Absence of CD36 alters systemic vitamin A homeostasis
Abstract 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 mobi...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2020-11-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-020-77411-5 |
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| Summary: | Abstract 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. |
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| ISSN: | 2045-2322 |