perinatologyРоссийский вестник перинатологии и педиатрииRossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics)1027-40652500-2228Ltd. “The National Academy of Pediatric Science and Innovation”10.21508/1027-4065-2025-70-4-22-28perinatology-2227Research ArticleОБЗОРЫ ЛИТЕРАТУРЫLITERATURE REVIEWSВлияние характера питания на формирование воспалительного процесса кишечникаInfluence of the nutritional model on the formation of the inflammatory bowel processhttps://orcid.org/0000-0002-4733-3262НалетовА. В.NalyotovA. V.

Налетов Андрей Васильевич — д.м.н., проф., зав. кафедрой педиатрии № 2; детский специалист гастроэнтеролог Министерства здравоохранения Донецкой Народной Республики

283003, Донецкая Народная Республика, г. Донецк, пр. Ильича, 16

283003, Donetsk

https://orcid.org/0000-0001-7308-7280ХавкинА. И.KhavkinA. I.

Хавкин Анатолий Ильич — д.м.н., проф., руководитель Московского областного центра детской гастроэнтерологии и гепатологии; проф. кафедры педиатрии с курсом детских хирургических болезней Медицинского института 

115093, г. Москва, ул. Большая Серпуховская, д. 62

115093, Moscow

308015, Belgorod

МацынинаМ. А.MatsyninaM. A.

Мацынина Мария Александровна — к.м.н., доцент кафедры педиатрии и неонатологии

191015, г. Санкт-Петербург, ул. Кирочная, д.41

191015, Saint-Petersburg

ФГБОУ ВО «Донецкий государственный медицинский университет имени М. Горького» Минздрава РоссииРоссияGorky Donetsk State Medical UniversityRussian FederationГБУЗ МО «Научно-исследовательский клинический институт детства Минздрава Московской области»; ФГАОУ ВО «Белгородский государственный национальный исследовательский университет»РоссияResearch Clinical Institute of Childhood; Belgorod National Research UniversityRussian FederationФГБОУ ВО «Северо-Западный государственный медицинский университет имени И.И. Мечникова» Минздрава РоссииРоссияMechnikov North-Western State Medical UniversityRussian Federation20252808202570422–28Copyright © Ltd. “The National Academy of Pediatric Science and Innovation”, 20252025Ltd. “The National Academy of Pediatric Science and Innovation”Ltd. “The National Academy of Pediatric Science and Innovation”https://www.ped-perinatology.ru/jour/about/submissions#copyrightNoticehttps://www.ped-perinatology.ru/jour/article/view/2227

Возросшая заболеваемость воспалительными заболеваниями кишечника тесно связана с переходом населения планеты на западную модель питания, которая характеризуется высоким потреблением переработанных и рафинированных продуктов, красного мяса, сахара, насыщенных и транс-жиров и сниженным потреблением фруктов, овощей и пищевых волокон. Так, диета с высоким содержанием сахаров способствует развитию воспалительных заболеваний кишечника, вызывая существенные изменения в составе кишечного микробиома и иммунных реакций в слизистой оболочке, а также повышенному образованию активных форм кислорода, что нарушает функцию кишечного барьера и способствует воспалению. Диета с высоким содержанием жиров изменяет разнообразие кишечной микробиоты за счет колонизации кишечника адгезивно-инвазивными штаммами бактерий и вызывает воспаление низкой степени интенсивности в стенке кишки, воздействуя на функцию белков плотных контактов слизистой оболочки, нарушая барьерную функцию кишечника. Полученные результаты подчеркивают необходимость проведения целенаправленных мероприятий в области питания, которые принесут пользу пациентам с воспалительными заболеваниями кишечника. Интеграция диетотерапии с традиционным медикаментозным лечением может оптимизировать комплексный подход к лечению пациентов с воспалительными заболеваниями кишечника.

