Nature communications · 2026
Atypical protein kinase C activation drives intestinal glucose excretion in diabetes mellitus.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kang Chan Woo, Hong Zhen-Yu, Oh Ju Hun, Farh Mohamed El-Agamy, Wang Eun Kyung, Lee Soohyun, Kang Un Ho, Nam Jung Ho, Lee Yang Jong, Shin Hyeju, Kim Ye Bin, Jeon Hyeonuk, Jeong Jae Woong, Kim Doyeon, Kim Jung Seung, Hong Seung Soo, Park Jong-Pil, Cho Hyo Je, Fang Sungsoon, Kim Hyongbum Henry, Cho Arthur, Lim Byung Kook, Sohn Insuk, Ku Cheol Ryong
Аннотация
Intestinal glucose excretion, defined as increased intestinal serum glucose uptake and secretion into the lumen, influences bariatric surgery-associated glycaemic control. Here, we investigate molecular mechanisms that activate intestinal glucose excretion. We evaluate altered transcriptomes in variable intestinal glucose excretion models and big data-based drug discovery systems. We show that protein kinase C (PKC) activation mimics transcriptome alterations observed during intestinal glucose excretion. Among PKC subfamilies, atypical PKC (aPKC) facilitates glucose transporter 1 (GLUT1)-mediated intestinal glucose excretion without inducing oncogenic proliferation. Intestinal aPKC activation via transposon expression vector induces serum glucose uptake into intestinal tissues and excretion into the lumen. Prostratin, a non-tumorigenic phorbol ester, activates aPKC and induces a similar effect on intestinal glucose excretion. We identify the prostratin and aPKC/GLUT1 signalling pathways as putative targets for treating diabetes, providing insights into the future development of antidiabetic and weight-loss drugs.