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Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways

Vaspin (visceral adipose tissue-derived serine protease inhibitor) is a recently discovered adipokine that has been implicated in diabetes mellitus and other metabolic disorders. However, the effects of vaspin on pancreatic β cell function and related mechanisms are not fully understood. Thus, the p...

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Detalles Bibliográficos
Autores principales: Liu, Shiwei, Li, Xin, Wu, Yaru, Duan, Ruixue, Zhang, Jiaxin, Du, Fang, Zhang, Qi, Li, Yuanbin, Li, Naishi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5730172/
https://www.ncbi.nlm.nih.gov/pubmed/29240812
http://dx.doi.org/10.1371/journal.pone.0189722
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author Liu, Shiwei
Li, Xin
Wu, Yaru
Duan, Ruixue
Zhang, Jiaxin
Du, Fang
Zhang, Qi
Li, Yuanbin
Li, Naishi
author_facet Liu, Shiwei
Li, Xin
Wu, Yaru
Duan, Ruixue
Zhang, Jiaxin
Du, Fang
Zhang, Qi
Li, Yuanbin
Li, Naishi
author_sort Liu, Shiwei
collection PubMed
description Vaspin (visceral adipose tissue-derived serine protease inhibitor) is a recently discovered adipokine that has been implicated in diabetes mellitus and other metabolic disorders. However, the effects of vaspin on pancreatic β cell function and related mechanisms are not fully understood. Thus, the present study was performed to investigate the effects of vaspin on pancreatic β cell function and the potential underlying mechanisms. Both in vitro (rat insulinoma cells, INS-1) and in vivo (high fat diet fed rats) experiments were conducted. The results showed that vaspin significantly increased INS-1 cell secretory function. Potential mechanisms were explored using inhibitors, western blot and real-time PCR techniques. We found that vaspin increased the levels of IRS-2 mRNA and IRS-2 total protein, while decreased the serine phosphorylation level of IRS-2 protein. Moreover, vaspin increased the Akt phosphorylation protein level which was reversed by PI3K inhibitor ly294002. In addition, vaspin increased the phosphorylation levels of mTOR and p70S6K, which was inhibited by rapamycin. Meanwhile, we found that the NF-κB mRNA and protein levels were reduced after vaspin treatment, similar to the effect of NF-κB inhibitor TPCK. Furthermore, vaspin increased the glucose stimulated insulin secretion (GSIS) level, lowered blood glucose level and improved the glucose tolerance and insulin sensitivity of high fat diet fed rats. Hyperglycemic clamp test manifested that vaspin improved islet β cell function. Together, these findings provide a new understanding of the function of vaspin on pancreatic β cell and suggest that it may serve as a potential agent for the prevention and treatment of type 2 diabetes.
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spelling pubmed-57301722017-12-22 Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways Liu, Shiwei Li, Xin Wu, Yaru Duan, Ruixue Zhang, Jiaxin Du, Fang Zhang, Qi Li, Yuanbin Li, Naishi PLoS One Research Article Vaspin (visceral adipose tissue-derived serine protease inhibitor) is a recently discovered adipokine that has been implicated in diabetes mellitus and other metabolic disorders. However, the effects of vaspin on pancreatic β cell function and related mechanisms are not fully understood. Thus, the present study was performed to investigate the effects of vaspin on pancreatic β cell function and the potential underlying mechanisms. Both in vitro (rat insulinoma cells, INS-1) and in vivo (high fat diet fed rats) experiments were conducted. The results showed that vaspin significantly increased INS-1 cell secretory function. Potential mechanisms were explored using inhibitors, western blot and real-time PCR techniques. We found that vaspin increased the levels of IRS-2 mRNA and IRS-2 total protein, while decreased the serine phosphorylation level of IRS-2 protein. Moreover, vaspin increased the Akt phosphorylation protein level which was reversed by PI3K inhibitor ly294002. In addition, vaspin increased the phosphorylation levels of mTOR and p70S6K, which was inhibited by rapamycin. Meanwhile, we found that the NF-κB mRNA and protein levels were reduced after vaspin treatment, similar to the effect of NF-κB inhibitor TPCK. Furthermore, vaspin increased the glucose stimulated insulin secretion (GSIS) level, lowered blood glucose level and improved the glucose tolerance and insulin sensitivity of high fat diet fed rats. Hyperglycemic clamp test manifested that vaspin improved islet β cell function. Together, these findings provide a new understanding of the function of vaspin on pancreatic β cell and suggest that it may serve as a potential agent for the prevention and treatment of type 2 diabetes. Public Library of Science 2017-12-14 /pmc/articles/PMC5730172/ /pubmed/29240812 http://dx.doi.org/10.1371/journal.pone.0189722 Text en © 2017 Liu et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Liu, Shiwei
Li, Xin
Wu, Yaru
Duan, Ruixue
Zhang, Jiaxin
Du, Fang
Zhang, Qi
Li, Yuanbin
Li, Naishi
Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways
title Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways
title_full Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways
title_fullStr Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways
title_full_unstemmed Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways
title_short Effects of vaspin on pancreatic β cell secretion via PI3K/Akt and NF-κB signaling pathways
title_sort effects of vaspin on pancreatic β cell secretion via pi3k/akt and nf-κb signaling pathways
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5730172/
https://www.ncbi.nlm.nih.gov/pubmed/29240812
http://dx.doi.org/10.1371/journal.pone.0189722
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