The increased incidence of inflammatory bowel diseases is closely related to the transition of the world’s population to the Western model of nutrition, which is characterized by high consumption of processed and refined foods, red meat, sugar, saturated and trans fats, and reduced consumption of fruits, vegetables and dietary fiber. Thus, a diet high in sugars contributes to the development of inflammatory bowel diseases, causing significant changes in the composition of the intestinal microbiome and immune responses in the mucous membrane, as well as increased formation of reactive oxygen species, which disrupts the function of the intestinal barrier and promotes inflammation. A high-fat diet alters the diversity of the intestinal microbiota due to colonization of the intestine by adhesive-invasive bacterial strains and causes low-intensity inflammation in the intestinal wall, affecting the function of proteins of the dense contacts of the mucous membrane, disrupting the barrier function of the intestine. The results obtained emphasize the need for targeted nutrition interventions that will benefit patients with inflammatory bowel diseases. The integration of diet therapy with traditional drug treatment can optimize a comprehensive approach to the treatment of patients with inflammatory bowel diseases.

диетотерапиявоспалительные заболевания кишечниказападная модель питанияжирысахараdiet therapyinflammatory bowel diseasesWestern model of nutritionfatssugarsReferencesХавкин А.И., Налетов А.В., Шумилов П.В., Ситкин С.И. Эффективность пищевых волокон при воспалительных заболеваниях кишечника. Вопросы детской диетологии. 2024; 22 (2): 74–81.Khavkin A.I., Nalyotov A.V., Shumilov P.V., Sitkin S.I. The effectiveness of dietary fiber in inflammatory bowel disease. Voprosy detskoj dietologii. 2024; 22 (2): 74–81. (in Russ)]. DOI: 10.20953/1727–5784–2024–2–74–81Налетов А.В., Хавкин А.И., Мацынин А.Н. Сухофрукты — важный компонент диетотерапии. Педиатрическая фармакология. 2024; 21 (5): 462–467.Nalyotov AV, Khavkin AI, Matsynin AN. Dried fruits are an important component of diet therapy. Pediatricheskaja farmakologija. 2024; 21 (5): 462–467. (in Russ)]. DOI: 10.15690/pf.v21i5.2789Хавкин А.И., Налетов А.В., Шумилов П.В., Мацынин А.Н., Ситкин С.И. Ультрапереработанные продукты и микробиота кишечника. Вопросы детской диетологии. 2024; 22 (5): 79–86.Khavkin A.I., Nalyotov A.V., Shumilov P.V., Matsynin A.N., Sitkin S.I. Ultra-processed foods and gut microbiome. Voprosy detskoj dietologii. 2024; 22 (5): 79–86. (in Russ)]. DOI: 10.20953/1727–5784–2024–5–79–86Хавкин А.И., Налетов А.В., Шумилов П.В., Ситкин С.И., Марченко Н.А. Диетические аспекты лечения воспалительных заболеваний кишечника. Вопросы детской диетологии. 2024; 22 (1): 51–62.Khavkin AI, Nalyotov A.V., Shumilov P.V., Sitkin S.I., Marchenko N.A. Dietary aspects in the treatment of inflammatory bowel disease. Voprosy detskoj dietologii. 2024; 22 (1): 51–62. (in Russ). DOI: 10.20953/1727–5784–2024–1–51–62Хавкин А.И., Налетов А.В., Куропятник П.И. Фрукты и их влияние на состояние кишечной микробиоты и моторику кишечника. Вопросы диетологии. 2024; 14 (3): 49–56.Khavkin A.I., Nalyotov A.V., Kuropyatnik P.I. Fruits and their effect on the state of the intestinal microbiota and intestinal motility. Voprosy dietologii. 2024; 14 (3): 49– 56. (in Russ)]. DOI: 10.20953/2224–5448–2024–3–49–56Камалова А.