Nat Commun: Pharmacology rather than physiological GDF15 inhibits eating and exercise 

GDF15 was originally discovered as a macrophage suppressor cytokine (MIC-1), but in recent years it has attracted considerable attention due to its anti-obesity potential.
the treatment of GDF15 for rodents and monkeys, which promotes substantial anorexia and weight loss.
, however, the GDF15 treatment also promotes rodent disgust and nausea.
now, there is growing evidence that pharmacological application of growth differentiation factor 15 (GDF15) inhibits appetite, but also promotes pathological behavior in rodents through GDNF family-like α-like (GFRAL) dependence mechanisms.
, the endomorphic regulation of GDF15 and its physiological effects on energy stabilization and behavior are still not fully available.
recently, researchers showed that in four separate human studies, prolonged endurance exercise increased the level of circulatory GDF15, which is generally observed only under pathophysiological conditions.
this exercise-induced increase can be reproduced in mice, along with an increase in Gdf15 expression in the liver, skeletal muscle, and heart muscle.
, however, the drug GDF15 inhibits appetite and voluntary running through GFRAL, while exercise does not induce physical activity in GDF15.
, the exercise-induced cycle GDF15 is associated with the duration of endurance exercise.
, however, higher levels of GDF15 after exercise are not sufficient to evoke the effects of pharmacological GDF15 on appetite, nor are they responsible for reducing motivation.