Research

Hormonal

The PPARδ agonist GW501516 increases glucose uptake in human skeletal muscle cells via an AMPK-dependent mechanism that is independent of PPARδ expression.

This research identifies a specific mechanism by which PPARδ activation improves glucose handling in muscle cells: it bypasses the PPARδ receptor itself to activate AMPK, a key energy sensor. While GW501516 is a research chemical and not a consumer supplement, this finding suggests that strategies which activate AMPK (such as exercise or specific metabolic stressors) may mimic this glucose-uptake benefit independently of PPARδ expression levels.

ModerateSupportsMEDIUM confidence
Finally, we have also demonstrated that the GW501516-mediated increase in glucose uptake requires AMPK but not PPARδ.
David Kramer et al. · Journal of Biological Chemistry · 2007

Why this rating

The study uses primary human muscle cells (high translational relevance) but relies on in vitro siRNA knockdown and acute incubation rather than long-term clinical outcomes.

Source

Role of AMP Kinase and PPARδ in the Regulation of Lipid and Glucose Metabolism in Human Skeletal Muscle

David Kramer et al. · Journal of Biological Chemistry · 2007

DOI 10.1074/jbc.m702329200

mechanism_only · n=7Cited 180×
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DOI resolved against Crossref · corpus check 2026-06-10

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