Defective glucose-stimulated insulin release in the diabetic Goto-Kakizaki (GK) rat coincides with reduced activity of the islet carbon monoxide signaling pathway.

@article{Mosn2005DefectiveGI,
  title={Defective glucose-stimulated insulin release in the diabetic Goto-Kakizaki (GK) rat coincides with reduced activity of the islet carbon monoxide signaling pathway.},
  author={Henrik Mos{\'e}n and Albert Salehi and Per Alm and Ragnar Henningsson and Javier Jimenez-Feltstr{\"o}m and C. G. Ostenson and Suad Efend{\'i}c and Ingmar Lundquist},
  journal={Endocrinology},
  year={2005},
  volume={146 3},
  pages={1553-8}
}
The Goto-Kakizaki (GK) rat displays a markedly reduced insulin response to glucose, a defect that is thought to be coupled to an impaired glucose signaling in the beta-cell. We have examined whether carbon monoxide (CO), derived from beta-cell heme oxygenase (HO), might be involved in the secretory dysfunction. Immunocytochemical labeling of constitutive HO (HO-2) showed no overt difference in fluorescence pattern in islets from GK vs. Wistar controls. However, isolated islets from GK rats… CONTINUE READING