IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function

Type 2 diabetes is associated with islet amyloid deposits derived from islet amyloid polypeptide (IAPP) expressed by β-cells. Here the authors show that IAPP misfolded protein stress induces the hypoxia inducible factor 1 alpha injury repair pathway and activates survival metabolic changes mediated...

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Main Authors:	Chiara Montemurro, Hiroshi Nomoto, Lina Pei, Vishal S. Parekh, Kenny E. Vongbunyong, Suryakiran Vadrevu, Tatyana Gurlo, Alexandra E. Butler, Rohan Subramaniam, Eleni Ritou, Orian S. Shirihai, Leslie S. Satin, Peter C. Butler, Slavica Tudzarova
Format:	Article
Language:	English
Published:	Nature Publishing Group 2019-06-01
Series:	Nature Communications
Online Access:	https://doi.org/10.1038/s41467-019-10444-1

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spelling	doaj-386002cb2bd14399b8b10d3e7c881ca52021-05-11T11:33:50ZengNature Publishing GroupNature Communications2041-17232019-06-0110111710.1038/s41467-019-10444-1IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell functionChiara Montemurro0Hiroshi Nomoto1Lina Pei2Vishal S. Parekh3Kenny E. Vongbunyong4Suryakiran Vadrevu5Tatyana Gurlo6Alexandra E. Butler7Rohan Subramaniam8Eleni Ritou9Orian S. Shirihai10Leslie S. Satin11Peter C. Butler12Slavica Tudzarova13Larry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesDepartment of Pharmacology and Brehm Diabetes Research Center, University of MichiganLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesDepartment of Pharmacology and Brehm Diabetes Research Center, University of MichiganLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesDivision of Endocrinology, Department of Medicine, David Geffen School of Medicine, University of California, Los AngelesDivision of Endocrinology, Department of Medicine, David Geffen School of Medicine, University of California, Los AngelesDepartment of Pharmacology and Brehm Diabetes Research Center, University of MichiganLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los AngelesType 2 diabetes is associated with islet amyloid deposits derived from islet amyloid polypeptide (IAPP) expressed by β-cells. Here the authors show that IAPP misfolded protein stress induces the hypoxia inducible factor 1 alpha injury repair pathway and activates survival metabolic changes mediated by PFKFB3.https://doi.org/10.1038/s41467-019-10444-1
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Chiara Montemurro Hiroshi Nomoto Lina Pei Vishal S. Parekh Kenny E. Vongbunyong Suryakiran Vadrevu Tatyana Gurlo Alexandra E. Butler Rohan Subramaniam Eleni Ritou Orian S. Shirihai Leslie S. Satin Peter C. Butler Slavica Tudzarova
spellingShingle	Chiara Montemurro Hiroshi Nomoto Lina Pei Vishal S. Parekh Kenny E. Vongbunyong Suryakiran Vadrevu Tatyana Gurlo Alexandra E. Butler Rohan Subramaniam Eleni Ritou Orian S. Shirihai Leslie S. Satin Peter C. Butler Slavica Tudzarova IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function Nature Communications
author_facet	Chiara Montemurro Hiroshi Nomoto Lina Pei Vishal S. Parekh Kenny E. Vongbunyong Suryakiran Vadrevu Tatyana Gurlo Alexandra E. Butler Rohan Subramaniam Eleni Ritou Orian S. Shirihai Leslie S. Satin Peter C. Butler Slavica Tudzarova
author_sort	Chiara Montemurro
title	IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function
title_short	IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function
title_full	IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function
title_fullStr	IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function
title_full_unstemmed	IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function
title_sort	iapp toxicity activates hif1α/pfkfb3 signaling delaying β-cell loss at the expense of β-cell function
publisher	Nature Publishing Group
series	Nature Communications
issn	2041-1723
publishDate	2019-06-01
description	Type 2 diabetes is associated with islet amyloid deposits derived from islet amyloid polypeptide (IAPP) expressed by β-cells. Here the authors show that IAPP misfolded protein stress induces the hypoxia inducible factor 1 alpha injury repair pathway and activates survival metabolic changes mediated by PFKFB3.
url	https://doi.org/10.1038/s41467-019-10444-1
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IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function

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