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Glucosamine-induced beta-cell dysfunction: a possible involvement of glucokinase or glucose-transporter type 2
Hiroyasu Yoshikawa1, Yuji Tajiri, Yasuhiro Sako
1Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hiroyasi.yoshikawa@medisin.ntnu.no
Introduction:
The mechanism for beta-cell dysfunction induced by glucosamine has not yet fully been investigated previously.
Aim:
To investigate the effects of glucosamine on insulin release or gene expression related to glucose metabolism in rat islets cultured with glucosamine for 24 hours.
Methodology:
After islets were cultured with glucosamine or diazoxide, we measured glucose- or arginine-induced insulin release by using radioimmunoassay (RIA) and gene expressions by semiquantitative polymerase/chain reaction.
Results:
Coculture with glucosamine inhibited 27 mmol/L glucose-induced insulin release with no effects on 20 mmol/L arginine-induced insulin release. Coculture with diazoxide did not restore the impaired glucose-induced insulin release. In glucosamine-cultured islets, glucose-transporter type 2 or glucokinase mRNA expression decreased, whereas hexokinase mRNA increased. Phosphofructokinase-A, pyruvate dehydrogenase E1alpha, or pyruvate carboxylase mRNA was not affected by the addition of glucosamine. Pancreatic and duodenal homeobox-1, preproinsulin, or p21 (induced by oxidative stress) mRNA expression did not change, whereas uncoupling protein 2 mRNA, which plays an important role in thermogenesis, decreased in glucosamine-cultured islets.
Conclusion:
These data imply that glucosamine impairs glucose-induced insulin release probably through the inhibition of glucose metabolism.