Insulin resistance in the ХХІ century: multimodal approach to assessing causes and effective correction
DOI:
https://doi.org/10.18370/2309-4117.2021.62.97-103Keywords:
insulin resistance, metabolic syndrome, melatonin, vitamin D, proinsulin, chronorhythms, biorhythmsAbstract
In a broad sense, insulin resistance (IR) is the impairment of the biological response of target tissues to insulin stimulation. IR plays a leading role in the development of metabolic syndrome, the global prevalence of which continues to grow, despite the significant efforts of medical systems. The multicomponent nature of metabolic syndrome implies its complex and heterogeneous pathogenesis, knowledge about which is annually updated with new details as a result of scientific research.
This review systematizes the results of recent studies on risk factors and pathogenetic links in the development of IR, prospects and existing experience of using these data in clinical practice with an emphasis on assessing the level of melatonin and vitamin D. The issue of timely and reliable laboratory confirmation of IR is relevant not only for endocrinologists, but also for specialists in almost all areas. In clinical use apart from indirect methods of IR-assessment like HOMA-IR, there is an informative test intact proinsulin.
Recently, the increasing attention of researchers is attracted by such factors of the development of IR as vitamin D deficiency and disturbances in chrono- and biorhythms. Today, their role in the pathogenesis of IR can be considered proven, which makes it possible to consider vitamin D and melatonin as therapeutic agents in an integrated approach to the prevention and correction of IR. Statistical analysis of the research results of the “DILA” Medical Laboratory and clinical data provided by the Department of Endocrinology of the O.O. Bogomolets National Medical University also showed an association of vitamin D and melatonin levels with IR.
Thus, a review of scientific sources over the last 5 years clearly demonstrates the growing urgency of the problem of IR and metabolic syndrome, the need to reconsider their management from assessing traditional etiopathogenetic factors (alimentary) to taking into account the maximum spectrum of genetic aspects and exogenous impacts. An important place among the latter belongs to an objective assessment of the vitamin D and melatonin levels for adequate pharmacological correction.
References
- World Health Organization. “The top 10 causes of death.” Available from: [https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death], accessed Dec. 02, 2021.
- Centers for Disease Control and Prevention. “FastStats – Leading Causes of Death.” Available from: [https://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm], accessed Dec. 02, 2021.
- Nsiah, K., Shang, V.O., Boateng, K.A., Mensah, F. “Prevalence of metabolic syndrome in type 2 diabetes mellitus patients.” Int J Appl Basic Med Res 5.2 (2015): 133. DOI: 10.4103/2229-516X.157170
- Gathirua-Mwangi, W.G., Monahan, P.O., Murage, M.J., Zhang, J. “Metabolic syndrome and total cancer mortality in the Third National Health and Nutrition Examination Survey.” Cancer Causes Control 28.2 (2017): 127–36. DOI: 10.1007/S10552-016-0843-1
- Tune, J.D., Goodwill, A.G., Sassoon, D.J., Mather, K.J. “Cardiovascular consequences of metabolic syndrome.” Transl Res 183 (2017): 57–70. DOI: 10.1016/J.TRSL.2017.01.001
- Albitar, O., Ballouze, R., Ooi, J.P., Sheikh Ghadzi, S.M. “Risk factors for mortality among COVID-19 patients.” Diabetes Res Clin Pract 166 (2020): 108293. DOI: 10.1016/J.DIABRES.2020.108293
- Marhl, M., Grubelnik, V., Magdič, M., Markovič, R. “Diabetes and metabolic syndrome as risk factors for COVID-19.” Diabetes Metab Syndr Clin Res Rev 14.4 (2020): 671–7. DOI: 10.1016/J.DSX.2020.05.013
- Martinez-Ferran, M., de la Guía-Galipienso, F., Sanchis-Gomar, F., Pareja-Galeano, H. “Metabolic Impacts of Confinement during the COVID-19 Pandemic Due to Modified Diet and Physical Activity Habits.” Nutr 12.6 (2020): 1549. DOI: 10.3390/NU12061549
