26 Mar 2015
Impaired glucose-stimulated insulin secretion (GSIS) and increasing β-cell death are two typical dysfunctions of pancreatic β-cells in individuals that are destined to develop type 2 diabetes, and improvement of β-cell function through GSIS enhancement and/or inhibition of β-cell death is a promising strategy for anti-diabetic therapy. Yao and colleagues discovered that the small molecule, N-(2-benzoylphenyl)-5-bromo-2-thiophenecarboxamide (BBT), was effective in both potentiating GSIS and protecting β-cells from cytokine- or streptozotocin (STZ)-induced cell death. Further studies revealed the pathways involved, that BBT administration efficiently restored β-cell function, and decreased β-cell loss.
Read the full article at Yao et al. (2015) Journal of Endocrinology 224 327–341.
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