А., Сафина Э.Р., Низамова Р.А., Зайнетдинова М.Ш., Квитко Э.М. Питание при воспалительных заболеваниях кишечника у детей. Рос вестн перинатол и педиатр. 2020; 65: (5): 145–151Kamalova A.A., Safina E.R., Nizamova R.A., Zaynetdinova M.Sh., Kvitko E.M. Nutrition of children with inflammatory bowel disease. Ros Vestn Perinatol i Pediatr. 2020; 65: (5): 145–151 (in Russ)]. DOI: 10.21508/1027–4065–2020–65–5–145–151Khalili H., Chan S., Lochhead P., Ananthakrishnan A.N., Hart A.R. The role of diet in the aetiopathogenesis of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2018; 15: 525–535. DOI: 10.1038/s41575–018–0022–9Khalili H., Chan S., Lochhead P., Ananthakrishnan A.N., Hart A.R. The role of diet in the aetiopathogenesis of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2018; 15: 525–535. DOI: 10.1038/s41575–018–0022–9Камалова А.А., Сафина Э.Р., Гарина Г.А., Гайфутдинова А.Р. Практическое руководство ESPEN: клиническое питание при воспалительных заболеваниях кишечника. Практическая медицина. 2021; 19 (5): 67–74.Kamalova A.A, Safina E.R, Garina G.A, Gayfutdinova A.R. ESPEN practical guideline: Clinical Nutrition in inflammatory bowel disease. Prakticheskaja medicina. 2021; 19 (5): 67–74. (in Russ)]Hou J.K., Abraham B., El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol. 2011; 106: 563–573. DOI: 10.1038/ajg.2011.44Hou J.K., Abraham B., El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol. 2011; 106: 563–573. DOI: 10.1038/ajg.2011.44Witek K., Wydra K., Filip M.A. high-sugar diet consumption, metabolism and health impacts with a focus on the development of substance use disorder: A narrative review. Nutrients. 2022; 14: 2940. DOI: 10.3390/nu14142940Witek K., Wydra K., Filip M.A. high-sugar diet consumption, metabolism and health impacts with a focus on the development of substance use disorder: A narrative review. Nutrients. 2022; 14: 2940. DOI: 10.3390/nu14142940Pacheco L.S., Tobias D.K., Li Y., Bhupathiraju S.N., Willett W.C., Ludwig D.S., et al. Sugar-sweetened or artificially-sweetened beverage consumption, physical activity, and risk of cardiovascular disease in adults: a prospective cohort study. Am J Clin Nutr. 2024; 119: 669–681. DOI: 10.1016/j.ajcnut.2024.01.001Pacheco L.S., Tobias D.K., Li Y., Bhupathiraju S.N., Willett W.C., Ludwig D.S., et al. Sugar-sweetened or artificially-sweetened beverage consumption, physical activity, and risk of cardiovascular disease in adults: a prospective cohort study. Am J Clin Nutr. 2024; 119: 669–681. DOI: 10.1016/j.ajcnut.2024.01.001Basson A.R., Katz J., Singh S., Celio F., Cominelli F., Rodriguez-Palacios A. Sweets and inflammatory bowel disease: patients favor artificial sweeteners and diet foods/drinks over table sugar and consume less fruits/ vegetables. Inflamm Bowel Dis. 2023; 29: 1751–1759. DOI: 10.1093/ibd/izac272Basson A.R., Katz J., Singh S., Celio F., Cominelli F., Rodriguez-Palacios A. Sweets and inflammatory bowel disease: patients favor artificial sweeteners and diet foods/drinks over table sugar and consume less fruits/ vegetables. Inflamm Bowel Dis. 2023; 29: 1751–1759. DOI: 10.1093/ibd/izac272Racine A., Carbonnel F., Chan S.S., Hart A.R., Bueno-deMesquita H.B., Oldenburg B., et al. Dietary patterns and risk of inflammatory bowel disease in europe: results from the EPIC study. Inflammation Bowel Dis. 2016; 22: 345–354. DOI: 10.1097/MIB.0000000000000638Racine A., Carbonnel