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      SREBP-regulated lipid metabolism: convergent physiology — divergent pathophysiology

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      Journal: Nature Reviews Endocrinology
      Publisher: Springer Nature

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          Abstract

          In addition to controlling cellular lipid metabolism and homeostasis, sterol regulatory element-binding proteins (SREBPs) act as nodes of convergence and divergence within myriad physiological and pathophysiological processes. Here, Shimano and Sato provide a comprehensive overview of the role of SREBPs in health and disease, at the cell, organ and organism levels.

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          On the origin of cancer cells.

          O WARBURG (1956)
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            Pancreatic β cell dedifferentiation as a mechanism of diabetic β cell failure.

            Chutima Talchai, Shouhong Xuan, Hua V. Lin … (2012)
            Diabetes is associated with β cell failure. But it remains unclear whether the latter results from reduced β cell number or function. FoxO1 integrates β cell proliferation with adaptive β cell function. We interrogated the contribution of these two processes to β cell dysfunction, using mice lacking FoxO1 in β cells. FoxO1 ablation caused hyperglycemia with reduced β cell mass following physiologic stress, such as multiparity and aging. Surprisingly, lineage-tracing experiments demonstrated that loss of β cell mass was due to β cell dedifferentiation, not death. Dedifferentiated β cells reverted to progenitor-like cells expressing Neurogenin3, Oct4, Nanog, and L-Myc. A subset of FoxO1-deficient β cells adopted the α cell fate, resulting in hyperglucagonemia. Strikingly, we identify the same sequence of events as a feature of different models of murine diabetes. We propose that dedifferentiation trumps endocrine cell death in the natural history of β cell failure and suggest that treatment of β cell dysfunction should restore differentiation, rather than promoting β cell replication. Copyright © 2012 Elsevier Inc. All rights reserved.
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              ER stress induces cleavage of membrane-bound ATF6 by the same proteases that process SREBPs.

              Jin Ye, Robert Rawson, Ryutaro Komuro … (2000)
              ATF6 is a membrane-bound transcription factor that activates genes in the endoplasmic reticulum (ER) stress response. When unfolded proteins accumulate in the ER, ATF6 is cleaved to release its cytoplasmic domain, which enters the nucleus. Here, we show that ATF6 is processed by Site-1 protease (S1P) and Site-2 protease (S2P), the enzymes that process SREBPs in response to cholesterol deprivation. ATF6 processing was blocked completely in cells lacking S2P and partially in cells lacking S1P. ATF6 processing required the RxxL and asparagine/proline motifs, known requirements for S1P and S2P processing, respectively. Cells lacking S2P failed to induce GRP78, an ATF6 target, in response to ER stress. ATF6 processing did not require SCAP, which is essential for SREBP processing. We conclude that S1P and S2P are required for the ER stress response as well as for lipid synthesis.
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                Author and article information

                Journal
                Title: Nature Reviews Endocrinology
                Abbreviated Title: Nat Rev Endocrinol
                Publisher: Springer Nature
                ISSN (Print): 1759-5029
                ISSN (Electronic): 1759-5037
                Publication date Created: August 29 2017
                Publication date (Print): August 29 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrendo.2017.91
                PubMed ID: 28849786
                SO-VID: 71c951b6-e3db-4843-9c83-41cd29b9c3cf
                Copyright © © 2017
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