Analysis of plasma ghrelin in patients with medium-chain acyl-CoA dehydrogenase deficiency and glutaric aciduria type II

  • Akamizu T
  • Sakura N
  • Shigematsu Y
 et al. 
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Abstract

Objective: Ghrelin requires a fatty acid modification for binding to the growth hormone 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 desacyl (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 appeared to be elevated in patients with MCAD deficiency or GA2 than in comparison to those in normal subjects. Reverse-phase high-performance liquid chromatography 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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Authors

  • T Akamizu

  • N Sakura

  • Y Shigematsu

  • G Tajima

  • A Ohtake

  • H Hosoda

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