sibmedСибирский научный медицинский журналСибирский научный медицинский журнал2410-25122410-2520ИЦиГ СО РАН10.18699/SSMJ20230601sibmed-1301Research ArticleОБЗОРЫREVIEWSДиабетический кетоацидоз и окислительный стресс: патофизиологические механизмыDiabetic ketoacidosis and oxidative stress: pathophysiological mechanismshttps://orcid.org/0000-0003-4705-3823БыковЮ. В.BykovYu. V.

Быков Юрий Витальевич - к.м.н.

355017, Ставрополь, ул. Мира; 310 355002, Ставрополь, ул. Пономарева, 5

Yuri V. Bykov, candidate of medical sciences.

355017, Stavropol, Mira st., 310; 355002, Stavropol, Ponomareva st., 5

yubykov@gmail.comСтавропольский государственный медицинский университет Минздрава России; Детская городская клиническая больница им. Г.К. ФилиппскогоРоссияStavropol State Medical University of Minzdrav of Russia; Children’s City Clinical Hospital named G.K. FilippskyRussian Federation202310012024436613Copyright © Быков Ю.В., 20242024Быков Ю.В.Bykov Y.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://sibmed.elpub.ru/jour/article/view/1301

Сахарный диабет (СД) – распространенная эндокринная патология с большим количеством острых и хронических осложнений, среди которых диабетический кетоацидоз (ДКА) является наиболее частым и тяжелым осложнением, особенно у детей и подростков с СД 1 типа. Окислительный стресс (ОС) – патологического состояние, которое возникает в результате дисбаланса между образованием свободных радикалов и неэффективностью антиоксидантной системы. ОС служит мощным фактором риска развития многих диабетических осложнений. В последнее время он рассматривается как важная составляющая ДКА, патофизиологические механизмы развития которого изучены еще недостаточно хорошо. Описаны гипотезы, согласно которым ОС не только провоцирует и утяжеляет проявления ДКА, но и представляет собой тяжелое последствие самого ДКА, что приводит к прогрессированию многих микро- и макроскопических диабетических осложнений. Среди основных патофизиологических механизмов развития ОС при ДКА рассматриваются образование конечных продуктов гликирования, активация протеинкиназы C, полиолового и гексозаминового путей. Улучшение понимания патогенеза ОС при ДКА позволит оптимизировать диагностику ОС и подходы к коррекции ДКА за счет своевременного назначения антиоксидантов.

Diabetes mellitus (DM) is a common endocrine disease with a large number of acute and chronic complications, among which diabetic ketoacidosis (DKA) is the most frequent and severe, especially in children and adolescents with type 1 DM. Oxidative stress (OS) is a pathological condition that develops due to an imbalance between free radicals formation and inefficiency of the antioxidant system. OS is a strong risk factor for the development of numerous diabetic complications. Recently OS has been considered as an important component of DKA, the pathophysiological mechanisms of which have not yet been fully elucidated. This paper describes hypotheses according to which OS not only triggers and exacerbates manifestations of DKA, but itself represents a severe consequence of DKA, leading to the progression of numerous micro- and macroscopic diabetic complications. The formation of glycation end products, activation of protein kinase C, polyol and hexosamine pathways are considered among the key pathophysiologic mechanisms of OS development in DKA. Achieving a better understanding of OS pathogenesis in DKA will optimize the diagnosis of OS and approaches to DKA correction through timely prescription of antioxidants.