- Alberti, K.G.M.M., et al. “Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.” Circulation 120.16 (2009): 1640–5. DOI: 10.1161/CIRCULATIONAHA.109.192644
- Zimmet, P., Magliano, D., Matsuzawa, Y., et al. “The Metabolic Syndrome: A Global Public Health Problem and A New Definition.” J Atheroscler Thromb 12.6 (2005): 295–300. DOI: 10.5551/JAT.12.295
- Go, A.S., et al. “Executive summary: heart disease and stroke statistics – 2013 update: a report from the American Heart Association.” Circulation 127.1 (2013): 143–52. DOI: 10.1161/CIR.0B013E318282AB8F
- Alexander, C.M., Landsman, P.B., Teutsch, S.M., Haffner, S.M. “NCEP-Defined Metabolic Syndrome, Diabetes, and Prevalence of Coronary Heart Disease Among NHANES III Participants Age 50 Years and Older.” Diabetes 52.5 (2003): 1210–4. DOI: 10.2337/DIABETES.52.5.1210
- Eckel, R.H., Grundy, S.M., Zimmet, P.Z. “The metabolic syndrome.” Lancet (London, England) 365.9468 (2005): 1415–28. DOI: 10.1016/S0140-6736(05)66378-7
- Desroches, S., Lamarche, B. “The evolving definitions and increasing prevalence of the metabolic syndrome.” Appl Physiol Nutr Metab 32.1 (2007): 23–32. DOI: 10.1139/h06-095
- Roomi, M.A., Mohammadnezhad, M. “Prevalence of Metabolic Syndrome Among Apparently Healthy Workforce.” J Ayub Med Coll Abbottabad 31.2 (2019): 252–4. Available from: [https://europepmc.org/article/med/31094127], accessed Dec. 03, 2021.
- Fazleen, N.E., Whittaker, M., Mamun, A. “Risk of metabolic syndrome in adolescents with polycystic ovarian syndrome: A systematic review and meta-analysis.” Diabetes Metab Syndr Clin Res Rev 12.6 (2018): 1083–90. DOI: 10.1016/J.DSX.2018.03.014
- Nolan, P.B., Carrick-Ranson, G., Stinear, J.W., et al. “Prevalence of metabolic syndrome and metabolic syndrome components in young adults: A pooled analysis.” Prev Med Reports 7 (2017): 211–5. DOI: 10.1016/J.PMEDR.2017.07.004
- Petersen, M.C., Shulman, G.I. “Mechanisms of insulin action and insulin resistance.” Physiol Rev 98.4 (2018): 2133–223. DOI: 10.1152/physrev.00063.2017
- Wang, C.H., Wei, Y.H. “Role of mitochondrial dysfunction and dysregulation of Ca2+ homeostasis in the pathophysiology of insulin resistance and type 2 diabetes.” J Biomed Sci 24.1 (2017): 1–11. DOI: 10.1186/s12929-017-0375-3
- Pinti, M.V., Fink, G.K., Hathaway, Q.A., et al. “Mitochondrial dysfunction in type 2 diabetes mellitus: An organ-based analysis.” Am J Physiol Endocrinol Metab 316.2 (2019): E268–85. DOI: 10.1152/ajpendo.00314.2018
- Yaribeygi, H., Farrokhi, F.R., Butler, A.E, Sahebkar, A. “Insulin resistance: Review of the underlying molecular mechanisms.” J Cell Physiol 234.6 (2019): 8152–61. DOI: 10.1002/JCP.27603
- Chernyaeva, A.О., et al. “State of glucose homeostasis in women with type 2 diabetes mellitus with hyperuricemia.” Problems of endocrine pathology 4 (2019): 103–9. DOI: 10.21856/j-PEP.2019.4.14
- Fonseca, V.A. “Defining and Characterizing the Progression of Type 2 Diabetes.” Diabetes Care 32.2 (2009): S151–6. DOI: 10.2337/DC09-S301
- Nguyen, T.T., Ta, Q.T.H., Nguyen, T.K.O., et al. “Type 3 Diabetes and Its Role Implications in Alzheimer’s Disease.” Int J Mol Sci 21.9 (2020). DOI: 10.3390/IJMS21093165
- Hendrickx, J.O., et al. “Serum Corticosterone and Insulin Resistance as Early Biomarkers in the hAPP23 Overexpressing Mouse Model of Alzheimer’s Disease.” Int J Mol Sci 22.13 (2021). DOI: 10.3390/IJMS22136656
- Ferreira, L.S.S., Fernandes, C.S., Vieira, M.N.N., De Felice, F.G. “Insulin resistance in Alzheimer’s disease.” Front Neurosci 12 (2018): 830. DOI: 10.3389/fnins.2018.00830
- Holt, R.I.G., Hanley, N.A. “Essential Endocrinology and Diabetes.” Available from: [https://books. google.com.ua/books?hl=uk&lr=&id=EjAhEAAAQBAJ&oi=fnd&pg=PP7 &dq=Essential+endocrinology+and+diabetes&ots=zuDBoR3WyR&sig= _y_q97GxC0fwUhu7GFvIzN87yAM&redir_esc=y#v=onepage&q=Essential endocrinology and diabetes&f=false], accessed Dec. 03, 2021.
