
Gut transporter MCT6 identified as required for metformin-linked weight loss
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Researchers have identified the orphan transporter MCT6 as the main route by which Lac-Phe, a metabolite raised after meals and exercise, leaves intestinal cells and enters the bloodstream. In mice, deleting intestinal MCT6 collapsed normal circulating Lac-Phe levels and made the animals resistant to the weight loss typically associated with metformin. The work, published in Cell, positions metabolite export from the gut as a regulatory node controlling Lac-Phe's systemic effects, rather than merely its production. The finding is from mouse studies; whether the same pathway governs metformin-associated weight loss in humans, and whether MCT6 can be safely targeted to treat obesity, are open questions. Follow-up work on the transporter's physiology and pharmacology would be the expected next step.
Written by a model from the reports · updated 3 hours ago
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- cell.comPickMCT6 is an intestinal Lac-Phe exporter required for metformin-associated weight loss
The orphan transporter MCT6 is the key route by which the meal- and exercise-associated metabolite Lac-Phe exits intestinal cells and enters the blood. Mice lacking intestinal MCT6 cannot maintain normal circulating Lac-Phe levels and are resistant to metformin-associated weight loss, establishing metabolite secretion as a regulatory node for systemic action.
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