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Cardiovascular diseases are a leading cause of death worldwide, with excessive platelet activity and blood clots (thrombosis) playing a key role. While intermittent fasting is known for its benefits like better metabolism, weight loss, and longer lifespan, its impact on platelet function and clot formation is less clear.
A recent study by Professor Junbo Ge team at Fudan University unveiled a novel mechanism by which intermittent fasting can significantly reduce the risk of platelet hyperactivity and thrombosis. That is, intermittent fasting elevates levels of the metabolite indole-3-propionic acid (IPA) by modulating gut microbiota, which in turn suppresses platelet activation — a critical factor in cardiovascular events such as heart attacks and strokes.
The findings of the study are published in the journal Life Metabolism (1✔ ✔Trusted Source
Intermittent fasting inhibits platelet activation and thrombosis through the intestinal metabolite indole-3-propionate
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IPA was previously known as a tryptophan-derived metabolite with anti-inflammatory properties. By integrating clinical data from patients with coronary artery disease and experimental ApoE knockout mice, as well as utilizing metabolomic and transcriptomic analyses, the present study reported a novel role of gut microbiota-derived IPA in modulating platelet activation by binding to the pregnane X receptor (PXR), thereby decreasing the phosphorylation of Src, Lyn, Syk, LAT, PLCγ, and PKC, as well as reducing Ca2+ influx.
The findings reveal a previously unknown relationship between dietary patterns and platelet activation and thrombosis, which suggests that nonpharmacological interventions could substantially lower the risk of life-threatening cardiovascular events.
Reference:
Source-Eurekalert
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