- Belfiore, A., et al. “Insulin Receptor Isoforms in Physiology and Disease: An Updated View.” Endocr Rev 38.5 (2017): 379–431. DOI: 10.1210/ER.2017-00073
- Carson, C., Lawson, H.A. “Epigenetics of metabolic syndrome.” Physiol Genomics 50.11 (2018): 947–55. DOI: 10.1152/physiolgenomics.00072.2018
- Stepto, N.K., et al. “Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic-hyperinsulaemic clamp.” Hum Reprod 28.3 (2013): 777–84. DOI: 10.1093/humrep/des463
- Karelis, A.D., St-Pierre, D.H., Conus, F., et al. “Metabolic and Body Composition Factors in Subgroups of Obesity: What Do We Know?” J Clin Endocrinol Metab 89.6 (2004): 2569–75. DOI: 10.1210/JC.2004-0165
- Di Lorenzo, N., et al. “Clinical practice guidelines of the European Association for Endoscopic Surgery (EAES) on bariatric surgery: update 2020 endorsed by IFSO-EC, EASO and ESPCOP.” Surg Endosc 34.6 (2020): 2332–58. DOI: 10.1007/s00464-020-07555-y
- Borzan, V., et al. “Risk of Insulin Resistance and Metabolic Syndrome in Women with Hyperandrogenemia: A Comparison between PCOS Phenotypes and Beyond.” J Clin Med 10.4 (2021): 829. DOI: 10.3390/JCM10040829
- Condorelli, R.A., et al. “Androgen excess and metabolic disorders in women with PCOS: beyond the body mass index.” J Endocrinol Invest 41.4 (2018): 383–8. DOI: 10.1007/s40618-017-0762-3
- Pan, A., et al. “Bidirectional association between depression and metabolic syndrome: A systematic review and meta-analysis of epidemiological studies.” Diabetes Care 35.5 (2012): 1171–80. DOI: 10.2337/dc11-2055
- Dimopoulou, C., Goulis, D.G., Corona, G., Maggi, M. “The complex association between metabolic syndrome and male hypogonadism.” Metabolism 86 (2018): 61–8. DOI: 10.1016/J.METABOL.2018.03.024
- Singh, B., Saxena, A. “Surrogate markers of insulin resistance: A review.” World J Diabetes 1.2 (2010): 36–47. DOI: 10.4239/wjd.v1.i2.36
- Pfützner, P.A., et al. “IRIS II Study: Intact Proinsulin Is Confirmed as a Highly Specific Indicator for Insulin Resistance in a Large Cross-Sectional Study Design.” Diabetes Technol Ther 7.3 (2005): 478–86. DOI: 10.1089/DIA.2005.7.478
- Pfützner, A., Pfützner, A.H., Kann, P.H., Burgard, G. “Clinical and Laboratory Evaluation of a New Specific Point-of-Care Test for Intact Proinsulin.” J Diabetes Sci Technol 11.2 (2017): 278–83. DOI: 10.1177/1932296816663745
- Pfützner, A., et al. “Fasting Intact Proinsulin Is a Highly Specific Predictor of Insulin Resistance in Type 2 Diabetes.” Diabetes Care 27.3 (2004): 682–7. DOI: 10.2337/DIACARE.27.3.682
- Røder, M.E. “Hyperproinsulinemia in obesity and in type 2 diabetes and its relation to cardiovascular disease.” Expert Rev Endocrinol Metab 12.4 (2017): 227–39. DOI: 10.1080/17446651.2017.1331735
