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. 2022 Jul 28;146(10):724–739. doi: 10.1161/CIRCULATIONAHA.121.057978

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© 2022 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 4. — E97G alters hepatic lipase substrate specificity. A and B, Triglyceride (TG) lipase activity and phospholipase A1 (PLA1) activity in medium of heparin-treated immortalized human hepatocytes with overexpression of wild-type LIPC (LIPC-WT), LIPC-E97G, or LIPC-S168G. C and D, Triglyceride lipase activity and PLA1 activity in medium of heparin-treated immortalized human hepatocytes with a wild-type allele, a heterozygous presence of the E97G variant, or a corrected wild-type allele. Each enzymatic activity was corrected for the amount of released hepatic lipase (HL). E, Lipidomics data of plasma of control individuals (n=5) or E97G carriers (n=3). Values are depicted in nanomoles per liter (phosphatidylethanolamine [PE], lysophosphatidylethanolamine [LysoPE], phosphatidylinositol [PI], ceramides [Cer]) or micromoles per liter (fatty acids [FAs], phosphatidylcholine [PC], lysophosphatidylcholine [LysoPC], sphingomyelin [SM]). F, Ratios of plasma FA levels between control individuals (n=5) and E97G carriers (n=3). G, Phospholipid (PL) ratios of lysophospholipids/phospholipids in control individuals (n=5) or family members (n=3). Cell culture data are of 3 independent experiments with a technical duplicate. Statistical significance determined by Mann-Whitney tests. ns Indicates not significant; and RFU, relative fluorescence units. *P<0.05; **P<0.01; ***P<0.001.