сахарный диабетдиабетический кетоацидозокислительный стресссвободные радикалыdiabetes mellitusdiabetic ketoacidosisoxidative stressfree radicalsReferencesPasupuleti V.R., Arigela C.S., Gan S.H., Salam S.K.N., Krishnan K.T., Rahman N.A., Jeffree M.S. A review on oxidative stress, diabetic complications, and the roles of honey polyphenols. Oxid. Med. Cell. Longev. 2020;2020:8878172. doi: 10.1155/2020/8878172Pasupuleti V.R., Arigela C.S., Gan S.H., Salam S.K.N., Krishnan K.T., Rahman N.A., Jeffree M.S. A review on oxidative stress, diabetic complications, and the roles of honey polyphenols. Oxid. Med. Cell. Longev. 2020;2020:8878172. doi: 10.1155/2020/8878172Black H.S. A synopsis of the associations of oxidative stress, ROS, and antioxidants with diabetes mellitus. Antioxidants (Basel). 2022;11(10):2003. doi: 10.3390/antiox11102003Black H.S. A synopsis of the associations of oxidative stress, ROS, and antioxidants with diabetes mellitus. Antioxidants (Basel). 2022;11(10):2003. doi: 10.3390/antiox11102003Papachristoforou E., Lambadiari V., Maratou E., Makrilakis K. Association of glycemic indices (hyperglycemia, glucose variability, and hypoglycemia) with oxidative stress and diabetic complications. J. Diabetes Res. 2020;2020:7489795. doi: 10.1155/2020/7489795Papachristoforou E., Lambadiari V., Maratou E., Makrilakis K. Association of glycemic indices (hyperglycemia, glucose variability, and hypoglycemia) with oxidative stress and diabetic complications. J. Diabetes Res. 2020;2020:7489795. doi: 10.1155/2020/7489795Li J., Shen X. Leptin concentration and oxidative stress in diabetic ketoacidosis. Eur. J. Clin. Invest. 2018;48(10):e13006. doi: 10.1111/eci.13006Li J., Shen X. Leptin concentration and oxidative stress in diabetic ketoacidosis. Eur. J. Clin. Invest. 2018;48(10):e13006. doi: 10.1111/eci.13006Li J., Shen X. Oxidative stress and adipokine levels were significantly correlated in diabetic patients with hyperglycemic crises. Diabetol. Metab. Syndr. 2019;11:13. doi: 10.1186/s13098-019-0410-5Li J., Shen X. Oxidative stress and adipokine levels were significantly correlated in diabetic patients with hyperglycemic crises. Diabetol. Metab. Syndr. 2019;11:13. doi: 10.1186/s13098-019-0410-5Mayer-Davis E.J., Lawrence J.M., Dabelea D., Divers J., Isom S., Dolan L., Imperatore G., Linder B., Marcovina S., Pettitt D.J., … SEARCH for Diabetes in Youth Study. Incidence trends of type 1 and type 2 diabetes among youths, 2002–2012. N. Engl. J. Med. 2017;376(15):1419–1429. doi: 10.1056/NEJMoa1610187Mayer-Davis E.J., Lawrence J.M., Dabelea D., Divers J., Isom S., Dolan L., Imperatore G., Linder B., Marcovina S., Pettitt D.J., … SEARCH for Diabetes in Youth Study. Incidence trends of type 1 and type 2 diabetes among youths, 2002–2012. N. Engl. J. Med. 2017;376(15):1419–1429. doi: 10.1056/NEJMoa1610187Saeedi P., Petersohn I., Salpea P., Malanda B., Karuranga S., Unwin N., Colagiuri S., Guariguata L., Motala A.A., Ogurtsova K., … IDF Diabetes Atlas Committee. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res. Clin. Pract. 2019;157:107843. doi: 10.1016/j.diabres.2019.107843Saeedi P., Petersohn I., Salpea P., Malanda B., Karuranga S., Unwin N., Colagiuri S., Guariguata L., Motala A.A., Ogurtsova K., … IDF Diabetes Atlas Committee. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res. Clin. Pract. 