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CELA2A mutations predispose to early-onset atherosclerosis and metabolic syndrome and affect plasma insulin and platelet activation.

Nat Genet. 2019-08; 
EsteghamatFatemehsadat,BroughtonJames S,SmithEmily,CardoneRebecca,TyagiTarun,GuerraMateus,SzabóAndrás,UgwuNelson,ManiMitra V,AzariBani,KayingoGerald,ChungSunny,FathzadehMohsen,WeissEphraim,BenderJeffrey,ManeShrikant,LiftonRichard P,AdeniranAdebowale,NathansonMichael H,GorelickFred S,HwaJohn,Sahin-TóthMiklós,Belfort-DeAguiarRenata,KibbeyRichard G,Mani
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Proteins, Expression, Isolation and Analysis To explore the in vivo effect of CELA2A on glucose and triglyceride homeostasis, 3-month-old male hyperlipidemic and diabetic Ldlr−/− mice on a Western diet were injected intravenously with exogenous endotoxin-free (<0.1EUml−1 ; L00338; GenScript) mouse rCela2a (2.5mg kg−1 ; n=10) or vehicle (n=10) after 16h of fasting. Get A Quote

摘要

Factors that underlie the clustering of metabolic syndrome traits are not fully known. We performed whole-exome sequence analysis in kindreds with extreme phenotypes of early-onset atherosclerosis and metabolic syndrome, and identified novel loss-of-function mutations in the gene encoding the pancreatic elastase chymotrypsin-like elastase family member 2A (CELA2A). We further show that CELA2A is a circulating enzyme that reduces platelet hyperactivation, triggers both insulin secretion and degradation, and increases insulin sensitivity. CELA2A plasma levels rise postprandially and parallel insulin levels in humans. Loss of these functions by the mutant proteins provides insight into disease mechanisms and... More

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