F., Chan S.S., Hart A.R., Bueno-deMesquita H.B., Oldenburg B., et al. Dietary patterns and risk of inflammatory bowel disease in europe: results from the EPIC study. Inflammation Bowel Dis. 2016; 22: 345–354. DOI: 10.1097/MIB.0000000000000638Fu T., Chen H., Chen X., Sun Y., Xie Y., Deng M., et al. Sugarsweetened beverages, artificially sweetened beverages and natural juices and risk of inflammatory bowel disease: a cohort study of 121,490 participants. Aliment Pharmacol Ther. 2022; 56: 1018–1029. DOI: 10.1111/apt.17149Fu T., Chen H., Chen X., Sun Y., Xie Y., Deng M., et al. Sugarsweetened beverages, artificially sweetened beverages and natural juices and risk of inflammatory bowel disease: a cohort study of 121,490 participants. Aliment Pharmacol Ther. 2022; 56: 1018–1029. DOI: 10.1111/apt.17149Bischoff S.C., Kaden-Volynets V., Filipe Rosa L., Guseva D., Seethaler B. Regulation of the gut barrier by carbohydrates from diet — Underlying mechanisms and possible clinical implications. Int J OF Med Microbiol. 2021; 311: 151499. DOI: 10.1016/j.ijmm.2021.151499Bischoff S.C., Kaden-Volynets V., Filipe Rosa L., Guseva D., Seethaler B. Regulation of the gut barrier by carbohydrates from diet — Underlying mechanisms and possible clinical implications. Int J OF Med Microbiol. 2021; 311: 151499. DOI: 10.1016/j.ijmm.2021.151499Khan S., Waliullah S., Godfrey V., Khan M., Ramachandran R.A., Cantarel B.L., et al. Dietary simple sugars alter microbial ecology in the gut and promote colitis in mice. Sci Trans Med. 2020; 12: eaay6218. DOI: 10.1126/scitranslmed.aay6218Khan S., Waliullah S., Godfrey V., Khan M., Ramachandran R.A., Cantarel B.L., et al. Dietary simple sugars alter microbial ecology in the gut and promote colitis in mice. Sci Trans Med. 2020; 12: eaay6218. DOI: 10.1126/scitranslmed.aay6218Kim S., Shin Y.C., Kim T.Y., Kim Y., Lee Y.S., Lee S.H., et al. Mucin degrader Akkermansia muciniphila accelerates intestinal stem cell-mediated epithelial development. Gut Microbes. 2021; 13: 1–20. DOI: 10.1080/19490976.2021.1892441Kim S., Shin Y.C., Kim T.Y., Kim Y., Lee Y.S., Lee S.H., et al. Mucin degrader Akkermansia muciniphila accelerates intestinal stem cell-mediated epithelial development. Gut Microbes. 2021; 13: 1–20. DOI: 10.1080/19490976.2021.1892441Ashrafian F., Behrouzi A., Shahriary A., Ahmadi Badi S., Davari M., Khatami S., et al. Comparative study of effect of Akkermansia muciniphila and its extracellular vesicles on toll-like receptors and tight junction. Gastroenterol Hepatol bed to bench. 2019; 12: 163–168Ashrafian F., Behrouzi A., Shahriary A., Ahmadi Badi S., Davari M., Khatami S., et al. Comparative study of effect of Akkermansia muciniphila and its extracellular vesicles on toll-like receptors and tight junction. Gastroenterol Hepatol bed to bench. 2019; 12: 163–168Montrose D.C., Nishiguchi R., Basu S., Staab H.A., Zhou X.K., Wang H., et al. Dietary fructose alters the composition, localization, and metabolism of gut microbiota in association with worsening colitis. Cell Mol Gastroenterol Hepatol. 2021; 11: 525–550. DOI: 10.1016/j.jcmgh.2020.09.008Montrose D.C., Nishiguchi R., Basu S., Staab H.A., Zhou X.K., Wang H., et al. Dietary fructose alters the composition, localization, and metabolism of gut microbiota in association with worsening colitis. Cell Mol Gastroenterol Hepatol. 