- Tokarz, V.L., MacDonald, P.E., Klip, A. “The cell biology of systemic insulin function.” J Cell Biol 217.7 (2018): 2273–89. DOI: 10.1083/JCB.201802095
- Shorakae, S., et al. “Inter-related effects of insulin resistance, hyperandrogenism, sympathetic dysfunction and chronic inflammation in PCOS.” Clin Endocrinol (Oxf) 89.5 (2018): 628–33. DOI: 10.1111/cen.13808
- Saad, M.J.A., Santos, A., Prada, P.O. “Linking gut microbiota and inflammation to obesity and insulin resistance.” Physiology 31.4 (2016): 283–93. DOI: 10.1152/physiol.00041.2015
- Zatterale, F., et al. “Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes.” Front Physiol 10 (2020): 1607. DOI: 10.3389/fphys.2019.01607
- Kitade, H., Chen, G., Ni, Y., Ota, T. “Nonalcoholic Fatty Liver Disease and Insulin Resistance: New Insights and Potential New Treatments.” Nutr 9.4 (2017): 387. DOI: 10.3390/NU9040387
- Sassi, F., Tamone, C., D’amelio, P. “Vitamin D: Nutrient, Hormone, and Immunomodulator.” Nutr 10.11 (2018): 1656. DOI: 10.3390/NU10111656
- Kabadi, S.M., Lee, B.K., Liu, L. “Joint Effects of Obesity and Vitamin D Insufficiency on Insulin Resistance and Type 2 Diabetes.” Diabetes Care 35.10 (2012): 2048–54. DOI: 10.2337/DC12-0235
- Parker, J., et al. “Levels of vitamin D and cardiometabolic disorders: Systematic review and meta-analysis.” Maturitas 65.3 (2010): 225–36. DOI: 10.1016/j.maturitas.2009.12.013
- Hajhashemy, Z., Shahdadian, F., Moslemi, E., et al. “Serum vitamin D levels in relation to metabolic syndrome: A systematic review and dose-response meta-analysis of epidemiologic studies.” Obes Rev 22.7 (2021): e13223. DOI: 10.1111/OBR.13223
- Boucher, B.J. “Why do so many trials of vitamin D supplementation fail?” Endocr Connect 9.9 (2020): R195. DOI: 10.1530/EC-20-0274
- Ferreira, P.P., et al. “Vitamin D supplementation improves the metabolic syndrome risk profile in postmenopausal women.” Climacteric 23.1 (2020): 24–31. DOI: 10.1080/13697137.2019.1611761
- Pramono, A., Jocken, J.W.E., Blaak, E.E. “Vitamin D deficiency in the aetiology of obesity-related insulin resistance.” Diabetes Metab Res Rev 35.5 (2019): e3146. DOI: 10.1002/DMRR.3146
- Roizen, J.D., et al. “Obesity Decreases Hepatic 25-Hydroxylase Activity Causing Low Serum 25-Hydroxyvitamin D.” J Bone Miner Res 34.6 (2019): 1068–73. DOI: 10.1002/JBMR.3686
- Abbas, M.A. “Physiological functions of Vitamin D in adipose tissue.” J Steroid Biochem Mol Biol 165 (2017): 369–81. DOI: 10.1016/J.JSBMB.2016.08.004
- Krul-Poel, Y.H.M., et al. “Vitamin D and metabolic disturbances in polycystic ovary syndrome (PCOS): A cross-sectional study.” PLoS One 13.12 (2018): e0204748. DOI: 10.1371/JOURNAL.PONE.0204748
