Journal
MOLECULES
Volume 22, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/molecules22101718
Keywords
Hacl1; alpha-oxidation; pentadecanoic acid; heptadecanoic acid; C17:0; biomarker; odd chain fatty acid; peroxisomes
Funding
- Medical Research Council Human Nutrition Research in Cambridge [UD99999906, G0800783]
- Fonds Wetenschappelijk Onderzoek [G.0721.10N]
- KU Leuven [OT/14/100]
- NIHR BRC Core Metabolomics and Lipidomics Laboratory, University of Cambridge
- Biotechnology and Biological Sciences Research Council [BB/M027252/2, BB/P028195/1, BB/M027252/1] Funding Source: researchfish
- BBSRC [BB/M027252/2, BB/M027252/1, BB/P028195/1] Funding Source: UKRI
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Circulating heptadecanoic acid (C17:0) is reported to be a pathology risk/prognosis biomarker and a dietary biomarker. This pathology relationship has been shown to be reliably predictive even when independent of dietary contributions, suggesting that the endogenous biosynthesis of C17: 0 is related to the pathological aetiology. Little is known about C17: 0 biosynthesis, which tissues contribute to the circulating levels, and how C17:0 is related to pathology. Hacl1+/- mice were mated to obtain Hacl1-/- and Hacl1+/+ control mice. At 14 weeks, they were anesthetized for tissue collection and fatty acid analysis. Compared to Hacl1+/+, C15:0 was not significantly affected in any Hacl1-/- tissues. However, the Hacl1-/- plasma and liver C17:0 levels were significantly lower: similar to 26% and similar to 22%, respectively. No significant differences were seen in the different adipose tissues. To conclude, Hacl1 plays a significant role in the liver and plasma levels of C17:0, providing evidence it can be endogenously biosynthesized via alpha-oxidation. The strong inverse association of C17:0 with pathology raises the question whether there is a direct link between alpha-oxidation and these diseases. Currently, there is no clear evidence, warranting further research into the role of alpha-oxidation in relation to metabolic diseases.
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