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Nat. Commun., Feb 06 2026, | https://doi.org/10.1038/s41467-026-69193-7 Atypical protein kinase C activation drives intestinal glucose excretion in diabetes mellitus

Chan Woo Kang^1†, Zhen-Yu Hong^2†, Ju Hun Oh¹, Mohamed El-Agamy Farh^2,3, Eun Kyung Wang¹, Soohyun Lee¹, Un Ho Kang², Jung Ho Nam¹, Yang Jong Lee¹, Hyeju Shin¹, Ye Bin Kim⁴, Hyeonuk Jeon^4,5, Jae Woong Jeong⁶, Doyeon Kim¹, Jung Seung Kim⁷, Seung Soo Hong⁸, Jong-Pil Park⁹, Hyo Je Cho¹⁰, Sungsoon Fang^4,11, Hyongbum Henry Kim^4,12, Arthur Cho¹³, Byung Kook Lim¹⁴, Insuk Sohn², Cheol Ryong Ku^1*

¹Endocrinology, Institute of Endocrine Research, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
²Arontier Corporation, Seoul, 06735, Republic of Korea.
³AI-Bio Convergence Research Institute, Soongsil University, 369 Sangdo-Ro, Dongjak-Gu, Seoul 06978, Republic of Korea
⁴Graduate school of Medical Science, Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul, 03722, Republic of Korea.
⁵Data Intelligence-driven Integrated Disease Research Center, Yonsei University College of Medicine, Seoul, 03772, Republic of Korea.
⁶Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, 03772, Republic of Korea.
⁷NERIG Inc., Seoul 04166, Republic of Korea.
⁸Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
⁹Department of Forensic Medicine, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
¹⁰Department of Biochemistry, Chungbuk National University, Cheongju, 28644, Republic of Korea.
¹¹Department of Biomedical Sciences, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
¹²Department of Pharmacology, Yonsei University College of Medicine, Seoul, 03722 Republic of Korea.
¹³Department of Nuclear Medicine, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea
¹⁴Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA

^†C.W. Kang and Z. Hong contributed equally.
^*Corresponding author
Correspondence to Cheol Ryong Ku.

Abstract

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.

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