The discovery of apolipoprotein A5 (APOA5) in 2001 has raised a number of intriguing questions about its role in lipid transport and triglyceride (TG) homeostasis. Genome-wide association studies have consistently identified APOA5 as a regulator of plasma TG levels, which is further supported by studies in transgenic and knockout mouse models. The present review describes recent concepts pertaining to the roles of APOA5 in TG metabolism as related to the vascular compartment, liver, adipose tissue and the gut. Recent evidence indicates that APOA5 may also affect postprandial TG metabolism through influencing chylomicron formation and transport by the intestine into the intestinal lymph. While substantial evidence supports the notion that APOA5 plays both extracellular and intracellular roles in TG homeostasis, mysteries remain on how this low-abundance, liver-derived protein may modulate TG homeostasis, including via the gut. Given the strong correlation between elevated plasma TG and cardiometabolic diseases, there is great scientific and public interest in understanding the intriguing mysteries presented by APOA5.
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| http://dx.doi.org/10.1016/j.bbalip.2022.159185 | DOI Listing |
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Article Synopsis
- A study explored whole-exome sequencing (WES) to better understand severe hypertriglyceridemia by identifying genes linked to high triglyceride levels through a genome-wide association study (GWAS).
- The GWAS involved over 120,000 participants and found that the APOA5 locus on chromosome 11 has the strongest association with triglyceride levels, alongside other significant genes like BUD13, GCKR, and LPL.
- WES conducted on 29 patients with extreme hypertriglyceridemia identified additional genes such as ALDH1A2 and APOC1, highlighting both known and novel genetic factors that may influence lipid metabolism and open up possibilities for new treatments.
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