As anyone who's dabbled with MDMA and other serotonin-releasing compounds may have noticed, fatloss seems to be a pretty common side-effect. Obviously that's partly related to the poor nutrition, lack of appetite and high energy output that tends to accompany use.
However a new paper published in Nature on Friday is helping to uncover another of the probable links between serotonin release and fat metabolism: the neuropeptide FLP-7.
As the researchers state: "a neural circuit in the brain produces serotonin in response to sensory cues, such as food availability. This signals another set of neurons to begin producing FLP-7. FLP-7 then activates a receptor in intestinal cells, and the intestines begin turning fat into energy."
Now I'm not suggesting bodybuilders should go out and pop an E before training (!) since (as you probably know) serotonin is intricately involved in numerous other critical physiological functions. However this finding could have interesting implications for those suffering from depression and/or poor mood who often seem to put on weight. And unlike serotonin itself, FLP-7 appears to have fewer extraneous effects outside fatloss, so may be another potential miracle cutting agent (alongside asprosin blockers) to watch out for in the future.
Anyway for a magazine-style run through of the paper, read >>this<< article from ScienceDaily. For the abstract and link to the full (free) paper, read below:
A tachykinin-like neuroendocrine signalling axis couples central serotonin action and nutrient sensing with peripheral lipid metabolism (2017)
Lavinia Palamiuc, Tallie Noble, Emily Witham, Harkaranveer Ratanpal, Megan Vaughan & Supriya Srinivasan
Serotonin, a central neuromodulator with ancient ties to feeding and metabolism, is a major driver of body fat loss. However, mechanisms by which central serotonin action leads to fat loss remain unknown. Here, we report that the FLP-7 neuropeptide and its cognate receptor, NPR-22, function as the ligand-receptor pair that defines the neuroendocrine axis of serotonergic body fat loss in Caenorhabditis elegans. FLP-7 is secreted as a neuroendocrine peptide in proportion to fluctuations in neural serotonin circuit functions, and its release is regulated from secretory neurons via the nutrient sensor AMPK. FLP-7 acts via the NPR-22/Tachykinin2 receptor in the intestine and drives fat loss via the adipocyte triglyceride lipase ATGL-1. Importantly, this ligand-receptor pair does not alter other serotonin-dependent behaviours including food intake. For global modulators such as serotonin, the use of distinct neuroendocrine peptides for each output may be one means to achieve phenotypic selectivity.