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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">diaendo</journal-id><journal-title-group><journal-title xml:lang="ru">Сахарный диабет</journal-title><trans-title-group xml:lang="en"><trans-title>Diabetes mellitus</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-0351</issn><issn pub-type="epub">2072-0378</issn><publisher><publisher-name>Endocrinology research centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/DM12981</article-id><article-id custom-type="elpub" pub-id-type="custom">diaendo-12981</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Обзоры</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Взаимодействие воспаления и инсулиновой резистентности: молекулярные механизмы в инсулинопродуцирующих и инсулинозависимых тканях</article-title><trans-title-group xml:lang="en"><trans-title>The interactions between inflammation and insulin resistance: molecular mechanisms in insulin-producing and insulin-dependent tissues</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2940-0230</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Юдаева</surname><given-names>А. Д.</given-names></name><name name-style="western" xml:lang="en"><surname>Yudaeva</surname><given-names>A. D.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Юдаева Александра Дмитриевна</p><p>Researcher ID: GWN-0814-2022</p><p>Москва</p></bio><bio xml:lang="en"><p>Alexandra D. Yudaeva</p><p>Moscow</p></bio><email xlink:type="simple">alexa.yudaeva@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3514-3936</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Стафеев</surname><given-names>Ю. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Stafeev</surname><given-names>I. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Стафеев Юрий Сергеевич - кандидат биологических наук; Researcher ID: O-2949-2015; Scopus Author ID: 57204688438.</p><p>121552, Москва, ул. 3-я Черепковская, д. 15А</p></bio><bio xml:lang="en"><p>Iurii S. Stafeev - PhD in Biology; Researcher ID: O-2949-2015; Scopus Author ID: 57204688438.</p><p>15A 3rd Cherepkovskaya street, 121552 Moscow</p></bio><email xlink:type="simple">yuristafeev@gmail.com</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6027-2217</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Мичурина</surname><given-names>С. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Michurina</surname><given-names>S. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Мичурина Светлана Сергеевна; Scopus Author ID: 57202136814.</p><p>Москва</p></bio><bio xml:lang="en"><p>Svetlana S. Michurina; Scopus Author ID: 57202136814.</p><p>Moscow</p></bio><email xlink:type="simple">michurinas192@gmail.com</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-9949-0534</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Меньшиков</surname><given-names>М. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Menshikov</surname><given-names>M. Yu.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Меньшиков Михаил Юрьевич - доктор биологических наук; Researcher ID: O-2949-2015; Scopus Author ID: 6701418250.</p><p>Москва</p></bio><bio xml:lang="en"><p>Mikhail Yu. Menshikov - PhD in Biology; Researcher ID: O-2949-2015; Scopus Author ID: 6701418250.</p><p>Moscow</p></bio><email xlink:type="simple">myumensh@mail.ru</email><xref ref-type="aff" rid="aff-4"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5057-127X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шестакова</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shestakova</surname><given-names>M. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Шестакова Марина Владимировна - доктор медицинских наук, профессор, академик РАН; Researcher ID: D-9123-2012; Scopus Author ID: 7004195530.</p><p>Москва</p></bio><bio xml:lang="en"><p>Marina V. Shestakova - MD, PhD, Professor, Academician of the Russian Academy of Sciences; Researcher ID: D-9123-2012; Scopus Author ID: 7004195530.</p><p>Moscow</p></bio><email xlink:type="simple">shestakova.mv@gmail.com</email><xref ref-type="aff" rid="aff-5"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-0969-5780</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Парфенова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Parfyonova</surname><given-names>Y. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Парфенова Елена Викторовна - доктор медицинских наук, профессор, член-корреспондент РАН; Researcher ID: B-9307-2014; Scopus Author ID: 57190312316.</p><p>Москва</p></bio><bio xml:lang="en"><p>Yelena V. Parfyonova - MD, PhD, Professor; Researcher ID: B-9307-2014; Scopus Author ID: 57190312316.</p><p>Moscow</p></bio><email xlink:type="simple">yeparfyon@mail.ru</email><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр кардиологии им. академика Е.И. Чазова; Российский национальный исследовательский медицинский университет им. Н.И. Пирогова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>National Medical Research Centre of Cardiology named after academician E.I.Chazov; Pirogov Russian National Research Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр кардиологии им. академика Е.И. Чазова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>National Medical Research Centre of Cardiology named after academician E.I.Chazov; Pirogov Russian National Research Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр кардиологии им. академика Е.