“…With regard to BMS, the metabolome has been implicated both as a means to interpret the effects of BMS and as a scaffold of surrogate markers for predicting metabolic and bariatric outcomes on an individualized basis. Regarding the former area of interest, the trends of metabolites following BMS as documented in the literature are as follows— AA derivatives : decrease in BCAA (Leu, Ile, Val), AAA (Phe, Tyr, Trpؘ–kynurenine pathway), increase in serotonin, indoxysulfate, indole-3-propionic acid, glycine, and serine; lipid derivatives : decrease in free fatty acids (FFA), short-(C3, C5), medium-, and long-chain acylcarnitines, unsaturated and long-chain saturated fatty acids (LCSFA), triglycerides, ceramides, ketone bodies (late postoperatively), increase in medium-chain saturated fatty acids (MCSFA), decanoid acid, phosphatidylcholine, phosphatidylethanolamines, ketone bodies (early postoperatively); bile acids : increase in primary and secondary bile acids; microbiota-related metabolites : increase in trimethylamine-N-oxide, phenyl sulfate, p -cresol; TCA-related metabolites : decrease in pyruvate and lactate, increase in citrate, succinate, and malate; endocannabinoids : decrease in 2-arachidonoylglycerol, anandamide, arachidonic acid [ 13 , 14 ]. As far as prediction is concerned, relevant studies focus mainly on the relationship of various compounds with T2DM remission [ 12 , 15 , 16 , 17 , 18 , 19 ], and to a lesser extent, with (suboptimal) weight loss [ 20 , 21 ].…”