2019;157:107843. doi: 10.1016/j.diabres.2019.107843American Diabetes Association. 4. Comprehensive medical evaluation and assessment of comorbidities: standards of medical care in diabetes-2020. Diabetes care. 2019;43(Suppl 1):S37–S47. doi: 10.2337/dc20-S004American Diabetes Association. 4. Comprehensive medical evaluation and assessment of comorbidities: standards of medical care in diabetes-2020. Diabetes care. 2019;43(Suppl 1):S37–S47. doi: 10.2337/dc20-S004Baynest H.W. Classification, pathophysiology, diagnosis and management of diabetes mellitus. Journal of Diabetes & Metabolism. 2015;6(5):1–9. doi: 10.4172/2155-6156.1000541Baynest H.W. Classification, pathophysiology, diagnosis and management of diabetes mellitus. Journal of Diabetes & Metabolism. 2015;6(5):1–9. doi: 10.4172/2155-6156.1000541Bommer C., Heesemann E., Sagalova V., Manne-Goehler J., Atun R., Bärnighausen T., Vollmer S. The global economic burden of diabetes in adults aged 20–79 years: a cost-of-illness study. Lancet Diabetes Endocrinol. 2017;5(6):423–430. doi: 10.1016/S2213-8587(17)30097-9Bommer C., Heesemann E., Sagalova V., Manne-Goehler J., Atun R., Bärnighausen T., Vollmer S. The global economic burden of diabetes in adults aged 20–79 years: a cost-of-illness study. Lancet Diabetes Endocrinol. 2017;5(6):423–430. doi: 10.1016/S2213-8587(17)30097-9Быков Ю.В., Батурин В.А. Когнитивные нарушения при сахарном диабете 1 типа. Сиб. науч. мед. ж. 2023;43(1):4–12. doi: 10.18699/SSMJ20230101Bykov Yu.V., Baturin V.A. Cognitive impairment in type 1 diabetes mellitus. Sibirskij nauchnyj medicinskij zhurnal = Siberian Scientific Medical Journal. 2023;43(1):4–12. [In Russian]. doi: 10.18699/SSMJ20230101Быков Ю.В. Диабетический кетоацидоз у детей и подростков: от патофизиологии до профилактики. Забайк. мед. вестн. 2021;(2);85–95. doi: 10.52485/19986173_2021_2_85Bykov Yu.V. Diabetic ketoacidosis in children and adolescents: from pathophysiology to prevention. Zabaykal’skiy meditsinskiy vestnik = The Transbaikalian Medical Bulletin. 2021;(2);85–95. [In Russian]. doi: 10.52485/19986173_2021_2_85Yaribeygi H., Sathyapalan T., Atkin S.L., Sahebkar A. Molecular mechanisms linking oxidative stress and diabetes mellitus. Oxid. Med. Cell. Longev. 2020;2020:8609213. doi: 10.1155/2020/8609213Yaribeygi H., Sathyapalan T., Atkin S.L., Sahebkar A. Molecular mechanisms linking oxidative stress and diabetes mellitus. Oxid. Med. Cell. Longev. 2020;2020:8609213. doi: 10.1155/2020/8609213Yaribeygi H., Farrokhi F.R., Butler A.E., Sahebkar A. Insulin resistance: review of the underlying molecular mechanisms. J. Cell. Physiol. 2019;234(6):8152–8161. doi: 10.1002/jcp.27603Yaribeygi H., Farrokhi F.R., Butler A.E., Sahebkar A. Insulin resistance: review of the underlying molecular mechanisms. J. Cell. Physiol. 2019;234(6):8152–8161. doi: 10.1002/jcp.27603Ziegler R., Neu A. Diabetes in childhood and adolescence. Dtsch. Arztebl. Int. 2018;115(9):146–156. doi: 10.3238/arztebl.2018.0146Ziegler R., Neu A. Diabetes in childhood and adolescence. Dtsch. Arztebl. Int. 2018;115(9):146–156. doi: 10.3238/arztebl.2018.0146Otal Y., Kahraman F.A., Haydar F.G., Erel Ö. Dynamic thiol/disulfide homeostasis as oxidative stress marker in diabetic ketoacidosis. Turk. J. Med. Sci. 2021;51(2):743–748. doi: 10.3906/sag-1904-55Otal Y., Kahraman F.A., Haydar F.G., Erel Ö. Dynamic thiol/disulfide homeostasis as oxidative stress marker in diabetic ketoacidosis. Turk. J. Med. Sci. 2021;51(2):743–748. doi: 10.3906/sag-1904-55Быков Ю.