Current protein & peptide science · 2024
A Novel Peptide COX52-69 Inhibits High Glucose-induced Insulin Secretion by Modulating BK Channel Activity.
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Lin Qian, Liu Jingtao, Chen Hengling, Hu Wenwu, Lei Weiqiong, Wang Meijie, Lin Xianguang, Zhang Yongning, Ai Huiting, Chen Su, Li Chenhong
Аннотация
BACKGROUND: Excessive insulin is the leading cause of metabolic syndromes besides hyperinsulinemia. Insulin-lowering therapeutic peptides have been poorly studied and warrant urgent attention.
OBJECTIVES: The main purpose of this study, was to introduce a novel peptide COX52-69 that was initially isolated from the porcine small intestine and possessed the ability to inhibit insulin secretion under high-glucose conditions by modulating large conductance Ca2+-activated K+ channels (BK channels) activity.
METHODS AND RESULTS: Enzyme-linked immunosorbent assay results indicate that COX52-69 supressed insulin release induced by high glucose levels in pancreatic islets and animal models. Furthermore, electrophysiological data demonstrated that COX52-69 can increase BK channel currents and hyperpolarize cell membranes. Thus, cell excitability decreased, corresponding to a reduction in insulin secretion.
CONCLUSION: Our study provides a novel approach to modulate high glucose-stimulated insulin secretion in patients with hyperinsulinemia.
OBJECTIVES: The main purpose of this study, was to introduce a novel peptide COX52-69 that was initially isolated from the porcine small intestine and possessed the ability to inhibit insulin secretion under high-glucose conditions by modulating large conductance Ca2+-activated K+ channels (BK channels) activity.
METHODS AND RESULTS: Enzyme-linked immunosorbent assay results indicate that COX52-69 supressed insulin release induced by high glucose levels in pancreatic islets and animal models. Furthermore, electrophysiological data demonstrated that COX52-69 can increase BK channel currents and hyperpolarize cell membranes. Thus, cell excitability decreased, corresponding to a reduction in insulin secretion.
CONCLUSION: Our study provides a novel approach to modulate high glucose-stimulated insulin secretion in patients with hyperinsulinemia.