4 ms·
From the abstract, the supplement was B5. I would naively expect that if B5 suppressed appetite, someone would have previously noted this effect.
by 0cf8612b2e1e 2y ago
From the abstract, the supplement was B5. I would naively expect that if B5 suppressed appetite, someone would have previously noted this effect.
- gamblor956 2y agoI think you read the wrong article. The abstract states that gut bacteria is the key: "ugar preference is a key contributor to the overconsumption of sugar and the concomitant increase in the incidence of diabetes. However, the exact mechanism of its development remains ambiguous. Here we show that the expression of free fatty acid receptor Ffar4, a receptor for long-chain fatty acids, is decreased in patients and mouse models with diabetes, which is associated with high sugar intake. Deletion of intestinal Ffar4 in mice resulted in reduced gut Bacteroides vulgatus and its metabolite pantothenate, leading to dietary sugar preference. Pantothenate promoted the secretion of GLP-1 which inhibited sugar preference by stimulating hepatic FGF21 release, which in turn regulates energy metabolism. These findings uncover a previously unappreciated role of Ffar4 in negatively regulating sugar preference and suggest B. vulgatus-derived pantothenate as a potential therapeutic target for diabetes."
- 0cf8612b2e1e 2y agoMy reading from that blurb is that supplementing pantothenate (B5) leads to GLP-1 secretion and curbing of appetite. A proper gut flora already has B. vulgatus which secretes pantothenate, so no need to supplement.
- deleted 2y ago[deleted]
- toomuchtodo 2y agoWouldn’t people without weight challenges be the ones with a proper gut flora? And those without be the ones needing a repopulation of B. vulgatus?