В., Батурин В.А. Патофизиологические механизмы отека головного мозга при диабетическом кетоацидозе в детской практике. Медицина. 2021;(1):116–127. doi: 10.29234/23089113-2021-9-1-116-127Bykov Yu.V., Baturin V.A. Pathophysiological mechanisms of cerebral edema in diabetic ketoacidosis in children’s practice. Meditsina = Medicine. 2021;(1):116–127. [In Russian]. doi: 10.29234/23089113-2021-9-1-116-127Misra S., Oliver N.S. Diabetic ketoacidosis in adults. BMJ. 2015;351:h5660. doi: 10.1136/bmj.h5660Misra S., Oliver N.S. Diabetic ketoacidosis in adults. BMJ. 2015;351:h5660. doi: 10.1136/bmj.h5660Aldhaeefi M., Aldardeer N.F., Alkhani N., Alqarni S.M., Alhammad A.M., Alshaya A.I. Updates in the management of hyperglycemic crisis. Front. Clin. Diabetes Healthc. 2022;2:820728. doi: 10.3389/fcdhc.2021.820728Aldhaeefi M., Aldardeer N.F., Alkhani N., Alqarni S.M., Alhammad A.M., Alshaya A.I. Updates in the management of hyperglycemic crisis. Front. Clin. Diabetes Healthc. 2022;2:820728. doi: 10.3389/fcdhc.2021.820728Barski L., Golbets E., Jotkowitz A., Schwarzfuchs D. Management of diabetic ketoacidosis. Eur. J. Intern. Med. 2023;S0953–6205(23)00231-5. doi: 10.1016/j.ejim.2023.07.005Barski L., Golbets E., Jotkowitz A., Schwarzfuchs D. Management of diabetic ketoacidosis. Eur. J. Intern. Med. 2023;S0953–6205(23)00231-5. doi: 10.1016/j.ejim.2023.07.005Mays J.A., Jackson K.L., Derby T.A., Behrens J.J., Goel S., Molitch M.E., Kho A.N., Wallia A. An evaluation of recurrent diabetic ketoacidosis, fragmentation of care, and mortality across Chicago, Illinois. Diabetes Care. 2016;39(10):1671–1676. doi: 10.2337/dc16-0668Mays J.A., Jackson K.L., Derby T.A., Behrens J.J., Goel S., Molitch M.E., Kho A.N., Wallia A. An evaluation of recurrent diabetic ketoacidosis, fragmentation of care, and mortality across Chicago, Illinois. Diabetes Care. 2016;39(10):1671–1676. doi: 10.2337/dc16-0668Rugg-Gunn C.E., Deakin M., Hawcutt D.B. Update and harmonisation of guidance for the management of diabetic ketoacidosis in children and young people in the UK. BMJ Paediatr. Open. 2021;5(1):e001079. doi: 10.1136/bmjpo-2021-001079Rugg-Gunn C.E., Deakin M., Hawcutt D.B. Update and harmonisation of guidance for the management of diabetic ketoacidosis in children and young people in the UK. BMJ Paediatr. Open. 2021;5(1):e001079. doi: 10.1136/bmjpo-2021-001079Karslioglu French E., Donihi A.C., Korytkowski M.T. Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients. BMJ. 2019;365:I1141. doi: 10.1136/bmj.l1114Karslioglu French E., Donihi A.C., Korytkowski M.T. Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients. BMJ. 2019;365:I1141. doi: 10.1136/bmj.l1114Fayfman M., Pasquel F.J., Umpierrez G.E. Management of hyperglycemic crises. Med. Clinics. North. Am. 2017;101(3):587–606. doi: 10.1016/j.mcna.2016.12.011Fayfman M., Pasquel F.J., Umpierrez G.E. Management of hyperglycemic crises. Med. Clinics. North. Am. 2017;101(3):587–606. doi: 10.1016/j.mcna.2016.12.011Inci K., Gokcen T., Aylin B., Serdar U. Acute hyperglycemia causes oxidative stress which is prevented by vitamin E pretreatment in healthy rabbits. Journal of Research in Pharmacy. 