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  • Author: Ronald Gonzalez x
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Ronald Gonzalez Laboratory of Integrative Neuroendocrinology, Department of Biology, School of Kinesiology and Health Sciences, York University, 4700 Keele Street, Toronto, Ontario, Canada M3J 1P3

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Benjamin K Reingold Laboratory of Integrative Neuroendocrinology, Department of Biology, School of Kinesiology and Health Sciences, York University, 4700 Keele Street, Toronto, Ontario, Canada M3J 1P3

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Xiaodong Gao Laboratory of Integrative Neuroendocrinology, Department of Biology, School of Kinesiology and Health Sciences, York University, 4700 Keele Street, Toronto, Ontario, Canada M3J 1P3

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Mandeep P Gaidhu Laboratory of Integrative Neuroendocrinology, Department of Biology, School of Kinesiology and Health Sciences, York University, 4700 Keele Street, Toronto, Ontario, Canada M3J 1P3

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Robert G Tsushima Laboratory of Integrative Neuroendocrinology, Department of Biology, School of Kinesiology and Health Sciences, York University, 4700 Keele Street, Toronto, Ontario, Canada M3J 1P3

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Suraj Unniappan Laboratory of Integrative Neuroendocrinology, Department of Biology, School of Kinesiology and Health Sciences, York University, 4700 Keele Street, Toronto, Ontario, Canada M3J 1P3

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Nesfatin-1 is a recently discovered multifunctional metabolic hormone abundantly expressed in the pancreatic islets. The main objective of this study is to characterize the direct effects of nesfatin-1 on insulin secretion in vitro using MIN6 cells and islets isolated from C57BL/6 mice. We also examined the expression of the nesfatin-1 precursor protein, nucleobindin 2 (NUCB2) mRNA, and nesfatin-1 immunoreactivity (ir) in the islets of normal mice and in the islets from mice with streptozotocin-induced type 1 diabetes and diet-induced obese (DIO) mice with type 2 diabetes. Nesfatin-1 stimulated glucose-induced insulin release in vitro from mouse islets and MIN6 cells in a dose-dependent manner. No such stimulation in insulin secretion was found when MIN6 cells/islets were incubated with nesfatin-1 in low glucose. In addition, a fourfold increase in nesfatin-1 release from MIN6 cells was observed following incubation in high glucose (16.7 mM) compared to low glucose (2 mM). Furthermore, we observed a significant reduction in both NUCB2 mRNA expression and nesfatin-1-ir in the pancreatic islets of mice with type 1 diabetes, while a significant increase was observed in the islets of DIO mice. Together, our findings indicate that nesfatin-1 is a novel insulinotropic peptide and that the endogenous pancreatic islet NUCB2/nesfatin is altered in diabetes and diet-induced obesity.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-10-0492
Volume/Issue:
Volume 208: Issue 3
Free access