consumption. We will focus on mechanism by which brain regulates rewarding component of food intake and expose recent evolution in the field that might point toward a direct action of nutritional lipid in the mesolimbic pathway

Hedonic and motivational aspect of feeding: a focus on the mesolimbic pathway
Brain lipid sensing
Mesolimbic triglycerides sensing
Findings
Conclusion
Full Text
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