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PMID:11833042

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Citation

Yoshikawa, H, Tajiri, Y, Sako, Y, Hashimoto, T, Umeda, F and Nawata, H (2002) Effects of biotin on glucotoxicity or lipotoxicity in rat pancreatic islets. Metab. Clin. Exp. 51:163-8

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.

Links

PubMed

Keywords

Animals; Base Sequence; Biotin/pharmacology; DNA Primers; Fatty Acids, Nonesterified/pharmacology; Female; Glucose/pharmacology; Islets of Langerhans/drug effects; Islets of Langerhans/physiopathology; RNA, Messenger/genetics; Rats; Rats, Wistar

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

RAT:PDX1

involved_in

GO:0033273: response to vitamin

ECO:0000270: expression pattern evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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