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Metformin Increases Lac-Phe Levels, Potentially Aiding Weight Loss

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A recent study published in Nature Metabolism reveals that metformin, a commonly prescribed medication for type 2 diabetes, significantly increases levels of Lac-Phe, a metabolite linked to appetite suppression and weight loss. The study by a team at Stanford Medicine sheds new light on how metformin might promote weight loss through a previously undiscovered mechanism involving lac-Phe.

Metformin is widely known for its role in managing blood sugar levels. But its effects on weight loss have been a subject of interest and debate. The current study explores the biochemical pathways through which metformin influences body weight, focusing on its interaction with Lac-Phe, a metabolite previously identified for its role in reducing food intake and promoting weight loss during physical exercise.

The research demonstrated that metformin increases plasma Lac-Phe levels in both mice and humans. This increase is attributed to metformin’s inhibition of mitochondrial complex I, which shifts cellular metabolism towards glycolysis, thereby increasing lactate production. This lactate is then converted into Lac-Phe.

In one part of the study, the researchers administered metformin to a group of mice and measured the levels of Lac-Phe in their blood. They observed a significant rise in Lac-Phe levels post-treatment, confirming the drug’s role in enhancing Lac-Phe biosynthesis. Similarly, in human participants, Lac-Phe levels were found to be higher in those taking metformin compared to those who were not, even after adjusting for factors like age, sex, fasting glucose, and cholesterol levels.

The study further investigated the source of lactate used for Lac-Phe production. It was found that metformin predominantly increases Lac-Phe through intracellular lactate derived from glycolysis, rather than extracellular sources. Experiments using 13C-labeled glucose, which traced the metabolic pathways activated by metformin, supported this conclusion.

Additionally, the research highlighted the role of CNDP2, an enzyme crucial for Lac-Phe production. Mice genetically modified to lack CNDP2 did not show the same increase in Lac-Phe levels when treated with metformin, underscoring the enzyme’s importance in this metabolic pathway.

The implications of these findings are significant for the treatment of obesity and metabolic disorders. The study suggests that Lac-Phe could be a critical mediator of metformin’s weight-loss effects, offering a potential new target for therapeutic intervention. By enhancing Lac-Phe levels, either through pharmacological means or lifestyle changes like exercise, it might be possible to replicate the weight loss benefits observed with metformin.

But the researchers warn that even though the study provides strong evidence for Lac-Phe is role in weight loss, more research is needed to fully understand how it works and to create targeted treatments that can safely and effectively change Lac-Phe levels in humans.

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