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Abstract (1. The First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan 250014, China; 2. College of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 102488, China; 3. Weifang Hospital of Traditional Chinese Medicine, Weifang 261000, China; 4. Yanqing Hospital of Beijing Chinese Medicine Hospital, Beijing 102100, China; 5. Affiliated Hospital of Shandong University of Chinese Medicine, Jinan 250011, China)
Abstract: Islet β cells are the exclusive cellular source of insulin synthesis and secretion, playing a crucial role in regulating blood glucose homeostasis. The impairment of islet β cells due to sustained anaerobic glycolysis pressure represents a significant factor contributing to insulin deficiency or resistance in patients with type 2 diabetes mellitus (T2DM). Glucokinase (GK), serving as the principal rate-limiting step in glucose transport, exhibits close association with insulin secretion. Hypoxia-inducible factor 1α subunit (HIF-1α) and 6-phosphofructo-2-kinase (PFKFB3) act as pivotal regulatory factors within glycolysis. The HIF-1α/PFKFB3 signaling pathway participates in intricate pathophysiological processes involving islet β cell function and maintenance under high-glucose conditions. This review elucidates the mechanisms by which the HIF-1α/PFKFB3 signaling pathway mediates GK induction through anaerobic glycolysis, mitochondrial network adaptive fragmentation, oxidative stress, and dedifferentiation leading to pancreatic islet β cell dysfunction in T2DM, thereby offering novel insights for clinical prevention and treatment strategies targeting T2DM.
Key words: type 2 diabetes; glucokinase; HIF-1α/PFKFB3 signaling pathway; mitochondria; dedifferentiation
（Acta Laser Biology Sinica, 2024, 33(6): 512-522）
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. [J]. journal1, 2024, 33(6): 1-6. |
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