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

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.

Figure 1

Effects of L-DOPA treatment on body weight. Rats treated previously with L-DOPA had the same weight as rats treated with a vehicle solution before and immediately after the treatment, but gained more weight during a follow-up period. Results represent the means ± SD of body weight for each group measured at the respective time point. Asterisk indicates a significant difference (p < 0.05).

Figure 2

Individual data on increase in body weight. All but one rat from the vehicle group gained less weight than the mean weight gain of the L-DOPA group. About half of the rats from the L-DOPA group gained more weigh than almost all rats from the vehicle group. Results represent the individual difference in body weight for each rat from both groups between the last day of treatment and the 15-week follow-up.