И. Чазова; Московский государственный университет им. М.В. Ломоносова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>National Medical Research Centre of Cardiology named after academician E.I.Chazov; Lomonosov Moscow State University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-4"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр кардиологии им. академика Е.И. Чазова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>National Medical Research Centre of Cardiology named after academician E.I.Chazov</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-5"><aff xml:lang="ru"><institution>Национальный медицинский исследовательский центр эндокринологии</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Endocrinology Research Centre</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2023</year></pub-date><pub-date pub-type="epub"><day>10</day><month>02</month><year>2023</year></pub-date><volume>26</volume><issue>1</issue><fpage>75</fpage><lpage>81</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Юдаева А.Д., Стафеев Ю.С., Мичурина С.С., Меньшиков М.Ю., Шестакова М.В., Парфенова Е.В., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Юдаева А.Д., Стафеев Ю.С., Мичурина С.С., Меньшиков М.Ю., Шестакова М.В., Парфенова Е.В.</copyright-holder><copyright-holder xml:lang="en">Yudaeva A.D., Stafeev I.S., Michurina S.S., Menshikov M.Y., Shestakova M.V., Parfyonova Y.V.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.dia-endojournals.ru/jour/article/view/12981">https://www.dia-endojournals.ru/jour/article/view/12981</self-uri><abstract><p>В современном мире распространенность ожирения и сахарного диабета 2 типа (СД2) существенно возрастает. В связи с этим также повышаются риски развития сопутствующих осложнений, в том числе метаболических и сердечно-сосудистых. Звеном взаимосвязи между ожирением и его осложнениями является воспалительный процесс как на клеточном уровне, так и на уровнях межклеточной коммуникации и внутриклеточных сигнальных каскадов. Механизм этой связи довольно сходный в поджелудочной железе и инсулинозависимых тканях: катализаторами процесса нередко являются различные липиды (холестерин, свободные жирные кислоты, триглицериды), которые способны активировать Толл-подобные рецепторы — рецепторы врожденного иммунитета, запускающие воспалительный процесс. Далее через активацию IKK- и JNK-зависимых сигнальных каскадов происходит секреция провоспалительных цитокинов — фактора некроза альфа, интерлейкинов (ИЛ-1β, ИЛ-6) и других, которые, действуя паракринно и аутокринно, поддерживают процесс воспаления как на локальном, так и на системном уровне. Таким образом, инсулинопродуцирующие и инсулинозависимые ткани, вовлеченные в процесс патогенеза СД2, через процесс воспаления интегрируются в патогенетический самоподдерживающийся цикл, который в конечном счете приводит к снижению секреции инсулина, гибели β-клеток поджелудочной железы и развитию инсулиновой резистентности.</p></abstract><trans-abstract xml:lang="en"><p>In the modern world the prevalence of obesity and type 2 diabetes mellitus (T2DM) significantly increases. In this light the risks of obesity-associated complications also grow up. The crucial linkage between obesity and its metabolic and cardiovascular complications is inflammatory process. The mechanism of this linkage is similar in pancreas and insulin-dependent tissues both on cells, cell-to-cell communication and signaling pathway levels: the catalysts are different lipids (cholesterol, free fatty acids, triglycerides), which are able to activate Toll-like receptors of innate immunity and inflammation. Nextly, IKK- and JNK-dependent cascades activate the secretion of inflammatory cytokines TNFa, IL-1b, IL-6 and others, which act by paracrine and autocrine manner and support inflammation both in local and systemic levels. Thus, insulin-producing and insulin-dependent tissues, which are involved in T2DM pathogenesis, through the inflammatory process integrate in pathogenic and self-maintaining cycle, which leads to the suppression of insulin secretion, pancreatic β-cell failure and the development of insulin-dependent tissues insulin resistance.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>воспаление</kwd><kwd>ожирение</kwd><kwd>сахарный диабет 2 типа</kwd><kwd>иммунометаболизм</kwd><kwd>противовоспалительная терапия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Inflammation</kwd><kwd>obesity</kwd><kwd>type 2 diabetes mellitus</kwd><kwd>immunometabolism</kwd><kwd>anti-inflammatory therapy</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа выполнена при финансовой поддержке проекта РФФИ №20-015-00100</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Старостина Е.Г., Древаль A.B. Как врачи и пациенты смотрят на проблему ожирения // Терапевтический архив. — 2001. — Т. 73. — №10. — С. 14-20.</mixed-citation><mixed-citation xml:lang="en">Starostina EG, Dreval’ AV. How physicians and patients look at the problem of obesity. Therapeutic Archive. 2001;73(10):14-20. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Шестакова М.В., Викулова О.К., Железнякова А.