This study determined detailed metabolic effects of of genetically-induced ANGPTL3 deficiency in fasting and postprandial state.
ANGPTL3 loss-of-function carriers had lower levels of triglyceride and low-density lipoprotein cholesterol compred to controls. In addition, ANGPTL3 deficiency results in reduction of cholesterol proportion within triglyceride-rich lipoproteins and their remnants. Further, ANGPTL3 loss-of-function carriers had elevated ketone body production, suggesting enhanced hepatic fatty acid beta-oxidation. To conclude, the detailed metabolic profile in human knockouts of ANGPTL3 reinforces inactivation of ANGPTL3 as a promising therapeutic target for decreasing cardiovascular risk.
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