- Komisarenko, Y.I., Bobryk, M.I. “Vitamin D Deficiency and Immune Disorders in Combined Endocrine Pathology.” Front Endocrinol 9 (2018): 600. DOI: 10.3389/fendo.2018.00600
- Niroomand, M., Fotouhi, A., Irannejad, N., Hosseinpanah, F. “Does high-dose vitamin D supplementation impact insulin resistance and risk of development of diabetes in patients with pre-diabetes? A double-blind randomized clinical trial.” Diabetes Res Clin Pract 148 (2019): 1–9. DOI: 10.1016/J.DIABRES.2018.12.008
- Wimalawansa, S.J. “Associations of vitamin D with insulin resistance, obesity, type 2 diabetes, and metabolic syndrome.” J Steroid Biochem Mol Biol 175 (2018): 177–89. DOI: 10.1016/J.JSBMB.2016.09.017
- Totonchi, H., Rezaei, R., Noori, S., et al. “Vitamin D Receptor Gene Polymorphisms and the Risk of Metabolic Syndrome (MetS): A Meta-Analysis.” Endocrine Metab Immune Disord Drug Targets 21.5 (2020): 943–55. DOI: 10.2174/1871530320666200805101302
- Liang, F., et al. “A meta-analysis of the relationship between vitamin D receptor gene ApaI polymorphisms and polycystic ovary syndrome.” Adv Clin Exp Med 28.2 (2019): 255–62. DOI: 10.17219/ACEM/85882
- Vulcan, T., Filip, G.A., Lenghel, L.M., et al. “Polymorphisms of Vitamin D Receptor and the Effect on Metabolic and Endocrine Abnormalities in Polycystic Ovary Syndrome: A Review.” Horm Metab Res 53.10 (2021): 645–53. DOI: 10.1055/a-1587-9336
- Cooper, C.B., Neufeld, E.V., Dolezal, B.A., Martin, J.L. “Sleep deprivation and obesity in adults: a brief narrative review.” BMJ Open Sport Exerc Med 4.1 (2018): e000392. DOI: 10.1136/BMJSEM-2018-000392
- Cardinali, D.P. “Melatonin as a Medicament for the 24/7 Society: Metabolic Syndrome.” Ma Vie en Noir (2016): 185–213. DOI: 10.1007/978-3-319-41679-3_12
- Carpentieri, A., Díaz De Barboza, G., Areco, V., et al. “New perspectives in melatonin uses.” Pharmacol Res 65.4 (2012): 437–44. DOI: 10.1016/J.PHRS.2012.01.003
- Halpern, B., et al. “Melatonin increases brown adipose tissue volume and activity in patients with melatonin deficiency: A proof-of-concept study.” Diabetes 68.5 (2019): 947–52. DOI: 10.2337/db18-0956
- Yu, H.-S., Reiter, R.J. “Melatonin: Biosynthesis, Physiological Effects, and Clinical Applications.” Available from: [https://books.google.com.ua/books?hl=uk&lr=&id=LJEBEAAAQBAJ&oi=fnd&pg=PP11&dq=melatonin+physiology&ots=Maw0Md0ecm&sig=AIo_PhZfKDt1bqiE_Asza_gGZ04&redir_esc=y#v=onepage&q=melatonin physiology&f=false], accessed Dec. 05, 2021.
- Aulinas, A. “Physiology of the Pineal Gland and Melatonin.” Endotext (Dec. 2019). Available from: [https://www.ncbi.nlm.nih.gov/sites/books/NBK550972/], accessed: Dec. 05, 2021.
