Journal Article (Letter)

DZNE-2020-01371

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Creatine, guanidinoacetate and homoarginine in statin-induced myopathy.

Neu, A. ; Hornig, S. ; Sasani, A. ; Isbrandt, D.DZNE* ; Gerloff, C. ; Tsikas, D. ; Schwedhelm, E. ; Choe, C.-U. (Corresponding author)

2020
Springer Wien [u.a.]

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Please use a persistent id in citations: doi:10.1007/s00726-020-02865-w

Abstract: Our study evaluated the effect of creatine and homoarginine in AGAT- and GAMT-deficient mice after simvastatin exposure. Balestrino and Adriano suggest that guanidinoacetate might explain the difference between AGAT- and GAMT-deficient mice in simvastatin-induced myopathy. We agree with Balestrino and Adriano that our data shows that (1) creatine possesses a protective potential to ameliorate statin-induced myopathy in humans and mice and (2) homoarginine did not reveal a beneficial effect in statin-induced myopathy. Third, we agree that guanidinoacetate can be phosphorylated and partially compensate for phosphocreatine. In our study, simvastatin-induced damage showed a trend to be less pronounced in GAMT-deficient mice compared with wildtype mice. Therefore, (phospo) guanidinoacetate cannot completely explain the milder phenotype of GAMT-deficient mice, but we agree that it might contribute to ameliorate statin-induced myopathy in GAMT-deficient mice compared with AGAT-deficient mice. Finally, we agree with Balestino and Adriano that AGAT metabolites should further be evaluated as potential treatments in statin-induced myopathy.

Keyword(s): Amidinotransferases: deficiency (MeSH) ; Amino Acid Metabolism, Inborn Errors (MeSH) ; Animals (MeSH) ; Creatine: metabolism (MeSH) ; Creatine: pharmacology (MeSH) ; Developmental Disabilities (MeSH) ; Glycine: analogs & derivatives (MeSH) ; Glycine: metabolism (MeSH) ; Guanidinoacetate N-Methyltransferase: deficiency (MeSH) ; Homoarginine: metabolism (MeSH) ; Hydroxymethylglutaryl-CoA Reductase Inhibitors (MeSH) ; Intellectual Disability (MeSH) ; Mice (MeSH) ; Muscular Diseases: chemically induced (MeSH) ; Muscular Diseases: metabolism (MeSH) ; Phosphocreatine: metabolism (MeSH) ; Speech Disorders (MeSH)

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Contributing Institute(s):

1. Experimental Neurophysiology (AG Isbrandt)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2020

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DEAL Springer ; Ebsco Academic Search ; Essential Science Indicators ; IF < 5 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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