Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases.

@article{Maedler2008GlucoseAL,
  title={Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases.},
  author={Kathrin Maedler and Fabienne T. Schulthess and Christelle Bielman and Thierry Berney and Christophe Bonny and Marc Prentki and Marc Yves Donath and Raphael Roduit},
  journal={FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
  year={2008},
  volume={22 6},
  pages={1905-13}
}
c-Jun N-terminal kinases (SAPK/JNKs) are activated by inflammatory cytokines, and JNK signaling is involved in insulin resistance and beta-cell secretory function and survival. Chronic high glucose concentrations and leptin induce interleukin-1beta (IL-1beta) secretion from pancreatic islets, an event that is possibly causal in promoting beta-cell dysfunction and death. The present study provides evidence that chronically elevated concentrations of leptin and glucose induce beta-cell apoptosis… CONTINUE READING

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