Research

Energy balance

Adropin34-76 treatment reduces incomplete fatty acid oxidation and increases the CoA/acetyl-CoA ratio in skeletal muscle, indicating improved mitochondrial function in obese mice.

This study indicates that obesity can lead to mitochondrial dysfunction, specifically incomplete fatty acid oxidation, which contributes to metabolic issues. Adropin treatment was shown to correct this by improving mitochondrial function. This suggests that maintaining healthy mitochondrial function is crucial for metabolic health, and future therapies may target these pathways.

ModerateSupportsMEDIUM confidence
Reduced incomplete fatty acid oxidation and increased CoA/acetyl-CoA ratio suggested improved mitochondrial function.
Su Gao et al. · Molecular Metabolism · 2015

Why this rating

Controlled animal study with specific biochemical assays. The findings are robust within the model but are mechanistic details rather than primary clinical outcomes.

Source

Therapeutic effects of adropin on glucose tolerance and substrate utilization in diet-induced obese mice with insulin resistance

Su Gao et al. · Molecular Metabolism · 2015

DOI 10.1016/j.molmet.2015.01.005

mechanism_onlyCited 191×
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DOI resolved against Crossref · corpus check 2026-06-10

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