| First Author | Trites MJ | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 20386 |
| PubMed ID | 33230291 | Mgi Jnum | J:299714 |
| Mgi Id | MGI:6491073 | Doi | 10.1038/s41598-020-77411-5 |
| Citation | Trites MJ, et al. (2020) Absence of CD36 alters systemic vitamin A homeostasis. Sci Rep 10(1):20386 |
| abstractText | Fatty acid translocase (CD36) is a scavenger receptor with multiple ligands and diverse physiological actions. We recently reported that alcohol-induced hepatic retinoid mobilization is impaired in Cd36(-/-) mice, leading us to hypothesize that CD36 has a novel role in hepatic vitamin A mobilization. Given the central role of the liver in systemic vitamin A homeostasis we also postulated that absence of CD36 would affect whole-body vitamin A homeostasis. We tested this hypothesis in aging wild type and Cd36(-/-) mice, as well as mice fed a vitamin A-deficient diet. In agreement with our hypothesis, Cd36(-/-) mice accumulated hepatic retinyl ester stores with age to a greater extent than wild type mice. However, contrary to expectations, Cd36(-/-) mice consuming a vitamin A-deficient diet mobilized hepatic retinoid similar to wild type mice. Interestingly, we observed that Cd36(-/-) mice had significantly reduced white adipose tissue retinoid levels compared to wild type mice. In conclusion, we demonstrate that the absence of CD36 alters whole-body vitamin A homeostasis and suggest that this phenotype is secondary to the impaired chylomicron metabolism previously reported in these mice. |