2022; 26(3):534– 542. doi:10.29228/jrp.150Inci K., Gokcen T., Aylin B., Serdar U. Acute hyperglycemia causes oxidative stress which is prevented by vitamin E pretreatment in healthy rabbits. Journal of Research in Pharmacy. 2022; 26(3):534– 542. doi:10.29228/jrp.150Asmat U., Abad K., Ismail K. Diabetes mellitus and oxidative stress – A concise review. Saudi Pharm. J. 2016;24(5):547–553. doi: 10.1016/j.jsps.2015.03.013Asmat U., Abad K., Ismail K. Diabetes mellitus and oxidative stress – A concise review. Saudi Pharm. J. 2016;24(5):547–553. doi: 10.1016/j.jsps.2015.03.013Yaribeygi H., Farrokhi F.R., Rezaee R., Sahebkar A. Oxidative stress induces renal failure: a review of possible molecular pathways. J. Cell. Biochem. 2018;119(4):2990–2998. doi: 10.1002/jcb.26450Yaribeygi H., Farrokhi F.R., Rezaee R., Sahebkar A. Oxidative stress induces renal failure: a review of possible molecular pathways. J. Cell. Biochem. 2018;119(4):2990–2998. doi: 10.1002/jcb.26450Rajlic S., Treede H., Münzel T., Daiber A., Duerr G.D. Early detection is the best prevention-characterization of oxidative stress in diabetes mellitus and its consequences on the cardiovascular system. Cells. 2023;12(4):583. doi: 10.3390/cells12040583Rajlic S., Treede H., Münzel T., Daiber A., Duerr G.D. Early detection is the best prevention-characterization of oxidative stress in diabetes mellitus and its consequences on the cardiovascular system. Cells. 2023;12(4):583. doi: 10.3390/cells12040583Nowotny K., Jung T., Höhn A., Weber D., Grune T. Advanced glycation end products and oxidative stress in type 2 diabetes mellitus. Biomolecules. 2015;5(1):194–222. doi: 10.3390/biom5010194Nowotny K., Jung T., Höhn A., Weber D., Grune T. Advanced glycation end products and oxidative stress in type 2 diabetes mellitus. Biomolecules. 2015;5(1):194–222. doi: 10.3390/biom5010194Halliwell B., Gutteridge J.M. Free radicals in biology and medicine. Oxford University Press, 2015. 896 p.Halliwell B., Gutteridge J.M. Free radicals in biology and medicine. Oxford University Press, 2015. 896 p.Sindhu S., Akhter N., Kochumon S., Thomas R., Wilson A., Shenouda S., Tuomilehto J., Ahmad R. Increased expression of the innate immune receptor TLR10 in obesity and type-2 diabetes: association with ROS-mediated oxidative stress. Cell. Physiol. Biochem. 2018;45(2):572–590. doi: 10.1159/000487034Sindhu S., Akhter N., Kochumon S., Thomas R., Wilson A., Shenouda S., Tuomilehto J., Ahmad R. Increased expression of the innate immune receptor TLR10 in obesity and type-2 diabetes: association with ROS-mediated oxidative stress. Cell. Physiol. Biochem. 2018;45(2):572–590. doi: 10.1159/000487034Ghasemi M., Amini-Khoei H., Lorigooini Z., Rafieian-Kopaei M. Oxidative stress and antioxidants in diabetes mellitus. Asian Pacific Journal of Tropical Medicine. 2020;13(10):431–438. doi: 10.4103/19957645.291036Ghasemi M., Amini-Khoei H., Lorigooini Z., Rafieian-Kopaei M. Oxidative stress and antioxidants in diabetes mellitus. Asian Pacific Journal of Tropical Medicine. 