Volume 52 Issue 1
Jan.  2021
Turn off MathJax
Article Contents
YUAN Ke-fei, SHI Jia-yan, PENG Li-yuan, et al. A Review of Progress of the Relation Between Stress Response and Diabetes Mellitus[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCE EDITION), 2021, 52(1): 64-69. doi: 10.12182/20210160103
Citation: YUAN Ke-fei, SHI Jia-yan, PENG Li-yuan, et al. A Review of Progress of the Relation Between Stress Response and Diabetes Mellitus[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCE EDITION), 2021, 52(1): 64-69. doi: 10.12182/20210160103

A Review of Progress of the Relation Between Stress Response and Diabetes Mellitus

doi: 10.12182/20210160103
More Information
  • Corresponding author: E-mail:zhangyy@scu.edu.cn
  • Received Date: 2020-11-11
  • Rev Recd Date: 2020-12-30
  • Publish Date: 2021-01-20
  • Stress response is an adaptive process of the organism to confront environmental perturbation. Moderate stress response induces the organism to establish effective adaptive strategies for survival, while excessive stress response results in stress injury, which is a major cause of a variety of physical or psychological diseases, including diabetes mellitus. Diabetes mellitus is a typical stress-related disease, with numerous evidence indicating that the development and progression of diabetes mellitus are closely related to stress response, such as metabolic stress, oxidative stress and endoplasmic reticulum stress. However, the detailed mechanisms of stress response mediated regulation of diabetes mellitus and how to prevent or treat diabetes mellitus via modification of stress response remain to be further investigated. Here, we will introduce the definition and regulatory mechanisms of stress response, as well as discuss the biological functions and mechanisms of various stress responses during the pathogenesis of diabetes mellitus. This review highlights recent advances of stress medicine associated with diabetes mellitus, in order to provide theoretical basis and reference for prevention and treatment of diabetes mellitus. Future studies should focus on elucidating the clinical application potential of the key factors of stress response that mediate the pathogenesis of diabetes mellitus, as well as boosting the related translational medicine studies.
  • loading
  • [1]
    RUSSELL G, LIGHTMAN S. The human stress response. Nat Rev Endocrinol,2019,15(9): 525–534. doi: 10.1038/s41574-019-0228-0
    FAN W. Epidemiology in diabetes mellitus and cardiovascular disease. Cardiovasc Endocrinol,2017,6(1): 8–16. doi: 10.1097/XCE.0000000000000116
    American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care,2014,37(Suppl 1): S81–S90.
    SZABLEWSKI L. Glucose transporters in healthy heart and in cardiac disease. Int J Cardiol,2017,230: 70–75. doi: 10.1016/j.ijcard.2016.12.083
    ZHANG Y, SOWERS J R, REN J. Targeting autophagy in obesity: from pathophysiology to management. Nat Rev Endocrinol,2018,14(6): 356–376. doi: 10.1038/s41574-018-0009-1
    WELLEN K E, THOMPSON C B. Cellular metabolic stress: considering how cells respond to nutrient excess. Mol Cell,2010,40(2): 323–332. doi: 10.1016/j.molcel.2010.10.004
    WANG Y, HU H, YIN J, et al. TLR4 participates in sympathetic hyperactivity post-MI in the PVN by regulating NF-κB pathway and ROS production. Redox Biol, 2019, 24: 101186[2020-12-28]. https://doi.org/10.1016/j.redox.2019.101186.
    LIN L, CAO L, LIU Y, et al. B7-H3 promotes multiple myeloma cell survival and proliferation by ROS-dependent activation of Src/STAT3 and c-Cbl-mediated degradation of SOCS3. Leukemia,2019,33(6): 1475–1486. doi: 10.1038/s41375-018-0331-6
    ZHANG Y, QU Y, LIN Y, et al. Enoyl-CoA hydratase-1 regulates mTOR signaling and apoptosis by sensing nutrients. Nat Commun, 2017, 8(1): 464[2020-12-28]. https://www.nature.com/articles/s41467-017-00489-5. doi: 10.1038/s41467-017-00489-5.
