Международный эндокринологический журнал Том 22, №5, 2026

Ожиріння, метаболічний синдром (МС) і цукровий діабет (ЦД) 2-го типу супроводжуються порушеннями структури і функції підшлункової залози. Експериментальні моделі на щурах широко використовують для дослідження механізмів дисфункції β-клітин, інсулінорезистентності (ІР), оксидативного стресу (ОС) та хронічного запалення низької інтенсивності (ХЗНІ). Ожиріння, МС та гіперглікемія асоціюються зі значними патофізіологічними змінами в підшлунковій залозі, що включають деструкцію β-клітин, порушення архітектоніки панкреатичних острівців, розвиток ХЗНІ, ОС, порушення метаболізму гліколіпідів та фіброзу. Ключову роль у прогресуванні цих змін відіграють ХЗНІ, ОС та ІР. Острівці підшлункової залози, як ключова ланка ендокринної системи, відіграють вирішальну роль у регуляції гомеостазу глюкози та є особливо чутливими до особливостей внутрішньоутробного енергетичного метаболічного мікросередовища. Порушення внутрішньоутробного балансу поживних речовин може спричинити зміни у процесах розвитку острівців, що, у свою чергу, зумовлює структурні та функціональні аномалії. Однак вплив ЦД та ожиріння на морфофункціональний стан підшлункової залози, особливо у контексті міжпоколіннєвих змін, все ще залишається недостатньо вивченим. Метою цього огляду було провести аналіз сучасних літературних даних щодо морфологічних і функціональних змін підшлункової залози у щурів за умов експериментального ЦД та ожиріння. Особливий акцент в огляді зроблено на дослідженнях, які застосовують стрептозотоцин-індуковані моделі ЦД як класичний підхід до відтворення дисфункції β-клітин, а також високожирові або гіперкалорійні дієти. Розглянуто основні положення теорії походження здоров’я та хвороб у процесі розвитку, а також теорії фетального програмування в контексті ожиріння, прегестаційного (ПГЦД) і гестаційного цукрового діабету (ГЦД). Окремо висвітлено дослідження, спрямовані на комплексний аналіз морфофункціональних змін острівців Лангерганса в експериментальних умовах ПГЦД і ГЦД. Пошук літератури проводився в Scopus, Science Direct (від Elsevier) і PubMed, включно з базами даних Medline. Використані ключові слова «цукровий діабет», «ожиріння», «метаболічний синдром», «хронічне запалення», «оксидативний стрес», «інсулінорезистентність», «підшлункова залоза», «β-клітини», «морфофункціональні зміни». Для виявлення результатів досліджень, які не вдалося знайти під час онлайн-пошуку, використовувався ручний пошук бібліографії публікацій.

Obesity, metabolic syndrome, and type 2 diabetes mellitus (DM) are accompanied by abnormalities in the structure and function of the pancreas. Experimental models in rats are widely used to study the mechanisms of β-cell dysfunction, insulin resistance (IR), oxidative stress (OS), and low-grade chronic inflammation (LGCI). Obesity, metabolic syndrome, and hyperglycemia are associated with significant pathophysiological changes in the pancreas, including β-cell destruction, disruption of pancreatic islet architecture, development of LGCI, OS, impaired glycolipid metabolism, and fibrosis. LGCI, OS, and IR play a key role in the progression of these changes. The pancreatic islets, as a key component of the endocrine system, play a decisive role in regulating glucose homeostasis and are particularly sensitive to the characte­ristics of the intrauterine energy metabolic microenvironment. Disruptions in the intrauterine balance of nutrients can cause changes in islet development, which, in turn, lead to structural and functional abnormalities. However, the impact of DM and obesity on the morphofunctional state of the pancreas, particularly in the context of intergenerational changes, remains understudied. The aim of this review was to analyze current literature data on morphological and functional changes in the pancreas of rats under conditions of experimental diabetes and obesity. The review places particular emphasis on studies that use streptozotocin-induced models of DM as a classic approach to replicating β-cell dysfunction, as well as the use of high-fat or high-calorie diets. The main tenets of the Deve­lopmental Origins of Health and Disease concept are discussed, as well as the theory of fetal programming in the context of obesity, pregestational, and gestational DM. Separate attention is given to studies aimed at a comprehensive analysis of the morphofunctional changes in the islets of Langerhans under experimental conditions of pregestational, and gestational DM. The literature search was conducted in Scopus, Science Direct (from Elsevier), and PubMed, including the MEDLINE databases. The keywords used were “dia­betes mellitus”, “obesity”, “metabolic syndrome”, “chronic inflammation”, “oxidative stress”, “insulin resistance”, “pancreas”, “β-cells”, “morphofunctional changes”. To identify study results that could not be found during the online search, a manual search of the publications’ bibliographies was conducted.

цукровий діабет; гестаційний цукровий діабет; метаболічний синдром; підшлункова залоза; β-клітини; морфофункціональні зміни

diabetes mellitus; gestational diabetes mellitus; metabo­lic syndrome; pancreas; β-cells; morphofunctional changes

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