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<p>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.</p>

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Atypical protein kinase C activation drives intestinal glucose excretion in diabetes mellitus

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月6日

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  • Chan Woo Kang,
  • Zhen-Yu Hong,
  • Ju Hun Oh,
  • Mohamed El-Agamy Farh,
  • Eun Kyung Wang,
  • Soohyun Lee,
  • Un Ho Kang,
  • Jung Ho Nam,
  • Yang Jong Lee,
  • Hyeju Shin,
  • Ye Bin Kim,
  • Hyeonuk Jeon,
  • Jae Woong Jeong,
  • Doyeon Kim,
  • Jung Seung Kim,
  • Seung Soo Hong,
  • Jong-Pil Park,
  • Hyo Je Cho,
  • Sungsoon Fang,
  • Hyongbum Henry Kim,
  • Arthur Cho,
  • Byung Kook Lim,
  • Insuk Sohn,
  • Cheol Ryong Ku

摘要

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.