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Effects of biotin on glucotoxicity or lipotoxicity in rat pancreatic islets.

Authors
  • Yoshikawa, H
  • Tajiri, Y
  • Sako, Y
  • Hashimoto, T
  • Umeda, F
  • Nawata, H
Type
Published Article
Journal
Metabolism
Publisher
Elsevier
Publication Date
Feb 01, 2002
Volume
51
Issue
2
Pages
163–168
Identifiers
PMID: 11833042
Source
Medline
License
Unknown

Abstract

Biotin (vitamin H) plays an important role as a cofactor in glucose or lipid metabolism. We showed that biotin potentiated glucose-induced insulin release in isolated rat islets, while biotin alone did not affect insulin release. Coculture with biotin in islets for 48 hours significantly enhanced glucose-induced insulin release or islet insulin content. Similarly, preproinsulin or pancreatic/duodenal homeobox-1 (PDX-1) mRNA was also enhanced in islets cultured with biotin for 48 hours. Furthermore, we measured effects of biotin on beta-cell function under glucotoxic or lipotoxic states. In islets cultured with high glucose or palmitate for 48 hours, glucose-induced insulin release or islet insulin content deteriorated. Coculture with biotin significantly restored glucose-induced insulin release or islet insulin content together with the restoration of preproinsulin or PDX-1 mRNA. We conclude that biotin exerts its beneficial effects on beta-cell dysfunction induced by glucose or free fatty acids probably through the enhancement of insulin biosynthesis.

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