- Socaciu, A.I., et al. “Melatonin, an ubiquitous metabolic regulator: functions, mechanisms and effects on circadian disruption and degenerative diseases.” Rev Endocr Metab Disord 21.4 (2020): 465–78. DOI: 10.1007/S11154-020-09570-9
- NaveenKumar, S.K., et al. “Melatonin restores neutrophil functions and prevents apoptosis amid dysfunctional glutathione redox system.” J Pineal Res 69.3 (2020): e12676. DOI: 10.1111/JPI.12676
- Lynch, H.J., Wurtman, R.J. “Melatonin Levels as they Relate to Reproductive Physiology.” Pineal Gland 123 (2020): 103–23. DOI: 10.1201/9780429280931-5
- Pevet, P., Klosen, P., Felder-Schmittbuhl, M.P. “The hormone melatonin: Animal studies.” Best Pract Res Clin Endocrinol Metab 31.6 (2017): 547–59. DOI: 10.1016/J.BEEM.2017.10.010
- Owino, S., et al. “Nocturnal activation of melatonin receptor type 1 signaling modulates diurnal insulin sensitivity via regulation of PI3K activity.” J Pineal Res 64.3 (2018): e12462. DOI: 10.1111/JPI.12462
- Tuomi, T., et al. “Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes.” Cell Metab 23.6 (2016): 1067–77. DOI: 10.1016/J.CMET.2016.04.009
- Karamitri, A., Renault, N., Clement, N., et al. “Minireview: Toward the Establishment of a Link between Melatonin and Glucose Homeostasis: Association of Melatonin MT2 Receptor Variants with Type 2 Diabetes.” Mol Endocrinol 27.8 (2013): 1217–33. DOI: 10.1210/ME.2013-1101
- Peschke, E., Bähr, I., Mühlbauer, E. “Melatonin and Pancreatic Islets: Interrelationships between Melatonin, Insulin and Glucagon.” Int J Mol Sci 14.4 (2013): 6981–7015. DOI: 10.3390/IJMS14046981
- Mayo, J.C., et al. “Melatonin Uptake by Cells: An Answer to Its Relationship with Glucose?” Mol 23.8 (2018): 1999. DOI: 10.3390/MOLECULES23081999
- Ramracheya, R.D., et al. “Function and expression of melatonin receptors on human pancreatic islets.” J Pineal Res 44.3 (2008): 273–9. DOI: 10.1111/J.1600-079X.2007.00523.X
- Lo, C.C., Lin, S.H., Chang, J.S., Chien, Y.W. “Effects of Melatonin on Glucose Homeostasis, Antioxidant Ability, and Adipokine Secretion in ICR Mice with NA/STZ-Induced Hyperglycemia.” Nutr 9.11 (2017): 1187. DOI: 10.3390/NU9111187
- de Farias, T.D.S.M., et al. “Melatonin Supplementation Attenuates the Pro-Inflammatory Adipokines Expression in Visceral Fat from Obese Mice Induced by A High-Fat Diet.” Cells 8.9 (2019): 1041. DOI: 10.3390/CELLS8091041
- Stenvers, D.J., Scheer, F.A.J.L., Schrauwen, P., et al. “Circadian clocks and insulin resistance.” Nat Rev Endocrinol 15.2 (2018): 75–89. DOI: 10.1038/s41574-018-0122-1
- Garaulet, M., Qian, J., Florez, J.C., et al. “Melatonin Effects on Glucose Metabolism: Time To Unlock the Controversy.” Trends Endocrinol Metab 31.3 (2020): 192–204. DOI: 10.1016/J.TEM.2019.11.011
- Mok, J.X., Ooi, J.H., Ng, K.Y., et al. “A new prospective on the role of melatonin in diabetes and its complications.” Horm Mol Biol Clin Investig 40.1 (2019). DOI: 10.1515/hmbci-2019-0036
- Boutin, J.A., Jockers, R. “Melatonin controversies, an update.” J Pineal Res 70.2 (2021): e12702. DOI: 10.1111/JPI.12702
- Andersen, L.P.H., Gögenur, I., Rosenberg, J., Reiter, R.J. “The Safety of Melatonin in Humans.” Clin Drug Investig 36.3 (2015): 169–75. DOI: 10.1007/S40261-015-0368-5
- Xia, Q., et al. “Association between the Melatonin Receptor 1B Gene Polymorphism on the Risk of Type 2 Diabetes, Impaired Glucose Regulation: A Meta-Analysis.” PLoS One 7.11 (2012): e50107. DOI: 10.1371/JOURNAL.PONE.0050107
- Shen, L.L., Jin, Y. “Effects of MTNR1B genetic variants on the risk of type 2 diabetes mellitus: A meta-analysis.” Mol Genet Genomic Med 7.5 (2019): e611. DOI: 10.1002/MGG3.611
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2021 М.І. Бобрик, Т.М. Тутченко, І.В. Сідорова, О.А. Бурка, О.І. Кротик, А.В. Сербенюк
This work is licensed under a Creative Commons Attribution 4.0 International License.
Authors who publish with this journal agree to the following terms:
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.