В., и др. Эпидемиология сахарного диабета в Российской Федерации: что изменилось за последнее десятилетие? // Терапевтический архив. — 2019. — Т. 91. — №10. — С. 4-13. doi: https://doi.org/10.26442/00403660.2019.10.000364</mixed-citation><mixed-citation xml:lang="en">Shestakova MV, Vikulova OK, Zheleznyakova AV, et al. Diabetes epidemiology in Russia: what has changed over the decade? Therapeutic Archive. 2019;91(10):4-13. (In Russ.). doi: https://doi.org/10.26442/00403660.2019.10.000364</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Schmidt FM, Weschenfelder J, Sander C, et al. Inflammatory cytokines in general and central obesity and modulating effects of physical activity. PLoS One. 2015;10(3):e0121971. doi: https://doi.org/10.1371/journal.pone.0121971</mixed-citation><mixed-citation xml:lang="en">Schmidt FM, Weschenfelder J, Sander C, et al. Inflammatory cytokines in general and central obesity and modulating effects of physical activity. PLoS One. 2015;10(3):e0121971. doi: https://doi.org/10.1371/journal.pone.0121971</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Tsalamandris S, Antonopoulos AS, Oikonomou E, et al. The role of inflammation in diabetes: Current concepts and future perspectives. Eur Cardiol. 2019;14(1):50-59. doi: https://doi.org/10.15420/ecr.2018.33.1</mixed-citation><mixed-citation xml:lang="en">Tsalamandris S, Antonopoulos AS, Oikonomou E, et al. The role of inflammation in diabetes: Current concepts and future perspectives. Eur Cardiol. 2019;14(1):50-59. doi: https://doi.org/10.15420/ecr.2018.33.1</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Asrih M, Jornayvaz FR. Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance. J Endocrinol. 2013;218(3):R25-36. doi: https://doi.org/10.1530/JOE-13-0201</mixed-citation><mixed-citation xml:lang="en">Asrih M, Jornayvaz FR. Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance. J Endocrinol. 2013;218(3):R25-36. doi: https://doi.org/10.1530/JOE-13-0201</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Chen L, Chen R, Wang H, Liang F. Mechanisms Linking Inflammation to Insulin Resistance. Int J Endocrinol. 2015;2015:1-9. doi: https://doi.org/10.1155/2015/508409</mixed-citation><mixed-citation xml:lang="en">Chen L, Chen R, Wang H, Liang F. Mechanisms Linking Inflammation to Insulin Resistance. Int J Endocrinol. 2015;2015:1-9. doi: https://doi.org/10.1155/2015/508409</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Shimobayashi M, Albert V, Woelnerhanssen B, et al. Insulin resistance causes inflammation in adipose tissue. J Clin Invest. 2018;128(4):1538-1550. doi: https://doi.org/10.1172/JCI96139</mixed-citation><mixed-citation xml:lang="en">Shimobayashi M, Albert V, Woelnerhanssen B, et al. Insulin resistance causes inflammation in adipose tissue. J Clin Invest. 2018;128(4):1538-1550. doi: https://doi.org/10.1172/JCI96139</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Donath MY. Inflammation and type 2 diabetes: from basic science to treatment. Semin Immunopathol. 2019;41(4):411-412. doi: https://doi.org/10.1007/s00281-019-00749-0</mixed-citation><mixed-citation xml:lang="en">Donath MY. Inflammation and type 2 diabetes: from basic science to treatment. Semin Immunopathol. 2019;41(4):411-412. doi: https://doi.org/10.1007/s00281-019-00749-0</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Richardson SJ, Willcox A, Bone AJ, et al. Islet-associated macrophages in type 2 diabetes. Diabetologia. 2009;52(8):1686-1688. doi: https://doi.org/10.1007/s00125-009-1410-z</mixed-citation><mixed-citation xml:lang="en">Richardson SJ, Willcox A, Bone AJ, et al. Islet-associated macrophages in type 2 diabetes. Diabetologia. 2009;52(8):1686-1688. doi: https://doi.org/10.1007/s00125-009-1410-z</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Ying W, Lee YS, Dong Y, et al. Expansion of islet-resident macrophages leads to inflammation affecting β cell proliferation and function in obesity. Cell Metab. 2019;29(2):457-474.e5. doi: https://doi.org/10.1016/j.cmet.2018.12.003</mixed-citation><mixed-citation xml:lang="en">Ying W, Lee YS, Dong Y, et al. Expansion of islet-resident macrophages leads to inflammation affecting β cell proliferation and function in obesity. Cell Metab. 2019;29(2):457-474.e5. doi: https://doi.org/10.1016/j.cmet.2018.12.003</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Eguchi K, Manabe I, Oishi-Tanaka Y, et al. Saturated fatty acid and TLR signaling link β cell dysfunction and islet inflammation. Cell Metab. 2012;15(4):518-533. doi: https://doi.org/10.1016/j.cmet.2012.01.023</mixed-citation><mixed-citation xml:lang="en">Eguchi K, Manabe I, Oishi-Tanaka Y, et al. Saturated fatty acid and TLR signaling link β cell dysfunction and islet inflammation. Cell Metab. 2012;15(4):518-533. doi: https://doi.org/10.1016/j.cmet.2012.01.023</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Wu M, Lee MYY, Bahl V, et al. Single-cell analysis of the human pancreas in type 2 diabetes using multi-spectral imaging mass cytometry. Cell Rep. 2021;37(5):109919. doi: https://doi.org/10.1016/j.celrep.2021.109919</mixed-citation><mixed-citation xml:lang="en">Wu M, Lee MYY, Bahl V, et al. Single-cell analysis of the human pancreas in type 2 diabetes using multi-spectral imaging mass cytometry. Cell Rep. 2021;37(5):109919. doi: https://doi.org/10.1016/j.celrep.2021.109919</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Dalmas E, Lehmann FM, Dror E, et al. Interleukin-33-activated islet-resident innate lymphoid cells promote insulin secretion through myeloid cell retinoic acid production. Immunity. 