Inhibitory effect of chitooligosaccharides on retinol metabolism and bioavailability in mice

J Food Biochem. 2019 May;43(5):e12831. doi: 10.1111/jfbc.12831. Epub 2019 Mar 12.

Abstract

This study investigated the intervention effects of chitooligosaccharides (COS) on retinol metabolism and included comparisons of the retinol level, retinol binding protein 4 (RBP4) content, key genes, and protein expression between mice on a COS-enriched diet and a normal diet. The results showed that COS markedly decreased the retinol and RBP4 concentrations in the serum and liver. Furthermore, COS suppressed the mRNA and protein expression of RBP4, cellular retinol binding protein 1 (CRBP1), lecithin: retinol acyltransferase (LRAT) and cytochrome P45026A1 (CYP26A1). In addition, COS inhibited the mRNA expression of stimulated by retinoic acid 6 (STRA6). However, the protein expression of STRA6 was not significantly decreased. Thus, COS reduced the retinol concentration in the serum and disrupted the metabolism of retinol. The intervention mechanism of COS on retinol metabolism may be attributed to the modulation of RBP4, CRBP1, LRAT, STRA6, and CYP26A1 expression at the mRNA and protein levels. PRACTICAL APPLICATIONS: Chitooligosaccharides (COS), known to be the degradation products of chitosan, have been found to induce pinkeye in industrial workers who participate in the manufacturing of COS. Meanwhile, 5% population with COS dietary supplement also have similar phenomenon. The aim of this study is to explore the possible mechanism underlay of this potential risk. The results of this study showed that high exposure to COS during manufacture influences retinol metabolism and leads to a decrease in retinol content, ultimately causing pinkeye. These findings provide new evidence for understanding COS-induced retinol metabolism alteration and drawing attention toward the prevention of potential risk in high-exposure populations.

Keywords: chemical interaction; chitooligosaccharides; retinol; retinol bioavailability; retinol metabolism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acyltransferases / genetics
  • Acyltransferases / metabolism
  • Animals
  • Chitin / adverse effects
  • Chitin / analogs & derivatives*
  • Chitin / pharmacology
  • Chitosan / metabolism
  • Eye Diseases / prevention & control*
  • Humans
  • Mice
  • Occupational Exposure / prevention & control*
  • Oligosaccharides
  • Retinoic Acid 4-Hydroxylase / genetics
  • Retinoic Acid 4-Hydroxylase / metabolism
  • Retinol-Binding Proteins, Cellular / genetics
  • Retinol-Binding Proteins, Cellular / metabolism
  • Retinol-Binding Proteins, Plasma / genetics
  • Retinol-Binding Proteins, Plasma / metabolism*
  • Risk
  • Vitamin A / blood
  • Vitamin A / metabolism*

Substances

  • CrbpI protein, mouse
  • Oligosaccharides
  • Rbp4 protein, mouse
  • Retinol-Binding Proteins, Cellular
  • Retinol-Binding Proteins, Plasma
  • oligochitosan
  • Vitamin A
  • Chitin
  • Chitosan
  • Cyp26a1 protein, mouse
  • Retinoic Acid 4-Hydroxylase
  • Acyltransferases
  • lecithin-retinol acyltransferase