Commentary

Compensatory weight gain due to dopaminergic hypofunction: new evidence and own incidental observations

Julia Reinholz¹ , Oliver Skopp^1,2 , Caterina Breitenstein , Iwo Bohr¹ , Hilke Winterhoff² and Stefan Knecht¹

¹Department of Neurology, University of Muenster, Albert-Schweitzer-Strasse 33, 48129 Muenster, Germany

²Department of Pharmacology and Toxicology, University of Muenster, Domagkstrasse 12, 48149 Muenster, Germany

author email corresponding author email

Nutrition & Metabolism 2008, 5:35doi:10.1186/1743-7075-5-35

Published:	1 December 2008

Abstract

There is increasing evidence for a role of dopamine in the development of obesity. More specifically, dopaminergic hypofunction might lead to (over)compensatory food intake. Overeating and resulting weight gain may be induced by genetic predisposition for lower dopaminergic activity, but might also be a behavioral mechanism of compensating for decreased dopamine signaling after dopaminergic overstimulation, for example after smoking cessation or overconsumption of high palatable food. This hypothesis is in line with our incidental finding of increased weight gain after discontinuation of pharmaceutical dopaminergic overstimulation in rats. These findings support the crucial role of dopaminergic signaling for eating behaviors and offer an explanation for weight-gain after cessation of activities associated with high dopaminergic signaling. They further support the possibility that dopaminergic medication could be used to moderate food intake.