    WANG T, CAO Y, ZHENG Q, et al. SENP1-SIRT3 signaling controls mitochondrial protein acetylation and metabolism. Mol Cell,2019,75(4): 823–834. doi: 10.1016/j.molcel.2019.06.008
    CHIO I I C, TUVESON D A. ROS in cancer: the burning question. Trends Mol Med,2017,23(5): 411–429. doi: 10.1016/j.molmed.2017.03.004
    HAYES J D, DINKOVA-KOSTOVA A T, TEW K D. Oxidative stress in cancer. Cancer Cell,2020,38(2): 167–197. doi: 10.1016/j.ccell.2020.06.001
    SCHMIDLIN C J, DODSON M B, MADHAVAN L, et al. Redox regulation by NRF2 in aging and disease. Free Radic Biol Med,2019,134: 702–707. doi: 10.1016/j.freeradbiomed.2019.01.016
    KLOTZ L O, STEINBRENNER H. Cellular adaptation to xenobiotics: interplay between xenosensors, reactive oxygen species and FOXO transcription factors. Redox Biol,2017,13: 646–654. doi: 10.1016/j.redox.2017.07.015
    SONG M, CUBILLOS-RUIZ J R. Endoplasmic reticulum stress responses in intratumoral immune cells: implications for cancer immunotherapy. Trends Immunol,2019,40(2): 128–141. doi: 10.1016/j.it.2018.12.001
    FRAKES A E, DILLIN A. The UPRER: sensor and coordinator of organismal homeostasis. Mol Cell,2017,66(6): 761–771. doi: 10.1016/j.molcel.2017.05.031
    CAKIR I, NILLNI E A. Endoplasmic reticulum stress, the hypothalamus, and energy balance. Trends Endocrinol Metab,2019,30(3): 163–176. doi: 10.1016/j.tem.2019.01.002
    WANG M, KAUFMAN R J. Protein misfolding in the endoplasmic reticulum as a conduit to human disease. Nature,2016,529(7586): 326–335. doi: 10.1038/nature17041
    RUEGSEGGER G N, CREO A L, CORTES T M, et al. Altered mitochondrial function in insulin-deficient and insulin-resistant states. J Clin Invest,2018,128(9): 3671–3681. doi: 10.1172/JCI120843
    HOTAMISLIGIL G S. Inflammation, metaflammation and immunometabolic disorders. Nature,2017,542(7640): 177–185. doi: 10.1038/nature21363
    CHOUCHANI E T, KAZAK L, JEDRYCHOWSKI M P, et al. Mitochondrial ROS regulate thermogenic energy expenditure and sulfenylation of UCP1. Nature,2016,532(7597): 112–116. doi: 10.1038/nature17399
    FAKHRUDDIN S, ALANAZI W, JACKSON K E. Diabetes-induced reactive oxygen species: mechanism of their generation and role in renal injury. J Diabetes Res, 2017, 2017: 8379327[2020-12-28]. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5253173/. doi: 10.1155/2017/8379327.
    NOLAN C J, RUDERMAN N B, KAHN S E, et al. Insulin resistance as a physiological defense against metabolic stress: implications for the management of subsets of type 2 diabetes. Diabetes,2015,64(3): 673–686. doi: 10.2337/db14-0694
    USSHER J R, CAMPBELL J E, MULVIHILL E E, et al. Inactivation of the glucose-dependent insulinotropic polypeptide receptor improves outcomes following experimental myocardial infarction. Cell Metab,2018,27(2): 450–460. doi: 10.1016/j.cmet.2017.11.003
    JAIS A, SOLAS M, BACKES H, et al. Myeloid-cell-derived VEGF maintains brain glucose uptake and limits cognitive impairment in obesity. Cell,2016,165(4): 882–895. doi: 10.1016/j.cell.2016.03.033
    KENNY H C, ABEL E D. Heart failure in type 2 diabetes mellitus. Circ Res,2019,124(1): 121–141. doi: 10.1161/CIRCRESAHA.118.311371
    LEVASSEUR E M, YAMADA K, PIÑEROS A R, et al. Hypusine biosynthesis in β cells links polyamine metabolism to facultative cellular proliferation to maintain glucose homeostasis. Sci Signal, 2019, 12(610): eaax0715[2020-12-28]. https://stke.sciencemag.org/content/12/610/eaax0715.long. doi: 10.1126/scisignal.aax0715.
