urmjУральский медицинский журналUral Medical Journal2949-4389Ural State Medical University10.52420/umj.24.4.7AVWQFNurmj-1929Research ArticleОригинальные статьи | Original articlesOriginal articlesАнализ локализации коннексина 36 в эндокринной части ткани поджелудочной железы при моделировании различных подтипов гестационного сахарного диабета у крысAnalysis of the Localization of Connexin 36 in the Endocrine Part of Pancreatic Tissue in Modeling Various Subtypes of Gestational Diabetes Mellitus in Ratshttps://orcid.org/0000-0003-4874-7835ВолковаН. И.VolkovaN. I.

Волкова Наталья Ивановна — доктор медицинских наук, профессор, заведующий кафедрой внутренних болезней № 3.

Ростов-на-Дону

Natalya I. Volkova — Doctor of Sciences (Medicine), Professor, Head of the Department of Internal Medicine No. 3, Rostov State Medical University.

Rostov-on-Don

volkova_n_i@mail.ruhttps://orcid.org/0000-0002-8690-681XДавиденкоИ. Ю.DavidenkoI. Yu.

Давиденко Илья Юрьевич — кандидат медицинских наук, доцент, доцент кафедры внутренних болезней № 3.

Ростов-на-Дону

Ilya Yu. Davidenko — Candidate of Sciences (Medicine), Associate Professor, Associate Professor of the Department of Internal Medicine No. 3, Rostov State Medical University.

Rostov-on-Don

Davidenko.iu@gmail.comhttps://orcid.org/0000-0002-1929-6345ГоловинС. Н.GolovinS. N.

Головин Сергей Николаевич — старший преподаватель кафедры «Биоинженерия», факультет «Биоинженерия и ветеринарная медицина».

Ростов-на-Дону

Sergey N. Golovin — Senior Lecturer of the Department of Bioengineering, Faculty of Bioengineering and Veterinary Medicine, Don State Technical University.

Rostov-on-Don

labbiobez@yandex.ruhttps://orcid.org/0000-0001-9350-7588ШебекоС. К.ShebekoS. K.

Шебеко Сергей Константинович — доктор фармацевтических наук, профессор, заведующий кафедрой «Биотехнические и медицинские системы и технологии», факультет «Биоинженерия и ветеринарная медицина».

Ростов-на-Дону

Sergey K. Shebeko — Doctor of Sciences (Pharmaceutics), Professor, Head of the Department of Biotechnical and Medical Systems and Technologies, Faculty of Bioengineering and Veterinary Medicine, Don State Technical University.

Rostov-on-Don

shebeko_sk@mail.ruhttps://orcid.org/0000-0003-4703-1616КириченкоЕ. Ю.KirichenkoE. Yu.

Кириченко Евгения Юрьевна — доктор медицинских наук, профессор, профессор кафедры «Биоинженерия», факультет «Биоинженерия и ветеринарная медицина».

Ростов-на-Дону

Evgenia Yu. Kirichenko — Doctor of Sciences (Medicine), Professor, Professor of the Department of Bioengineering, Faculty of Bioengineering and Veterinary Medicine, Don State Technical University.

Rostov-on-Don

kiriche.evgeniya@yandex.ruРостовский государственной медицинский университетРоссияRostov State Medical UniversityRussian FederationДонской государственный технический университетРоссияDon State Technical UniversityRussian Federation2025270820252447–18Copyright © Волкова Н.И., Давиденко И.Ю., Головин С.Н., Шебеко С.К., Кириченко Е.Ю., 20252025Волкова Н.И., Давиденко И.Ю., Головин С.Н., Шебеко С.К., Кириченко Е.Ю.Volkova N.I., Davidenko I.Y., Golovin S.N., Shebeko S.K., Kirichenko E.Y.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.umjusmu.ru/jour/article/view/1929Введение

Введение. Согласно современным представлениям, гестационный сахарный диабет (ГСД) является гетерогенным заболеванием, включающим в себя несколько подтипов: с инсулинорезистентностью (ИР) и дисфункцией β-клеток поджелудочной железы. Выявлено, что клетки поджелудочной железы экспрессируют белок щелевых контактов — коннексин 36, — а содержащие этот белок щелевые контакты в норме координируют пульсирующую динамику Ca 2+ и высвобождение инсулина; нарушение этого процесса может являться одним из патогенетических механизмов ГСД.

Цель работы — изучить распределение коннексина 36 в ткани поджелудочной железы при моделировании различных подтипов ГСД у крыс.

Материалы и методы

Материалы и методы. Проведено проспективное исследование на белых нелинейных крысах: 50 самках и 15 самцах. Крысы-самки после подтверждения были разделены на 3 группы: I — 15 беременных крыс (контрольная); II — 12 беременных крыс (модель подтипа с дисфункцией β-клеток поджелудочной железы); III — 12 беременных крыс (модель подтипа с ИР). Всем крысам проведено иммуногистохимическое исследование на парафиновых срезах с использованием первичных кроличьих поликлональных антител к коннексину 36 (Invitrogen, США).

Результаты

Результаты. При исследовании образцов поджелудочной железы группы III отмечено резкое снижение уровня экспрессии коннексина 36. В образцах группы II выявлено, что в эндокринных участках железы мембранная реакция между клетками отрицательна. При морфометрическом исследовании определено достоверное снижение как удельной плотности иммунных комплексов, так и их средней площади в группах III и II (p < 0,050).

Обсуждение

Обсуждение. Проведенное иммуногистохимическое исследование распределения коннексина 36 свидетельствует о снижении электротонической сообщаемости посредством щелевых контактов как в модели подтипа ГСД с преобладающей ИР, так и дисфункцией β-клеток поджелудочной железы.

Заключение

Заключение. Полученные результаты позволяют предположить, что редукция коннексина 36 может сопровождать развитие патогенетических механизмов ГСД.

Introduction

Introduction. Gestational diabetes mellitus (GDM) is heterogeneous disease that includes several subtypes: subtype with predominant insulin resistance (IR) and subtype with predominant dysfunction of β-cell of pancreas. It was revealed that pancreatic cells express a gap junction protein, connexin 36, and gap junctions containing this protein normally coordinate the pulsating dynamics of Ca 2+ and the release of insulin, and disruption of this process may be one of the pathogenetic mechanisms of GDM.

The aim of work was to study distribution of connexin 36 in pancreatic tissue when modeling various subtypes of GDM in rats.

Materials and methods

Materials and methods. Prospective study was conducted on white nonlinear rats: 50 females and 15 males. Female rats were divided into 3 groups: I — 15 pregnant rats (control); II — 12 pregnant rats (pancreatic β-cell dysfunction); III — 12 pregnant rats (IR). All rats underwent histomorphological examination on paraffin sections using primary rabbit polyclonal antibodies to connexin 36 (Invitrogen, USA).

Results

Results. In study of pancreatic samples of group III, a sharp decrease in level of connexin 36 expression was noted. In samples of group II, it was revealed that in endocrine regions of gland, membrane reaction between cells is negative. Morphometric examination revealed a significant decrease in both the specific density of immune complexes and their average area in groups III and II (p < 0.050).

Discussion

Discussion. An immunohistochemical study of the distribution of connexin 36 indicates a decrease in electrotonic connectivity through gap contacts both in model of GDM subtype with predominant IR and pancreatic beta-cell dysfunction.

Conclusion

Conclusion. Results obtained suggest that reduction of connexin 36 may accompany development of pathogenetic mechanisms of GDM.

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