2021; 11: 525–550. DOI: 10.1016/j.jcmgh.2020.09.008Beisner J., Gonzalez-Granda A., Basrai M., DammsMaChado A., Bischoff S.C. Fructose-induced intestinal microbiota shift following two types of short-term highfructose dietary phases. Nutrients. 2020; 12: 3444. DOI: 10.3390/nu12113444Beisner J., Gonzalez-Granda A., Basrai M., DammsMaChado A., Bischoff S.C. Fructose-induced intestinal microbiota shift following two types of short-term highfructose dietary phases. Nutrients. 2020; 12: 3444. DOI: 10.3390/nu12113444Laffin M., Fedorak R., Zalasky A., Park H., Gill A., Agrawal A., et al. High-sugar diet rapidly enhances susceptibility to colitis via depletion of luminal short-chain fatty acids in mice. Sci Rep. 2019; 9: 12294. DOI: 10.1038/s41598–019–48749–2Laffin M., Fedorak R., Zalasky A., Park H., Gill A., Agrawal A., et al. High-sugar diet rapidly enhances susceptibility to colitis via depletion of luminal short-chain fatty acids in mice. Sci Rep. 2019; 9: 12294. DOI: 10.1038/s41598–019–48749–2Wang T., Yan H., Lu Y., Li X., Wang X., Shan Y., et al. Anti-obesity effect of Lactobacillus rhamnosus LS-8 and Lactobacillus crustorum MN047 on high-fat and high-fructose diet mice base on inflammatory response alleviation and gut microbiota regulation. Eur J Nutr. 2020; 59: 2709–2728. DOI: 10.1007/s00394–019–02117–yWang T., Yan H., Lu Y., Li X., Wang X., Shan Y., et al. Anti-obesity effect of Lactobacillus rhamnosus LS-8 and Lactobacillus crustorum MN047 on high-fat and high-fructose diet mice base on inflammatory response alleviation and gut microbiota regulation. Eur J Nutr. 2020; 59: 2709–2728. DOI: 10.1007/s00394–019–02117–yZhou M., Liu X., He J., Xu X., Ju C., Lou Sh., et al. High-fructose corn syrup aggravates colitis via microbiota dysbiosis-mediated Th17/Treg imbalance. Clin Sci (London England: 1979). 2023; 137: 1619–1635. DOI: 10.1042/CS20230788Zhou M., Liu X., He J., Xu X., Ju C., Lou Sh., et al. High-fructose corn syrup aggravates colitis via microbiota dysbiosis-mediated Th17/Treg imbalance. Clin Sci (London England: 1979). 2023; 137: 1619–1635. DOI: 10.1042/CS20230788Shon W.J., Jung M.H., Kim Y., Kang G.H., Choi E.Y., Shin D.M. Sugar-sweetened beverages exacerbate highfat diet-induced inflammatory bowel disease by altering the gut microbiome. J Nutr Biochem. 2023; 113: 109254. DOI: 10.1016/j.jnutbio.2022.109254Shon W.J., Jung M.H., Kim Y., Kang G.H., Choi E.Y., Shin D.M. Sugar-sweetened beverages exacerbate highfat diet-induced inflammatory bowel disease by altering the gut microbiome. J Nutr Biochem. 2023; 113: 109254. DOI: 10.1016/j.jnutbio.2022.109254Cho Y.E., Kim D.K., Seo W., Gao B., Yoo S.H., Song B.J. Fructose promotes leaky gut, endotoxemia, and liver fibrosis through ethanol-inducible cytochrome P450– 2E1–mediated oxidative and nitrative stress. Hepatology. 2021; 73: 2180–2195. DOI: 10.1002/hep.30652Cho Y.E., Kim D.K., Seo W., Gao B., Yoo S.H., Song B.J. Fructose promotes leaky gut, endotoxemia, and liver fibrosis through ethanol-inducible cytochrome P450– 2E1–mediated oxidative and nitrative stress. Hepatology. 2021; 73: 2180–2195. DOI: 10.1002/hep.30652Song G., Gan Q., Qi W., Wang Y., Xu M., Li Y. Fructose stimulated colonic arginine and proline metabolism dysbiosis, altered microbiota and aggravated intestinal barrier dysfunction in DSS-induced colitis rats. Nutrients. 