    WEIR G C. Glucolipotoxicity, β-cells, and diabetes: the emperor has no clothes. Diabetes,2020,69(3): 273–278. doi: 10.2337/db19-0138
    GERBER P A, RUTTER G A. The role of oxidative stress and hypoxia in pancreatic beta-cell dysfunction in diabetes mellitus. Antioxid Redox Signal,2017,26(10): 501–518. doi: 10.1089/ars.2016.6755
    LEE Y S, WOLLAM J, OLEFSKY J M. An integrated view of immunometabolism. Cell,2018,172(1/2): 22–40. doi: 10.1016/j.cell.2017.12.025
    KLEINER S, GOMEZ D, MEGRA B, et al. Mice harboring the human SLC30A8 R138X loss-of-function mutation have increased insulin secretory capacity. Proc Natl Acad Sci U S A,2018,115(32): E7642–E7649. doi: 10.1073/pnas.1721418115
    POCIOT F, LERNMARK Å. Genetic risk factors for type 1 diabetes. Lancet,2016,387(10035): 2331–2339. doi: 10.1016/S0140-6736(16)30582-7
    CATRYSSE L, VAN LOO G. Inflammation and the metabolic syndrome: the tissue-specific functions of NF-κB. Trends Cell Biol,2017,27(6): 417–429. doi: 10.1016/j.tcb.2017.01.006
    KITADA M, OGURA Y, MONNO I, et al. Sirtuins and type 2 diabetes: role in inflammation, oxidative stress, and mitochondrial function. Front Endocrinol, 2019, 10: 187[2020-12-28]. https://doi.org/10.3389/fendo.2019.00187.
    STUART C A, HOWELL M E, CARTWRIGHT B M, et al. Insulin resistance and muscle insulin receptor substrate‐1 serine hyperphosphorylation. Physiol Rev, 2014, 2(12): e12236[2020-12-28]. https://doi.org/10.14814/phy2.12236.
    PETERSEN M C, SHULMAN G I. Mechanisms of insulin action and insulin resistance. Physiol Rev,2018,98(4): 2133–2223. doi: 10.1152/physrev.00063.2017
    YANG J D, HAINAUT P, GORES G J, et al. A global view of hepatocellular carcinoma: trends, risk, prevention and management. Nat Rev Gastroenterol Hepatol,2019,16(10): 589–604. doi: 10.1038/s41575-019-0186-y
    KAHN C R, WANG G, LEE K Y. Altered adipose tissue and adipocyte function in the pathogenesis of metabolic syndrome. J Clin Invest,2019,129(10): 3990–4000. doi: 10.1172/JCI129187
    REILLY S M, SALTIEL A R. Adapting to obesity with adipose tissue inflammation. Nat Rev Endocrinol,2017,13(11): 633–643. doi: 10.1038/nrendo.2017.90
    ZHANG Y, KIM M S, JIA B, et al. Hypothalamic stem cells control ageing speed partly through exosomal miRNAs. Nature,2017,548(7665): 52–57. doi: 10.1038/nature23282
    SONG M, SANDOVAL T A, CHAE C S, et al. IRE1α–XBP1 controls T cell function in ovarian cancer by regulating mitochondrial activity. Nature,2018,562(7727): 423–428. doi: 10.1038/s41586-018-0597-x
    OLZMANN J A, CARVALHO P. Dynamics and functions of lipid droplets. Nat Rev Mol Cell Biol,2019,20(3): 137–155. doi: 10.1038/s41580-018-0085-z
    CUBILLOS-RUIZ J R, BETTIGOLE S E, GLIMCHER L H. Tumorigenic and immunosuppressive effects of endoplasmic reticulum stress in cancer. Cell,2017,168(4): 692–706. doi: 10.1016/j.cell.2016.12.004
    HETZ C, PAPA F R. The unfolded protein response and cell fate control. Mol Cell,2018,69(2): 169–181. doi: 10.1016/j.molcel.2017.06.017
    LEBEAUPIN C, VALLÉE D, HAZARI Y, et al. Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. J Hepatol,2018,69(4): 927–947. doi: 10.1016/j.jhep.2018.06.008
    CHEN S, HENDERSON A, PETRIELLO M C, et al. Trimethylamine N-oxide binds and activates PERK to promote metabolic dysfunction. Cell Metab, 2019, 30(6): 1141-1151. e5[2020-12-28]. https://doi.org/10.1016/j.cmet.2019.08.021.
    MEEX R C R, WATT M J. Hepatokines: linking nonalcoholic fatty liver disease and insulin resistance. Nat Rev Endocrinol,2017,13(9): 509–520. doi: 10.1038/nrendo.2017.56
    LI W, ZHU J, DOU J, et al. Phosphorylation of LAMP2A by p38 MAPK couples ER stress to chaperone-mediated autophagy. Nat Commun,2017,8(1): 1–14. doi: 10.1038/s41467-016-0009-6
    FUMAGALLI F, NOACK J, BERGMANN T J, et al. Translocon component Sec62 acts in endoplasmic reticulum turnover during stress recovery. Nat Cell Biol,2016,18(11): 1173–1184. doi: 10.1038/ncb3423
  • 加载中


    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索
    Article views (753) PDF downloads(58) Cited by()
    Proportional views


    DownLoad:  Full-Size Img  PowerPoint