Journal
EUROPEAN JOURNAL OF ENDOCRINOLOGY
Volume 166, Issue 2, Pages 235-240Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/EJE-11-0785
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Ministry of Health, Labour and Welfare of Japan
- Tokyo Biochemical Research Foundation
- Smoking Research Foundation
- Foundation for Growth Science
- Grants-in-Aid for Scientific Research [23791052, 23126510, 23791055, 22126002] Funding Source: KAKEN
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Objective: Ghrelin requires a fatty acid modification for binding to the GH secretagogue receptor. Acylation of the Ser3 residue of ghrelin is essential for its biological activities. We hypothesized that acyl-CoA is the fatty acid substrate for ghrelin acylation. Because serum octanoyl-CoA levels are altered by fatty acid oxidation disorders, we examined circulating ghrelin levels in affected patients. Materials and methods: Blood levels of acyl (A) and des-acyl (D) forms of ghrelin and acylcarnitine of patients with medium-chain acyl-CoA dehydrogenase (MCAD) deficiency and glutaric aciduria type II (GA2) were measured. Results: Plasma acyl ghrelin levels and A/D ratios increased in patients with MCAD deficiency or GA2 when compared with normal subjects. Reverse-phase HPLC confirmed that n-octanoylated ghrelin levels were elevated in these patients. Conclusion: Changing serum medium-chain acylcarnitine levels may affect circulating acyl ghrelin levels, suggesting that acyl-CoA is the substrate for ghrelin acylation.
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