LPL and metabolic syndrome: Therefore, we hypothesized that the observed upregulation of Lpl and Slc27a1 could represent a response to dyslipidemia triggered by circulating pro-inflammatory molecules in CC [37,38], while Agpat2 and Dgat2 may reflect a muscle adaptive response aimed at promoting lipid storage within the skeletal muscle to buffer against lipotoxicity-induced muscle damage in sedentary cachectic muscles.