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Abstract
Aims: The etiology of statin‑induced rhabdomyolysis (SIR) remains obscure. Most explanations claim deficiency of one of the main end products of the HMG‑CoA reductase pathway. Experimental work has rarely tested the skeletal muscle of humans after SIR. Methods: We compared muscle from ten SIR patients with muscle from eight age‑matched, statin‑naive control subjects. We evaluated differences in muscle histochemistry, sterol biochemistry, prenylated proteins, atrogin‑1 and mitochondrial content to assess which characteristics distinguished the rhabdomyolysis reaction from normal age‑matched muscle. Results: Plant sterols were significantly increased in muscle from SIR subjects compared with ontrol subjects. Ras was significantly reduced and there was a trend towards increased atrogin‑1 in SIR subjects compared with ontrol subject muscle. There was no difference in cholesterol concentrations, mitochondrial content or coenzyme Q10 between groups. Conclusions:This evaluation of muscle from a small sample of patients with SIR demonstrates that differences in sitosterol:cholesterol ratio, the prenylated protein Ras and signals for muscle atrophy like atrogin‑1, may distinguish this reaction from normal muscle.