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. 2019 Nov 25;9:17451. doi: 10.1038/s41598-019-53826-7

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Long-term exposure of kisspeptin inhibits insulin secretion in NIT-1 cells. (a) NIT-1 cells were transfected with or without pcDNA3.1 + mKiss1-T2A-GFP plasmid, then fixed and stained with Hoechst 33342. Nucleus and GFP signal are shown in blue and green, respectively. The overlay of signals was processed by ImageJ. (b) Representative blots of GFP and mouse kisspeptin from transfected NIT-1 cells are shown. (c) Insulin secretion ability of control and transfected NIT-1 cells were determined by the amount of secreted luciferase under basal and glucose-stimulated condition. The relative luciferase activity was normalized by total protein in cell lysates. Data represent the means ± standard errors of the mean (n = 3). *Compared with the basal level in the control group; **p < 0.01; ^#Compared with glucose-induced level in the control group; ^##p < 0.01. The full-length blots are presented in Supplementary Fig. S1.