2020;13(10):431–438. doi: 10.4103/19957645.291036Tibaut M. Oxidative stress genes, antioxidants and coronary artery disease in type 2 diabetes mellitus. Cardiovasc. Agent. Med. Chem. 2016;14(1):23–38. doi: 10.2174/1871525714666160407143416Tibaut M. Oxidative stress genes, antioxidants and coronary artery disease in type 2 diabetes mellitus. Cardiovasc. Agent. Med. Chem. 2016;14(1):23–38. doi: 10.2174/1871525714666160407143416Kanikarla-Marie P., Jain S.K. Hyperketonemia and ketosis increase the risk of complications in type 1 diabetes. Free Radic. Biol. Med. 2016;95:268–277. doi: 10.1016/j.freeradbiomed.2016.03.020Kanikarla-Marie P., Jain S.K. Hyperketonemia and ketosis increase the risk of complications in type 1 diabetes. Free Radic. Biol. Med. 2016;95:268–277. doi: 10.1016/j.freeradbiomed.2016.03.020Yazıcı M.U., Ayar G., Savas-Erdeve S., Azapağası E., Neşelioğlu S., Erel Ö., Çetinkaya S. Role of ischemia modified albumin serum levels as an oxidative stress marker in children with diabetic ketoacidosis. Comb. Chem. High. Throughput. Screen. 2019;22(8):577–581. doi: 10.2174/1386207322666191008214919Yazıcı M.U., Ayar G., Savas-Erdeve S., Azapağası E., Neşelioğlu S., Erel Ö., Çetinkaya S. Role of ischemia modified albumin serum levels as an oxidative stress marker in children with diabetic ketoacidosis. Comb. Chem. High. Throughput. Screen. 2019;22(8):577–581. doi: 10.2174/1386207322666191008214919Muriach M., Flores-Bellver M., Romero F.J., Barcia J.M. Diabetes and the brain: oxidative stress, inflammation, and autophagy. Oxid. Med. Cell. Longev. 2014;2014:102158. doi: 10.1155/2014/102158Muriach M., Flores-Bellver M., Romero F.J., Barcia J.M. Diabetes and the brain: oxidative stress, inflammation, and autophagy. Oxid. Med. Cell. Longev. 2014;2014:102158. doi: 10.1155/2014/102158Jha J.C., Banal C., Chow B.S.M., Cooper M.E., Jandeleit-Dahm K. Diabetes and kidney disease: role of oxidative stress. Antioxid. Redox. Signal. 2016;25(1):657–684. doi: 10.1089/ars.2016.6664Jha J.C., Banal C., Chow B.S.M., Cooper M.E., Jandeleit-Dahm K. Diabetes and kidney disease: role of oxidative stress. Antioxid. Redox. Signal. 2016;25(1):657–684. doi: 10.1089/ars.2016.6664Li J., Huang M., Shen X. The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis. J. Diabetes Complications. 2014;28(5):662–666. doi: 10.1016/j.jdiacomp.2014.06.008Li J., Huang M., Shen X. The association of oxidative stress and pro-inflammatory cytokines in diabetic patients with hyperglycemic crisis. J. Diabetes Complications. 2014;28(5):662–666. doi: 10.1016/j.jdiacomp.2014.06.008Glaser N., Chu S., Weiner J., Zdepski L., Wulff H., Tancredi D., ODonnell M.E. Acute and chronic neuroinflammation is triggered by diabetic ketoacidosis in a rat model. BMJ Open Diabetes Res.Care. 2020;8(2):e001793. doi: 10.1136/bmjdrc-2020-001793Glaser N., Chu S., Weiner J., Zdepski L., Wulff H., Tancredi D., ODonnell M.E. Acute and chronic neuroinflammation is triggered by diabetic ketoacidosis in a rat model. BMJ Open Diabetes Res.Care. 2020;8(2):e001793. doi: 10.1136/bmjdrc-2020-001793Li J., Pan L., Pan W., Li N., Tang B. Recent progress of oxidative stress associated biomarker detection. Chem. Commun. (Camb). 2023;59(48):7361– 7374. doi: 10.1039/d3cc00878aLi J., Pan L., Pan W., Li N., Tang B. Recent progress of oxidative stress associated biomarker detection. Chem. Commun. (Camb). 2023;59(48):7361– 7374. doi: 10.1039/d3cc00878aSehgal M., Batra M., Jha P., Sanchez O. Risk factors and laboratory findings associated with diabetic ketoacidosis in hospitalized pediatric patients. Cureus. 2022;14(5):e25410. doi: 10.7759/cureus.25410Sehgal M., Batra M., Jha P., Sanchez O. Risk factors and laboratory findings associated with diabetic ketoacidosis in hospitalized pediatric patients. Cureus. 