2023; 15: 782. DOI: 10.3390/nu15030782Song G., Gan Q., Qi W., Wang Y., Xu M., Li Y. Fructose stimulated colonic arginine and proline metabolism dysbiosis, altered microbiota and aggravated intestinal barrier dysfunction in DSS-induced colitis rats. Nutrients. 2023; 15: 782. DOI: 10.3390/nu15030782Burr A., Ji J., Ozler K., Mentrup H.L., Eskiocak O., Yueh B., et al. Excess dietary sugar alters colonocyte metabolism and impairs the proliferative response to damage. Cell Mol Gastroenterol Hepatol. 2023; 16: 287–316. DOI: 10.1016/j.jcmgh.2023.05.001Burr A., Ji J., Ozler K., Mentrup H.L., Eskiocak O., Yueh B., et al. Excess dietary sugar alters colonocyte metabolism and impairs the proliferative response to damage. Cell Mol Gastroenterol Hepatol. 2023; 16: 287–316. DOI: 10.1016/j.jcmgh.2023.05.001Zhang D., Jin W., Wu R., Li J., Park S.A., Tu E., et al. High glucose intake exacerbates autoimmunity through reactive-oxygen-species-mediated TGF-b Cytokine activation. Immunity. 2019; 51: 671–681.e5. DOI: 10.1016/j.immuni.2019.08.001Zhang D., Jin W., Wu R., Li J., Park S.A., Tu E., et al. High glucose intake exacerbates autoimmunity through reactive-oxygen-species-mediated TGF-b Cytokine activation. Immunity. 2019; 51: 671–681.e5. DOI: 10.1016/j.immuni.2019.08.001Tan J., Ni D., Wali J.A., Cox D.A., Pinget G.V., Taitz J., et al. Dietary carbohydrate, particularly glucose, drives B cell lymphopoiesis and function. iScience. 2021; 24: 102835. DOI: 10.1016/j.isci.2021.102835Tan J., Ni D., Wali J.A., Cox D.A., Pinget G.V., Taitz J., et al. Dietary carbohydrate, particularly glucose, drives B cell lymphopoiesis and function. iScience. 2021; 24: 102835. DOI: 10.1016/j.isci.2021.102835Jaiswal N., Agrawal S., Agrawal A. High fructose-induced metabolic changes enhance inflammation in human dendritic cells. Clin Exp Immunol. 2019; 197: 237–249. DOI: 10.1111/cei.13299Jaiswal N., Agrawal S., Agrawal A. High fructose-induced metabolic changes enhance inflammation in human dendritic cells. Clin Exp Immunol. 2019; 197: 237–249. DOI: 10.1111/cei.13299Jones N., Blagih J., Zani F., Rees A., Hill D.G., Jenkins B.J., et al. Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPSinduced inflammation. Nat Commun. 2021; 12: 1209. DOI: 10.1038/s41467–021–21461–4Jones N., Blagih J., Zani F., Rees A., Hill D.G., Jenkins B.J., et al. Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPSinduced inflammation. Nat Commun. 2021; 12: 1209. DOI: 10.1038/s41467–021–21461–4Buttó L.F., Haller D. Dysbiosis in intestinal inflammation: Cause or consequence. Int J Med Microbiol. 2016; 306: 302– 309. DOI: 10.1016/j.ijmm.2016.02.010Buttó L.F., Haller D. Dysbiosis in intestinal inflammation: Cause or consequence. Int J Med Microbiol. 2016; 306: 302– 309. DOI: 10.1016/j.ijmm.2016.02.010Wang L., Ji T., Yuan Y., Fu H., Wang Y., Tian S., et al. Highfructose corn syrup promotes proinflammatory Macrophage activation via ROS-mediated NF-kB signaling and exacerbates colitis in mice. Int Immunopharmacol. 2022; 109: 108814. DOI: 10.1016/j.intimp.2022.108814Wang L., Ji T., Yuan Y., Fu H., Wang Y., Tian S., et al. Highfructose corn syrup promotes proinflammatory Macrophage activation via ROS-mediated NF-kB signaling and exacerbates colitis in mice. Int Immunopharmacol. 2022; 109: 108814. DOI: 10.1016/j.intimp.2022.108814Velázquez K.T., Enos R.T., Bader J.E., Sougiannis A.T., Carson M.S., Chatzistamou I., et al. Prolonged high-fat-diet feeding promotes non-alcoholic fatty liver disease and alters gut microbiota in mice. World J Hepatol. 