Effects of biotin on glucotoxicity or lipotoxicity in rat pancreatic islets.
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.
Yoshikawa
H
H
Department of Medicine and Bioregulatory Science, Graduated School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tajiri
Y
Y
Sako
Y
Y
Hashimoto
T
T
Umeda
F
F
Nawata
H
H
D000818:Animals; D001483:Base Sequence; D001710:Biotin / Q000494:pharmacology*; D017931:DNA Primers; D005230:Fatty Acids, Nonesterified / Q000494:pharmacology*; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D066298:In Vitro Techniques; D007515:Islets of Langerhans / Q000187:drug effects* / Q000503:physiopathology; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar
D017931:DNA Primers; D005230:Fatty Acids, Nonesterified; D012333:RNA, Messenger; D001710:Biotin; D005947:Glucose