Cell and Tissue BiologyCell and Tissue BiologyЦитология0041-37713034-6061The Russian Academy of Sciences66961310.31857/S0041377124020051RKFSBWArticlesСтатьиResearch ArticleRole of calcium channels in glucose uptake regulation in the in vitro model of polarized intestinal epitheliumРоль кальциевых каналов в регуляции поглощения глюкозы в клеточной in vitro модели поляризованного кишечного эпителияBobkovD. E.БобковД. Е.
Russian Federation
svsem@incras.ruLukachevaA. V.ЛукачеваА. В.
Russian Federation
svsem@incras.ruKeverL. V.КеверЛ. В.
Russian Federation
svsem@incras.ruFurmanV. V.ФурманВ. В.
Russian Federation
svsem@incras.ruSemenovaS. B.СеменоваС. Б.
Russian Federation
svsem@incras.ruInstitute of Cytology, Russian Academy of SciencesИнститут цитологии РАН1503202466215016027022025Copyright ©; 2024, Russian Academy of SciencesCopyright ©; 2024, Российская академия наук2024Russian Academy of SciencesРоссийская академия наукhttps://vietnamjournal.ru/0041-3771/article/view/669613

Glucose is the main energy substrate that ensures metabolic processes in the human and animal bodies. Impaired carbohydrate metabolism is often associated with obesity and concomitant diseases, such as cardiovascular diseases, arterial hypertension, insulin resistance, etc. Current data indicate that intestinal glucose absorption is coupled with Ca2+ influx, but additional research is needed to confirm this interaction. We used a cellular model of human intestinal epithelium to elucidate the role of Ca2+ channels in the regulation of glucose absorption. The results of immunofluorescence and immunoelectron microscopy showed that high cellular glucose loading (50 mM) leads to an increase in the density of TRPV6 calcium channels on the apical membrane of the intestinal epithelium. The level of the calcium sensor STIM1, responsible for store-dependent calcium entry (SOCE), on the contrary, showed a decrease when Caco-2 cells were overloaded with glucose, which was accompanied by a decrease in SOCE. Excessive saturation of Caco-2 cells with glucose also led to a decrease in the expression level of the NF-kB transcription factor p65 subunit responsible for the expression of STIM1. The results showed that Ca2+ channels are not only involved in the regulation of glucose uptake, but may themselves be under the control of glucose.

Глюкоза является основным энергетическим субстратом, обеспечивающим метаболические процессы в организме человека и животных. Нарушение метаболизма углеводов часто ассоциировано с ожирением и сопутствующими заболеваниями, такими как сердечно-сосудистые заболевания, артериальная гипертензия, инсулинорезистентность и др. Современные данные указывают на сопряжение всасывания глюкозы в кишечнике со входом Ca2+, однако для подтверждения такого взаимодействия необходимы дополнительные исследования. Мы использовали клеточную in vitro модель кишечного эпителия человека для выяснения роли Ca2+-каналов в регуляции всасывания глюкозы. Результаты иммунофлуоресцентной и иммуноэлектронной микроскопии показали, что высокая нагрузка клеток глюкозой (50 мМ) приводит к увеличению плотности кальциевых каналов TRPV6 на апикальной мембране кишечного эпителия. Уровень кальциевого сенсора STIM1, ответственного за депо-зависимый вход кальция (SOCE), напротив, демонстрировал снижение при избыточной нагрузке клеток эпителия глюкозой, которое сопровождалось уменьшением SOCE. Кроме того, инкубация клеток кишечного эпителия в растворе с высокой концентрацией глюкозы приводила к подавлению образования субъединицы p65 транскрипционного фактора NF-kB, ответственной за экспрессию STIM1. Полученные данные показали, что Cа2+-каналы не только участвуют в регуляции поглощения глюкозы, но и сами могут находиться под контролем глюкозы.

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