2017;47(5):928-942.e7. doi: https://doi.org/10.1016/j.immuni.2017.10.015</mixed-citation><mixed-citation xml:lang="en">Dalmas E, Lehmann FM, Dror E, et al. Interleukin-33-activated islet-resident innate lymphoid cells promote insulin secretion through myeloid cell retinoic acid production. Immunity. 2017;47(5):928-942.e7. doi: https://doi.org/10.1016/j.immuni.2017.10.015</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Igoillo-Esteve M, Marselli L, Cunha DA, et al. Palmitate induces a pro-inflammatory response in human pancreatic islets that mimics CCL2 expression by beta cells in type 2 diabetes. Diabetologia. 2010;53(7):1395-1405. doi: https://doi.org/10.1007/s00125-010-1707-y</mixed-citation><mixed-citation xml:lang="en">Igoillo-Esteve M, Marselli L, Cunha DA, et al. Palmitate induces a pro-inflammatory response in human pancreatic islets that mimics CCL2 expression by beta cells in type 2 diabetes. Diabetologia. 2010;53(7):1395-1405. doi: https://doi.org/10.1007/s00125-010-1707-y</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Marselli L, Piron A, Suleiman M, et al. Persistent or transient human β cell dysfunction induced by metabolic stress: Specific signatures and shared gene expression with type 2 diabetes. Cell Rep. 2020;33(9):108466. doi: https://doi.org/10.1016/j.celrep.2020.108466</mixed-citation><mixed-citation xml:lang="en">Marselli L, Piron A, Suleiman M, et al. Persistent or transient human β cell dysfunction induced by metabolic stress: Specific signatures and shared gene expression with type 2 diabetes. Cell Rep. 2020;33(9):108466. doi: https://doi.org/10.1016/j.celrep.2020.108466</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Dror E, Dalmas E, Meier DT, et al. Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nat Immunol. 2017;18(3):283-292. doi: https://doi.org/10.1038/ni.3659</mixed-citation><mixed-citation xml:lang="en">Dror E, Dalmas E, Meier DT, et al. Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nat Immunol. 2017;18(3):283-292. doi: https://doi.org/10.1038/ni.3659</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Maedler K, Sergeev P, Ris F, et al. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. J Clin Invest. 2002;110(6):851-860. doi: https://doi.org/10.1172/JCI15318</mixed-citation><mixed-citation xml:lang="en">Maedler K, Sergeev P, Ris F, et al. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. J Clin Invest. 2002;110(6):851-860. doi: https://doi.org/10.1172/JCI15318</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Lanuza-Masdeu J, Arévalo MI, Vila C, et al. In vivo JNK activation in pancreatic β-cells leads to glucose intolerance caused by insulin resistance in pancreas. Diabetes. 2013;62(7):2308-2317. doi: https://doi.org/10.2337/db12-1097</mixed-citation><mixed-citation xml:lang="en">Lanuza-Masdeu J, Arévalo MI, Vila C, et al. In vivo JNK activation in pancreatic β-cells leads to glucose intolerance caused by insulin resistance in pancreas. Diabetes. 2013;62(7):2308-2317. doi: https://doi.org/10.2337/db12-1097</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Eguchi K, Nagai R. Islet inflammation in type 2 diabetes and physiology. J Clin Invest. 2017;127(1):14-23. doi: https://doi.org/10.1172/JCI88877</mixed-citation><mixed-citation xml:lang="en">Eguchi K, Nagai R. Islet inflammation in type 2 diabetes and physiology. J Clin Invest. 2017;127(1):14-23. doi: https://doi.org/10.1172/JCI88877</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Meyerovich K, Ortis F, Allagnat F, Cardozo AK. Endoplasmic reticulum stress and the unfolded protein response in pancreatic islet inflammation. J Mol Endocrinol. 2016;57(1):R1-R17. doi: https://doi.org/10.1530/jme-15-0306</mixed-citation><mixed-citation xml:lang="en">Meyerovich K, Ortis F, Allagnat F, Cardozo AK. Endoplasmic reticulum stress and the unfolded protein response in pancreatic islet inflammation. J Mol Endocrinol. 2016;57(1):R1-R17. doi: https://doi.org/10.1530/jme-15-0306</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Andreozzi F, D’Alessandris C, Federici M, et al. Activation of the hexosamine pathway leads to phosphorylation of insulin receptor substrate-1 on Ser307 and Ser612 and impairs the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin insulin biosynthetic pathway in RIN pancreatic beta-cells. Endocrinology. 2004;145(6):2845-2857. doi: https://doi.org/10.1210/en.2003-0939</mixed-citation><mixed-citation xml:lang="en">Andreozzi F, D’Alessandris C, Federici M, et al. Activation of the hexosamine pathway leads to phosphorylation of insulin receptor substrate-1 on Ser307 and Ser612 and impairs the phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin insulin biosynthetic pathway in RIN pancreatic beta-cells. Endocrinology. 2004;145(6):2845-2857. doi: https://doi.org/10.1210/en.2003-0939</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Arafat HA, Katakam AK, Chipitsyna G, et al. Osteopontin protects the islets and beta-cells from interleukin-1 beta-mediated cytotoxicity through negative feedback regulation of nitric oxide. Endocrinology. 