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Description

This article is not a recommendation for adding AOD-9604 to every stalled GLP-1 patient

Dev Biol

The Kraus 2014 study reported that adipocyte-specific NNMT knockdown in mice increased adipocyte energy expenditure through a mechanism interpreted as elevated methyl-donor availability for polyamine biosynthesis and for histone methylation that modulates adipocyte gene-expression programs [2]