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      Autophagy and its link to type II diabetes mellitus

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          Abstract

          Autophagy, a double-edged sword for cell survival, is the research object on 2016 Nobel Prize in Physiology or Medicine. Autophagy is a molecular mechanism for maintaining cellular physiology and promoting survival. Defects in autophagy lead to the etiology of many diseases, including diabetes mellitus (DM), cancer, neurodegeneration, infection disease and aging. DM is a metabolic and chronic disorder and has a higher prevalence in the world as well as in Taiwan. The character of diabetes mellitus is hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance and failure of producing insulin on pancreatic beta cells. In T2DM, autophagy is not only providing nutrients to maintain cellular energy during fasting, but also removes damaged organelles, lipids and miss-folded proteins. In addition, autophagy plays an important role in pancreatic beta cell dysfunction and insulin resistance. In this review, we summarize the roles of autophagy in T2DM.

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          Most cited references201

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          Autophagy: renovation of cells and tissues.

          Autophagy is the major intracellular degradation system by which cytoplasmic materials are delivered to and degraded in the lysosome. However, the purpose of autophagy is not the simple elimination of materials, but instead, autophagy serves as a dynamic recycling system that produces new building blocks and energy for cellular renovation and homeostasis. Here we provide a multidisciplinary review of our current understanding of autophagy's role in metabolic adaptation, intracellular quality control, and renovation during development and differentiation. We also explore how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease. Copyright © 2011 Elsevier Inc. All rights reserved.
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            The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis.

            RIP1 and RIP3 kinases are central players in TNF-induced programmed necrosis. Here, we report that the RIP homotypic interaction motifs (RHIMs) of RIP1 and RIP3 mediate the assembly of heterodimeric filamentous structures. The fibrils exhibit classical characteristics of β-amyloids, as shown by Thioflavin T (ThT) and Congo red (CR) binding, circular dichroism, infrared spectroscopy, X-ray diffraction, and solid-state NMR. Structured amyloid cores are mapped in RIP1 and RIP3 that are flanked by regions of mobility. The endogenous RIP1/RIP3 complex isolated from necrotic cells binds ThT, is ultrastable, and has a fibrillar core structure, whereas necrosis is partially inhibited by ThT, CR, and another amyloid dye, HBX. Mutations in the RHIMs of RIP1 and RIP3 that are defective in the interaction compromise cluster formation, kinase activation, and programmed necrosis in vivo. The current study provides insight into the structural changes that occur when RIP kinases are triggered to execute different signaling outcomes and expands the realm of amyloids to complex formation and signaling. Copyright © 2012 Elsevier Inc. All rights reserved.
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              Cell Death Signaling.

              In multicellular organisms, cell death is a critical and active process that maintains tissue homeostasis and eliminates potentially harmful cells. There are three major types of morphologically distinct cell death: apoptosis (type I cell death), autophagic cell death (type II), and necrosis (type III). All three can be executed through distinct, and sometimes overlapping, signaling pathways that are engaged in response to specific stimuli. Apoptosis is triggered when cell-surface death receptors such as Fas are bound by their ligands (the extrinsic pathway) or when Bcl2-family proapoptotic proteins cause the permeabilization of the mitochondrial outer membrane (the intrinsic pathway). Both pathways converge on the activation of the caspase protease family, which is ultimately responsible for the dismantling of the cell. Autophagy defines a catabolic process in which parts of the cytosol and specific organelles are engulfed by a double-membrane structure, known as the autophagosome, and eventually degraded. Autophagy is mostly a survival mechanism; nevertheless, there are a few examples of autophagic cell death in which components of the autophagic signaling pathway actively promote cell death. Necrotic cell death is characterized by the rapid loss of plasma membrane integrity. This form of cell death can result from active signaling pathways, the best characterized of which is dependent on the activity of the protein kinase RIP3.
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                Author and article information

                Journal
                Biomedicine (Taipei)
                Biomedicine (Taipei)
                bmdcn
                BioMedicine
                EDP Sciences
                2211-8020
                2211-8039
                14 June 2017
                June 2017
                : 7
                : 2 ( publisher-idID: bmdcn/2017/02 )
                : 8
                Affiliations
                [1 ] Department of Medical Research, China Medical University Hospital, China Medical University Taichung 404 Taiwan
                [2 ] School of Pharmacy, China Medical University Taichung 404 Taiwan
                [3 ] Department of Biological Science and Technology, China Medical University Taichung 404 Taiwan
                [4 ] Genetics Center, Department of Medical Research, China Medical University Hospital Taichung 404 Taiwan
                [5 ] School of Chinese Medicine, China Medical University Taichung 404 Taiwan
                [6 ] Institute of Biomedical Sciences, National Sun Yat-sen University Kaohsiung 804 Taiwan
                [7 ] Department of Medical Genetics, China Medical University Hospital, China Medical University Taichung 404 Taiwan
                Author notes
                [†]

                These authors contributed equally to this work.

                [* ]Corresponding author. Department of Medical Research, China Medical University Hospital, China Medical University, No. 2, Yuh-Der Road, Taichung 404, Taiwan, E-mail address: d0704@ 123456mail.cmuh.org.tw (F.-J. Tsai).
                Article
                bmdcn2017070201 10.1051/bmdcn/2017070201
                10.1051/bmdcn/2017070201
                5479440
                28612706
                8035602a-2f8d-49ce-afb6-ffc1c46843ef
                © Author(s) 2017. This article is published with open access by China Medical University

                Open Access This article is distributed under terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided original author(s) and source are credited.

                History
                : 11 April 2017
                : 02 May 2017
                Page count
                Figures: 6, Tables: 4, Equations: 0, References: 191, Pages: 12
                Categories
                Review Article

                autophagy,type 2 diabetes mellitus (t2dm),pancreatic β-cells,insulin resistance

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