2022;14(5):e25410. doi: 10.7759/cureus.25410Paoli A., Cerullo G. Investigating the link between ketogenic diet, NAFLD, mitochondria, and oxidative stress: a narrative review. Antioxidants (Basel). 2023;12(5):1065. doi: 10.3390/antiox12051065Paoli A., Cerullo G. Investigating the link between ketogenic diet, NAFLD, mitochondria, and oxidative stress: a narrative review. Antioxidants (Basel). 2023;12(5):1065. doi: 10.3390/antiox12051065Быков Ю.В., Батурин В.А., Волков Е.В. Уровень аутоантител к дофаминовым и NMDA рецепторам у детей в зависимости от степени тяжести диабетического кетоацидоза. Забайк. мед. вестн. 2022;(3):18–26. doi: 10.52485/19986173_2022_3_18Bykov Yu.V., Baturin V.A., Volkov E.V. Levels of autoantibodies against dopamine and NMDA receptors in children depending on the severity of diabetic ketoacidosis. Zabaykal’skiy meditsinskiy vestnik = The Transbaikalian Medical Bulletin. 2022;(3):18–26. [In Russian]. doi: 10.52485/19986173_2022_3_18Chowdhury S., Ghosh S., Das A.K., Sil P.C. Ferulic acid protects hyperglycemia-induced kidney damage by regulating oxidative insult, inflammation and autophagy. Front. Pharmacol. 2019;10:27. doi: 10.3389/fphar.2019.00027Chowdhury S., Ghosh S., Das A.K., Sil P.C. Ferulic acid protects hyperglycemia-induced kidney damage by regulating oxidative insult, inflammation and autophagy. Front. Pharmacol. 2019;10:27. doi: 10.3389/fphar.2019.00027Chen M.Y., Meng X.F., Han Y.P., Yan J.L., Xiao C., Qian L.B. Profile of crosstalk between glucose and lipid metabolic disturbance and diabetic cardiomyopathy: Inflammation and oxidative stress. Front. Endocrinol. (Lausanne). 2022;13:983713. doi: 10.3389/fendo.2022.983713Chen M.Y., Meng X.F., Han Y.P., Yan J.L., Xiao C., Qian L.B. Profile of crosstalk between glucose and lipid metabolic disturbance and diabetic cardiomyopathy: Inflammation and oxidative stress. Front. Endocrinol. (Lausanne). 2022;13:983713. doi: 10.3389/fendo.2022.983713Rains J.L., Jain S.K. Effect of hyperketonemia (Acetoacetate) on nuclear factor-kappaB and p38 mitogen-activated protein kinase activation mediated intercellular adhesion molecule 1 upregulation in endothelial cells. Metab. Syndr. Relat. Disord. 2015;13:71–77. doi: 10.1089/met.2014.0101Rains J.L., Jain S.K. Effect of hyperketonemia (Acetoacetate) on nuclear factor-kappaB and p38 mitogen-activated protein kinase activation mediated intercellular adhesion molecule 1 upregulation in endothelial cells. Metab. Syndr. Relat. Disord. 2015;13:71–77. doi: 10.1089/met.2014.0101Hoffman W.H., Ishikawa T., Blum J., Tani N., Ikeda T., Artlett C.M. Soluble receptor for glycation end-products concentration increases following the treatment of severe diabetic ketoacidosis. J. Clin. Res. Pediatr. Endocrinol. 2020;12(2):160–167. doi: 10.4274/jcrpe.galenos.2019.2019.0076Hoffman W.H., Ishikawa T., Blum J., Tani N., Ikeda T., Artlett C.M. Soluble receptor for glycation end-products concentration increases following the treatment of severe diabetic ketoacidosis. J. Clin. Res. Pediatr. Endocrinol. 2020;12(2):160–167. doi: 10.4274/jcrpe.galenos.2019.2019.0076Singh A., Kukreti R., Saso L., Kukreti S. Mechanistic insight into oxidative stress-triggered signaling pathways and type 2 diabetes. Molecules. 2022;27(3):950. doi: 10.3390/molecules27030950Singh A., Kukreti R., Saso L., Kukreti S. Mechanistic insight into oxidative stress-triggered signaling pathways and type 2 diabetes. Molecules. 