ArticlePhysiological reports2014
BLX-1002 restores glucose sensitivity and enhances insulin secretion stimulated by GLP-1 and sulfonylurea in type 2 diabetic pancreatic islets.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors at 1 institution in 2 countries.
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Abstract
BLX-1002 is a novel thiazolidinedione with no peroxisome proliferator-activated receptor (PPAR) activity that has been shown to improve glycemia in type 2 diabetes without weight gain. We previously found that BLX-1002 selectively augments glucose-sensitive (but not basal) insulin secretion in normal mouse β-cells. We have now extended these observations to other insulin secretagogues and to diabetic rat islets. To this end, dynamics of insulin secretion stimulated by glucose, GLP-1, and the sulfonylurea tolbutamide were examined in pancreatic islets from nondiabetic Wistar and type 2 diabetic Goto-Kakizaki rats ex vivo. BLX-1002 restored normal glucose-sensitive insulin secretion in otherwise "glucose-blind" islets from GK rats, but did not affect basal or glucose-stimulated secretion in normal Wistar rat islets. The stimulatory effect of BLX-1002 on insulin secretion at high glucose required Ca(2+) and involved phosphatidylinositol 3-kinase (PI3K) activity. Consistent with its effects on insulin secretion, BLX-1002 also augmented insulin secretion and cytoplasmic-free Ca(2+) concentrations ([Ca(2+)]i) stimulated by high glucose, GLP-1, and tolbutamide in islets from GK, but not Wistar, rats. The inactive analog BLX-1237 had no effects. In conclusion, our findings suggest that BLX-1002 potentiates insulin secretion by different stimuli in diabetic β-cells only, in a Ca(2+)-dependent manner and involving PI3K.
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