2007;148(2):575-584. doi: https://doi.org/10.1210/en.2006-0970</mixed-citation><mixed-citation xml:lang="en">Arafat HA, Katakam AK, Chipitsyna G, et al. Osteopontin protects the islets and beta-cells from interleukin-1 beta-mediated cytotoxicity through negative feedback regulation of nitric oxide. Endocrinology. 2007;148(2):575-584. doi: https://doi.org/10.1210/en.2006-0970</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Stancill JS, Kasmani MY, Khatun A, et al. Single-cell RNA sequencing of mouse islets exposed to proinflammatory cytokines. Life Sci Alliance. 2021;4(6):e202000949. doi: https://doi.org/10.26508/lsa.202000949</mixed-citation><mixed-citation xml:lang="en">Stancill JS, Kasmani MY, Khatun A, et al. Single-cell RNA sequencing of mouse islets exposed to proinflammatory cytokines. Life Sci Alliance. 2021;4(6):e202000949. doi: https://doi.org/10.26508/lsa.202000949</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Kubes P, Jenne C. Immune Responses in the Liver. Annu Rev Immunol. 2018;36(1):247-277. doi: https://doi.org/10.1146/annurev-immunol-051116-052415</mixed-citation><mixed-citation xml:lang="en">Kubes P, Jenne C. Immune Responses in the Liver. Annu Rev Immunol. 2018;36(1):247-277. doi: https://doi.org/10.1146/annurev-immunol-051116-052415</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Petersen MC, Shulman GI. Mechanisms of insulin action and insulin resistance. Physiol Rev. 2018;98(4):2133-2223. doi: https://doi.org/10.1152/physrev.00063.2017</mixed-citation><mixed-citation xml:lang="en">Petersen MC, Shulman GI. Mechanisms of insulin action and insulin resistance. Physiol Rev. 2018;98(4):2133-2223. doi: https://doi.org/10.1152/physrev.00063.2017</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Rinella ME. Nonalcoholic fatty liver disease: A systematic review. JAMA. 2015;313(22):2263. doi: https://doi.org/10.1001/jama.2015.5370</mixed-citation><mixed-citation xml:lang="en">Rinella ME. Nonalcoholic fatty liver disease: A systematic review. JAMA. 2015;313(22):2263. doi: https://doi.org/10.1001/jama.2015.5370</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Dowman JK, Tomlinson JW, Newsome PN. Pathogenesis of non-alcoholic fatty liver disease. QJM. 2010;103(2):71-83. doi: https://doi.org/10.1093/qjmed/hcp158</mixed-citation><mixed-citation xml:lang="en">Dowman JK, Tomlinson JW, Newsome PN. Pathogenesis of non-alcoholic fatty liver disease. QJM. 2010;103(2):71-83. doi: https://doi.org/10.1093/qjmed/hcp158</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Gregory SH, Cousens LP, van Rooijen N, et al. Complementary adhesion molecules promote neutrophil-Kupffer cell interaction and the elimination of bacteria taken up by the liver. J Immunol. 2002;168(1):308-315. doi: https://doi.org/10.4049/jimmunol.168.1.308</mixed-citation><mixed-citation xml:lang="en">Gregory SH, Cousens LP, van Rooijen N, et al. Complementary adhesion molecules promote neutrophil-Kupffer cell interaction and the elimination of bacteria taken up by the liver. J Immunol. 2002;168(1):308-315. doi: https://doi.org/10.4049/jimmunol.168.1.308</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">Kiziltas S. Toll-like receptors in pathophysiology of liver diseases. World J Hepatol. 2016;8(32):1354-1369. doi: https://doi.org/10.4254/wjh.v8.i32.1354</mixed-citation><mixed-citation xml:lang="en">Kiziltas S. Toll-like receptors in pathophysiology of liver diseases. World J Hepatol. 2016;8(32):1354-1369. doi: https://doi.org/10.4254/wjh.v8.i32.1354</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Li W, Yang GL, Zhu Q, et al. TLR4 promotes liver inflammation by activating the JNK pathway. Eur Rev Med Pharmacol Sci. 2019;23(17):7655-7662. doi: https://doi.org/10.26355/eurrev_201909_18889</mixed-citation><mixed-citation xml:lang="en">Li W, Yang GL, Zhu Q, et al. TLR4 promotes liver inflammation by activating the JNK pathway. Eur Rev Med Pharmacol Sci. 2019;23(17):7655-7662. doi: https://doi.org/10.26355/eurrev_201909_18889</mixed-citation></citation-alternatives></ref><ref id="cit31"><label>31</label><citation-alternatives><mixed-citation xml:lang="ru">Tosello-Trampont AC, Landes SG, Nguyen V, et al. Kuppfer cells trigger nonalcoholic steatohepatitis development in diet-induced mouse model through tumor necrosis factor-α production. J Biol Chem. 2012;287(48):40161-40172. doi: https://doi.org/10.1074/jbc.M112.417014</mixed-citation><mixed-citation xml:lang="en">Tosello-Trampont AC, Landes SG, Nguyen V, et al. Kuppfer cells trigger nonalcoholic steatohepatitis development in diet-induced mouse model through tumor necrosis factor-α production. J Biol Chem. 2012;287(48):40161-40172. doi: https://doi.org/10.1074/jbc.M112.417014</mixed-citation></citation-alternatives></ref><ref id="cit32"><label>32</label><citation-alternatives><mixed-citation xml:lang="ru">Mirea AM, Tack CJ, Chavakis T, et al. IL-1 family cytokine pathways underlying NAFLD: Towards new treatment strategies. Trends Mol Med. 2018;24(5):458-471. doi: https://doi.org/10.1016/j.molmed.2018.03.005</mixed-citation><mixed-citation xml:lang="en">Mirea AM, Tack CJ, Chavakis T, et al. IL-1 family cytokine pathways underlying NAFLD: Towards new treatment strategies. Trends Mol Med. 2018;24(5):458-471. doi: https://doi.org/10.1016/j.molmed.2018.03.005</mixed-citation></citation-alternatives></ref><ref id="cit33"><label>33</label><citation-alternatives><mixed-citation xml:lang="ru">Odegaard JI, Chawla A. Alternative macrophage activation and metabolism. Annu Rev Pathol. 