2022;27(3):950. doi: 10.3390/molecules27030950de Paula M.L.A., Rodrigues Villela A.M., Negri M.M., Kanaan S., de Carvalho Cardoso Weide L. Role of advanced glycation end products related to the onset of diabetic kidney disease complications. Clin. Biomed. Res. 2017;37(4):341–348.de Paula M.L.A., Rodrigues Villela A.M., Negri M.M., Kanaan S., de Carvalho Cardoso Weide L. Role of advanced glycation end products related to the onset of diabetic kidney disease complications. Clin. Biomed. Res. 2017;37(4):341–348.Ighodaro O.M. Molecular pathways associated with oxidative stress in diabetes mellitus Biomed. Pharmacother. 2018;108:656–662. doi: 10.1016/j.biopha.2018.09.058Ighodaro O.M. Molecular pathways associated with oxidative stress in diabetes mellitus Biomed. Pharmacother. 2018;108:656–662. doi: 10.1016/j.biopha.2018.09.058Twarda-Clapa A., Olczak A., Białkowska A.M., Koziołkiewicz M. Advanced glycation end-products (AGEs): formation, chemistry, classification, receptors, and diseases related to AGEs. Cells. 2022;11(8):1312. doi: 10.3390/cells11081312Twarda-Clapa A., Olczak A., Białkowska A.M., Koziołkiewicz M. Advanced glycation end-products (AGEs): formation, chemistry, classification, receptors, and diseases related to AGEs. Cells. 2022;11(8):1312. doi: 10.3390/cells11081312Gopalakrishna K., McNeill T.H., Elhia- ni A.A., Gundimeda U. Methods for studying oxidative regulation of protein kinase C. Methods. Enzymol. 2013;528:79–98. doi: 10.1016/B978-0-12-4058811.00005-7Gopalakrishna K., McNeill T.H., Elhia- ni A.A., Gundimeda U. Methods for studying oxidative regulation of protein kinase C. Methods. Enzymol. 2013;528:79–98. doi: 10.1016/B978-0-12-4058811.00005-7Lien C.F., Chen S.J., Tsai M.C., Lin C.S. Potential role of protein kinase C in the pathophysiology of diabetes-associated atherosclerosis. Front. Pharmacol. 2021;12:716332. doi: 10.3389/fphar.2021.716332Lien C.F., Chen S.J., Tsai M.C., Lin C.S. Potential role of protein kinase C in the pathophysiology of diabetes-associated atherosclerosis. Front. Pharmacol. 2021;12:716332. doi: 10.3389/fphar.2021.716332Behl T., Kaur I., Kotwani A. Implication of oxidative stress in progression of diabetic retinopathy. Surv. Ophthalmol. 2016;61(2):187–196. doi: 10.1016/j.survophthal.2015.06.001Behl T., Kaur I., Kotwani A. Implication of oxidative stress in progression of diabetic retinopathy. Surv. Ophthalmol. 2016;61(2):187–196. doi: 10.1016/j.survophthal.2015.06.001Yan L.J. Redox imbalance stress in diabetes mellitus: Role of the polyol pathway. Animal Model Exp. Med. 2018;1(1):7–13. doi: 10.1002/ame2.12001Yan L.J. Redox imbalance stress in diabetes mellitus: Role of the polyol pathway. Animal Model Exp. Med. 2018;1(1):7–13. doi: 10.1002/ame2.12001Kilanczyk E., Saraswat Ohri S., Whittemore S.R., Hetman M. Antioxidant protection of NADPH-depleted oligodendrocyte precursor cells is dependent on supply of reduced glutathione. ASN Neuro. 2016;8(4):1759091416660404. doi: 10.1177/1759091416660404Kilanczyk E., Saraswat Ohri S., Whittemore S.R., Hetman M. Antioxidant protection of NADPH-depleted oligodendrocyte precursor cells is dependent on supply of reduced glutathione. ASN Neuro. 2016;8(4):1759091416660404. doi: 10.1177/1759091416660404

The authors declare that there are no conflicts of interest present.