Olfactory inputs help animals coordinate food appreciation and selection. Previous studies say mice’s olfaction is linked to fat metabolism, and therefore is related to their weight gain. Ablation of adult olfactory sensory neurons (OSNs) reduces diet-induced obesity in mice. On the other hand, the findings is challenged by a study which shows enhancement of olfactory systems prevent high-fat induced obesity. These findings are conflicting and, hence, lead to the point that olfaction regulates fat metabolism in a complex way.
In March this year, Dr. Ayse Sena Mutlu and Meng C. Wang from Baylor College of Medicine described that some specific odors reduce fat metabolism in C. elegans by inhibiting the specific olfactory neurons, without changing food intake and energy expenditure. Authors screened 30 mutants with chemosensory neuronal defects and found that fat storage is increased in the intestine of the guanylate cyclase daf-11 mutants, meanwhile neither fatty-acid absorption nor lipid synthesis is increased. In the worms, daf-11 is identified to be expressed in seven pairs of head sensory neurons, among which, only AWC olfactory neurons play an important role in regulating fat metabolism.
In addition, the odor 2-butanone blocks the activity of AWC olfactory neurons. The study discovered that the exposure to 2-butanone causes an increase in fat storage levels in C. elegans. Worms exposed to 2-butanone show a rapid increase in fat storage levels within 4 hours compared to worms exposed to vehicle controls. And after removing the odor 2-butanone, the increased fat storage levels are rapidly recovered. The results suggest a reversible regulation of fat metabolism by specific environmental odors.