2011;6(1):275-297. doi: https://doi.org/10.1146/annurev-pathol-011110-130138</mixed-citation><mixed-citation xml:lang="en">Odegaard JI, Chawla A. Alternative macrophage activation and metabolism. Annu Rev Pathol. 2011;6(1):275-297. doi: https://doi.org/10.1146/annurev-pathol-011110-130138</mixed-citation></citation-alternatives></ref><ref id="cit34"><label>34</label><citation-alternatives><mixed-citation xml:lang="ru">Pradere J-P, Kluwe J, De Minicis S, et al. Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice. Hepatology. 2013;58(4):1461-1473. doi: https://doi.org/10.1002/hep.26429</mixed-citation><mixed-citation xml:lang="en">Pradere J-P, Kluwe J, De Minicis S, et al. Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice. Hepatology. 2013;58(4):1461-1473. doi: https://doi.org/10.1002/hep.26429</mixed-citation></citation-alternatives></ref><ref id="cit35"><label>35</label><citation-alternatives><mixed-citation xml:lang="ru">Mandal P, Pritchard MT, Nagy LE. Anti-inflammatory pathways and alcoholic liver disease: role of an adiponectin/interleukin-10/heme oxygenase-1 pathway. World J Gastroenterol. 2010;16(11):1330-1336. doi: https://doi.org/10.3748/wjg.v16.i11.1330</mixed-citation><mixed-citation xml:lang="en">Mandal P, Pritchard MT, Nagy LE. Anti-inflammatory pathways and alcoholic liver disease: role of an adiponectin/interleukin-10/heme oxygenase-1 pathway. World J Gastroenterol. 2010;16(11):1330-1336. doi: https://doi.org/10.3748/wjg.v16.i11.1330</mixed-citation></citation-alternatives></ref><ref id="cit36"><label>36</label><citation-alternatives><mixed-citation xml:lang="ru">Reneau J, Goldblatt M, Gould J, et al. Effect of adiposity on tissue-specific adiponectin secretion. PLoS One. 2018;13(6):e0198889. doi: https://doi.org/10.1371/journal.pone.0198889</mixed-citation><mixed-citation xml:lang="en">Reneau J, Goldblatt M, Gould J, et al. Effect of adiposity on tissue-specific adiponectin secretion. PLoS One. 2018;13(6):e0198889. doi: https://doi.org/10.1371/journal.pone.0198889</mixed-citation></citation-alternatives></ref><ref id="cit37"><label>37</label><citation-alternatives><mixed-citation xml:lang="ru">Kiechl S, Wittmann J, Giaccari A, et al. Blockade of receptor activator of nuclear factor-κB (RANKL) signaling improves hepatic insulin resistance and prevents development of diabetes mellitus. Nat Med. 2013;19(3):358-363. doi: https://doi.org/10.1038/nm.3084</mixed-citation><mixed-citation xml:lang="en">Kiechl S, Wittmann J, Giaccari A, et al. Blockade of receptor activator of nuclear factor-κB (RANKL) signaling improves hepatic insulin resistance and prevents development of diabetes mellitus. Nat Med. 2013;19(3):358-363. doi: https://doi.org/10.1038/nm.3084</mixed-citation></citation-alternatives></ref><ref id="cit38"><label>38</label><citation-alternatives><mixed-citation xml:lang="ru">Yang YM, Seki E. TNFα in Liver Fibrosis. Curr Pathobiol Rep. 2015;3(4):253-261. doi: https://doi.org/10.1007/s40139-015-0093-z</mixed-citation><mixed-citation xml:lang="en">Yang YM, Seki E. TNFα in Liver Fibrosis. Curr Pathobiol Rep. 2015;3(4):253-261. doi: https://doi.org/10.1007/s40139-015-0093-z</mixed-citation></citation-alternatives></ref><ref id="cit39"><label>39</label><citation-alternatives><mixed-citation xml:lang="ru">Fink LN, Costford SR, Lee YS, et al. Pro-inflammatory macrophages increase in skeletal muscle of high fat-fed mice and correlate with metabolic risk markers in humans: Muscle Macrophages in Obesity and Diabetes. Obesity (Silver Spring). 2014;22(3):747-757. doi: https://doi.org/10.1002/oby.20615</mixed-citation><mixed-citation xml:lang="en">Fink LN, Costford SR, Lee YS, et al. Pro-inflammatory macrophages increase in skeletal muscle of high fat-fed mice and correlate with metabolic risk markers in humans: Muscle Macrophages in Obesity and Diabetes. Obesity (Silver Spring). 2014;22(3):747-757. doi: https://doi.org/10.1002/oby.20615</mixed-citation></citation-alternatives></ref><ref id="cit40"><label>40</label><citation-alternatives><mixed-citation xml:lang="ru">Khan IM, Perrard XY, Brunner G, et al. Intermuscular and perimuscular fat expansion in obesity correlates with skeletal muscle T cell and macrophage infiltration and insulin resistance. Int J Obes (Lond). 2015;39(11):1607-1618. doi: https://doi.org/10.1038/ijo.2015.104</mixed-citation><mixed-citation xml:lang="en">Khan IM, Perrard XY, Brunner G, et al. Intermuscular and perimuscular fat expansion in obesity correlates with skeletal muscle T cell and macrophage infiltration and insulin resistance. Int J Obes (Lond). 