2019; 11: 619–637. DOI: 10.4254/wjh.v11.i8.619Velázquez K.T., Enos R.T., Bader J.E., Sougiannis A.T., Carson M.S., Chatzistamou I., et al. Prolonged high-fat-diet feeding promotes non-alcoholic fatty liver disease and alters gut microbiota in mice. World J Hepatol. 2019; 11: 619–637. DOI: 10.4254/wjh.v11.i8.619Arora T., Bäckhed F. The gut microbiota and metabolic disease: current understanding and future perspectives. J Intern Med. 2016; 280: 339–349. DOI: 10.1111/joim.2016.280.issue-4Arora T., Bäckhed F. The gut microbiota and metabolic disease: current understanding and future perspectives. J Intern Med. 2016; 280: 339–349. DOI: 10.1111/joim.2016.280.issue-4Dang Y., Ma C., Chen K., Chen Y., Jiang M., Hu K., et al. The effects of a high-fat diet on inflammatory bowel disease. Biomolecules. 2023; 13: 905. DOI: 10.3390/biom13060905Dang Y., Ma C., Chen K., Chen Y., Jiang M., Hu K., et al. The effects of a high-fat diet on inflammatory bowel disease. Biomolecules. 2023; 13: 905. DOI: 10.3390/biom13060905Martinez-Medina M., Denizot J., Dreux N., Robin F., Billard E., Bonnet R., et al. Western diet induces dysbiosis with increased E coli in CEABAC10 mice, alters host barrier function favouring AIEC colonisation. Gut. 2014; 63: 116–124. DOI: 10.1136/gutjnl-2012–304119Martinez-Medina M., Denizot J., Dreux N., Robin F., Billard E., Bonnet R., et al. Western diet induces dysbiosis with increased E coli in CEABAC10 mice, alters host barrier function favouring AIEC colonisation. Gut. 2014; 63: 116–124. DOI: 10.1136/gutjnl-2012–304119Haghikia A., Jörg S., Duscha A., Berg J., Manzel A., Waschbisch A., et al. Dietary fatty acids directly impact central nervous system autoimmunity via the small intestine. Immunity. 2015; 43: 817–829. DOI: 10.1016/j.immuni.2015.09.007Haghikia A., Jörg S., Duscha A., Berg J., Manzel A., Waschbisch A., et al. Dietary fatty acids directly impact central nervous system autoimmunity via the small intestine. Immunity. 2015; 43: 817–829. DOI: 10.1016/j.immuni.2015.09.007Xie R., Sun Y., Wu J., Huang S., Jin G., Guo Z., et al. Maternal high fat diet alters gut microbiota of offspring and exacerbates DSS-induced colitis in adulthood. Front Immunol. 2018; 9: 2608. DOI: 10.3389/fimmu.2018.02608Xie R., Sun Y., Wu J., Huang S., Jin G., Guo Z., et al. Maternal high fat diet alters gut microbiota of offspring and exacerbates DSS-induced colitis in adulthood. Front Immunol. 2018; 9: 2608. DOI: 10.3389/fimmu.2018.02608Kirpich I.A., Feng W., Wang Y., Liu Y., Barker D.F., Barve Sh.S., et al. The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease. Alcohol Clin Exp Res. 2012; 36: 835–846. DOI: 10.1111/j.1530–0277.2011.01673Kirpich I.A., Feng W., Wang Y., Liu Y., Barker D.F., Barve Sh.S., et al. The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease. Alcohol Clin Exp Res. 2012; 36: 835–846. DOI: 10.1111/j.1530–0277.2011.01673Murakami Y., Tanabe S., Suzuki T. High-fat diet-induced intestinal hyperpermeability is associated with increased bile acids in the large intestine of mice. J Food Sci. 2016; 81: H216– 22. DOI: 10.1111/jfds.2016.81.issue-1Murakami Y., Tanabe S., Suzuki T. High-fat diet-induced intestinal hyperpermeability is associated with increased bile acids in the large intestine of mice. J Food Sci. 2016; 81: H216– 22. DOI: 10.1111/jfds.2016.81.issue-1

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