Effects of dopamine on brown adipose tissue activity and brain energy levels in humans

Project Description:

Loss of body mass and fat mass are highly important nonmotor symptoms of Parkinson’s disease (PD) and predictors for faster disease progression. The determinants for body mass loss include disease severity and the presence of dyskinesias. Furthermore, data obtained in a PD rat model indicate that brown adipose tissue (BAT)-mediated thermogenesis may also contribute to body mass loss (1). Furthermore, stimulation of dopamine receptors (D2R) increases BAT activity in lean and diet-induced obese rodents in a food intake-independent manner. The clinical relevance of these findings is supported by the observation that patients treated with the D2R agonist cabergoline showed a significant body mass loss after 12 months, associated with augmented resting energy expenditure already 3 months after treatment initiation (2). With regard to short term effects of dopamine (DA), oxygen consumption rates, UCP1 and mitochondrial mass increased within 24 h after DA stimulation in a murine brown adipocyte cell model (3). 

References

1. Wang W, Meng X, Yang C, Fang D, Wang X, An J, u. a. Brown adipose tissue activation in a rat model of Parkinson’s disease. Am J Physiol-Endocrinol Metab. 1. Dezember 2017;313(6):E731–6.

2. Folgueira C, Beiroa D, Porteiro B, Duquenne M, Puighermanal E, Fondevila MF, u. a. Hypothalamic dopamine signalling regulates brown fat thermogenesis. Nat Metab. August 2019;1(8):811–29.

3. Kohlie R, Perwitz N, Resch J, Schmid SM, Lehnert H, Klein J, u. a. Dopamine directly increases mitochondrial mass and thermogenesis in brown adipocytes. J Mol Endocrinol. Februar 2017;58(2):57–66.