2015;39(11):1607-1618. doi: https://doi.org/10.1038/ijo.2015.104</mixed-citation></citation-alternatives></ref><ref id="cit41"><label>41</label><citation-alternatives><mixed-citation xml:lang="ru">Ciaraldi TP, Ryan AJ, Mudaliar SR, Henry RR. Altered myokine secretion is an intrinsic property of skeletal muscle in type 2 diabetes. PLoS One. 2016;11(7):e0158209. doi: https://doi.org/10.1371/journal.pone.0158209</mixed-citation><mixed-citation xml:lang="en">Ciaraldi TP, Ryan AJ, Mudaliar SR, Henry RR. Altered myokine secretion is an intrinsic property of skeletal muscle in type 2 diabetes. PLoS One. 2016;11(7):e0158209. doi: https://doi.org/10.1371/journal.pone.0158209</mixed-citation></citation-alternatives></ref><ref id="cit42"><label>42</label><citation-alternatives><mixed-citation xml:lang="ru">Frisard MI, McMillan RP, Marchand J, et al. Toll-like receptor 4 modulates skeletal muscle substrate metabolism. Am J Physiol Metab. 2010;298(5):E988-E998. doi: https://doi.org/10.1152/ajpendo.00307.2009</mixed-citation><mixed-citation xml:lang="en">Frisard MI, McMillan RP, Marchand J, et al. Toll-like receptor 4 modulates skeletal muscle substrate metabolism. Am J Physiol Metab. 2010;298(5):E988-E998. doi: https://doi.org/10.1152/ajpendo.00307.2009</mixed-citation></citation-alternatives></ref><ref id="cit43"><label>43</label><citation-alternatives><mixed-citation xml:lang="ru">Shi H, Kokoeva MV, Inouye K, et al. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest. 2006;116(11):3015-3025. doi: https://doi.org/10.1172/JCI28898</mixed-citation><mixed-citation xml:lang="en">Shi H, Kokoeva MV, Inouye K, et al. TLR4 links innate immunity and fatty acid-induced insulin resistance. J Clin Invest. 2006;116(11):3015-3025. doi: https://doi.org/10.1172/JCI28898</mixed-citation></citation-alternatives></ref><ref id="cit44"><label>44</label><citation-alternatives><mixed-citation xml:lang="ru">Plomgaard P, Bouzakri K, Krogh-Madsen R, et al. Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. Diabetes. 2005;54(10):2939-2945. doi: https://doi.org/10.2337/diabetes.54.10.2939</mixed-citation><mixed-citation xml:lang="en">Plomgaard P, Bouzakri K, Krogh-Madsen R, et al. Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. Diabetes. 2005;54(10):2939-2945. doi: https://doi.org/10.2337/diabetes.54.10.2939</mixed-citation></citation-alternatives></ref><ref id="cit45"><label>45</label><citation-alternatives><mixed-citation xml:lang="ru">Mesinovic J, Zengin A, De Courten B, et al. Sarcopenia and type 2 diabetes mellitus: a bidirectional relationship. Diabetes, Metab Syndr Obes Targets Ther. 2019;12(4):1057-1072. doi: https://doi.org/10.2147/DMSO.S186600</mixed-citation><mixed-citation xml:lang="en">Mesinovic J, Zengin A, De Courten B, et al. Sarcopenia and type 2 diabetes mellitus: a bidirectional relationship. Diabetes, Metab Syndr Obes Targets Ther. 2019;12(4):1057-1072. doi: https://doi.org/10.2147/DMSO.S186600</mixed-citation></citation-alternatives></ref><ref id="cit46"><label>46</label><citation-alternatives><mixed-citation xml:lang="ru">Kirwan AM, Lenighan YM, O’Reilly ME, et al. Nutritional modulation of metabolic inflammation. Biochem Soc Trans. 2017;45(4):979-985. doi: https://doi.org/10.1042/bst20160465</mixed-citation><mixed-citation xml:lang="en">Kirwan AM, Lenighan YM, O’Reilly ME, et al. Nutritional modulation of metabolic inflammation. Biochem Soc Trans. 2017;45(4):979-985. doi: https://doi.org/10.1042/bst20160465</mixed-citation></citation-alternatives></ref><ref id="cit47"><label>47</label><citation-alternatives><mixed-citation xml:lang="ru">Song N, Li T. Regulation of NLRP3 Inflammasome by Phosphorylation. Front Immunol. 2018;9(4):1057-1072. doi: https://doi.org/10.3389/fimmu.2018.02305</mixed-citation><mixed-citation xml:lang="en">Song N, Li T. Regulation of NLRP3 Inflammasome by Phosphorylation. Front Immunol. 2018;9(4):1057-1072. doi: https://doi.org/10.3389/fimmu.2018.02305</mixed-citation></citation-alternatives></ref><ref id="cit48"><label>48</label><citation-alternatives><mixed-citation xml:lang="ru">Tschopp J, Schroder K. NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production? Nat Rev Immunol. 2010;10(3):210-215. doi: https://doi.org/10.1038/nri2725</mixed-citation><mixed-citation xml:lang="en">Tschopp J, Schroder K. NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production? Nat Rev Immunol. 2010;10(3):210-215. doi: https://doi.org/10.1038/nri2725</mixed-citation></citation-alternatives></ref><ref id="cit49"><label>49</label><citation-alternatives><mixed-citation xml:lang="ru">Henriksen EJ, Diamond-Stanic MK, Marchionne EM. Oxidative stress and the etiology of insulin resistance and type 2 diabetes. Free Radic Biol Med. 2011;51(5):993-999. doi: https://doi.org/10.1016/j.freeradbiomed.2010.12.005</mixed-citation><mixed-citation xml:lang="en">Henriksen EJ, Diamond-Stanic MK, Marchionne EM. Oxidative stress and the etiology of insulin resistance and type 2 diabetes. Free Radic Biol Med. 2011;51(5):993-999. doi: https://doi.org/10.1016/j.freeradbiomed.2010.12.005</mixed-citation></citation-alternatives></ref><ref id="cit50"><label>50</label><citation-alternatives><mixed-citation xml:lang="ru">Zatterale F, Longo M, Naderi J, et al. Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes. Front Physiol. 2020;10(4):1057-1072. doi: https://doi.org/10.3389/fphys.2019.01607</mixed-citation><mixed-citation xml:lang="en">Zatterale F, Longo M, Naderi J, et al. Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes. Front Physiol. 2020;10(4):1057-1072. doi: https://doi.org/10.3389/fphys.2019.01607</mixed-citation></citation-alternatives></ref><ref id="cit51"><label>51</label><citation-alternatives><mixed-citation xml:lang="ru">Manna P, Jain SK. Obesity, oxidative stress, adipose tissue dysfunction, and the associated health risks: Causes and therapeutic strategies. Metab Syndr Relat Disord. 2015;13(10):423-444. doi: https://doi.org/10.1089/met.2015.0095</mixed-citation><mixed-citation xml:lang="en">Manna P, Jain SK. Obesity, oxidative stress, adipose tissue dysfunction, and the associated health risks: Causes and therapeutic strategies. Metab Syndr Relat Disord. 2015;13(10):423-444. doi: https://doi.org/10.1089/met.2015.0095</mixed-citation></citation-alternatives></ref><ref id="cit52"><label>52</label><citation-alternatives><mixed-citation xml:lang="ru">Dludla PV, Nkambule BB, Jack B, et al. Inflammation and oxidative stress in an obese state and the protective effects of Gallic acid. Nutrients. 2018;11(1):23. doi: https://doi.org/10.3390/nu11010023</mixed-citation><mixed-citation xml:lang="en">Dludla PV, Nkambule BB, Jack B, et al. Inflammation and oxidative stress in an obese state and the protective effects of Gallic acid. Nutrients. 2018;11(1):23. doi: https://doi.org/10.3390/nu11010023</mixed-citation></citation-alternatives></ref><ref id="cit53"><label>53</label><citation-alternatives><mixed-citation xml:lang="ru">Stafeev IS, Vorotnikov AV, Ratner EI, et al. Latent inflammation and insulin resistance in adipose tissue. Int J Endocrinol. 2017;2017(4):1-12. doi: https://doi.org/10.1155/2017/5076732</mixed-citation><mixed-citation xml:lang="en">Stafeev IS, Vorotnikov AV, Ratner EI, et al. Latent inflammation and insulin resistance in adipose tissue. Int J Endocrinol. 2017;2017(4):1-12. doi: https://doi.org/10.1155/2017/5076732</mixed-citation></citation-alternatives></ref><ref id="cit54"><label>54</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang C, Luo X, Zhang D, et al. Hypoxic adipocytes induce macrophages to release inflammatory cytokines that render skeletal muscle cells insulin resistant. Biochem Biophys Res Commun. 2020;521(3):625-631. doi: https://doi.org/10.1016/j.bbrc.2019.10.162</mixed-citation><mixed-citation xml:lang="en">Zhang C, Luo X, Zhang D, et al. Hypoxic adipocytes induce macrophages to release inflammatory cytokines that render skeletal muscle cells insulin resistant. Biochem Biophys Res Commun. 2020;521(3):625-631. doi: https://doi.org/10.1016/j.bbrc.2019.10.162</mixed-citation></citation-alternatives></ref><ref id="cit55"><label>55</label><citation-alternatives><mixed-citation xml:lang="ru">Corrales P, Vidal-Puig A, Medina-Gomez G. PPARs and metabolic disorders associated with challenged adipose tissue plasticity. Int J Mol Sci. 2018;19(7):2124. doi: https://doi.org/10.3390/ijms19072124</mixed-citation><mixed-citation xml:lang="en">Corrales P, Vidal-Puig A, Medina-Gomez G. PPARs and metabolic disorders associated with challenged adipose tissue plasticity. Int J Mol Sci. 2018;19(7):2124. doi: https://doi.org/10.3390/ijms19072124</mixed-citation></citation-alternatives></ref><ref id="cit56"><label>56</label><citation-alternatives><mixed-citation xml:lang="ru">Wang H, Shen L, Sun X, et al. Adipose group 1 innate lymphoid cells promote adipose tissue fibrosis and diabetes in obesity. Nat Commun. 2019;10(1):3254. doi: https://doi.org/10.1038/s41467-019-11270-1</mixed-citation><mixed-citation xml:lang="en">Wang H, Shen L, Sun X, et al. Adipose group 1 innate lymphoid cells promote adipose tissue fibrosis and diabetes in obesity. Nat Commun. 2019;10(1):3254. doi: https://doi.org/10.1038/s41467-019-11270-1</mixed-citation></citation-alternatives></ref><ref id="cit57"><label>57</label><citation-alternatives><mixed-citation xml:lang="ru">Klose CSN, Artis D. Innate lymphoid cells control signaling circuits to regulate tissue-specific immunity. Cell Res. 2020;30(6):475-491. doi: https://doi.org/10.1038/s41422-020-0323-8</mixed-citation><mixed-citation xml:lang="en">Klose CSN, Artis D. Innate lymphoid cells control signaling circuits to regulate tissue-specific immunity. Cell Res. 2020;30(6):475-491. doi: https://doi.org/10.1038/s41422-020-0323-8</mixed-citation></citation-alternatives></ref><ref id="cit58"><label>58</label><citation-alternatives><mixed-citation xml:lang="ru">Croce S, Avanzini MA, Regalbuto C, et al. Adipose tissue immunomodulation and Treg/Th17 imbalance in the impaired glucose metabolism of children with obesity. Children (Basel). 2021;8(7):554. doi: https://doi.org/10.3390/children8070554</mixed-citation><mixed-citation xml:lang="en">Croce S, Avanzini MA, Regalbuto C, et al. Adipose tissue immunomodulation and Treg/Th17 imbalance in the impaired glucose metabolism of children with obesity. Children (Basel). 2021;8(7):554. doi: https://doi.org/10.3390/children8070554</mixed-citation></citation-alternatives></ref><ref id="cit59"><label>59</label><citation-alternatives><mixed-citation xml:lang="ru">Chakarov S, Blériot C, Ginhoux F. Role of adipose tissue macrophages in obesity-related disorders. J Exp Med. 2022;219(7):1-12. doi: https://doi.org/10.1084/jem.20211948</mixed-citation><mixed-citation xml:lang="en">Chakarov S, Blériot C, Ginhoux F. Role of adipose tissue macrophages in obesity-related disorders. J Exp Med. 2022;219(7):1-12. doi: https://doi.org/10.1084/jem.20211948</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
