Section of Endocrinology, Department of Medicine, Tulane University School of Medicine, 1430 Tulane Ave, #8553,New Orleans, LA 70112, USA.
Regen Med. 2024 May 3;19(5):239-246. doi: 10.1080/17460751.2024.2343538. Epub 2024 May 10.
Type II diabetes (T2D) stems from insulin resistance, with β-cell dysfunction as a hallmark in its progression. Studies reveal that β cells undergo apoptosis or dedifferentiation during T2D development. The transcription factor PAX4 is vital for β differentiation and survival, thus may be a potential enhancer of β-cell function in T2D islets. Human PAX4 cDNA was delivered into T2D human islets with an adenoviral vector, and its effects on β cells were examined. PAX4 gene delivery significantly improved β-cell survival, and increased β-cell composition in the T2D human islets. Basal insulin and glucose-stimulated insulin secretion in PAX4-expressing islets were substantially higher than untreated or control-treated T2D human islets. Introduced PAX4 expression in T2D human islets improves β-cell function, thus could provide therapeutic benefits for T2D treatment.
2 型糖尿病（T2D）源于胰岛素抵抗，其进展的标志是β细胞功能障碍。研究表明，在 T2D 发展过程中β细胞会发生细胞凋亡或去分化。转录因子 PAX4 对β细胞分化和存活至关重要，因此可能是 T2D 胰岛中β细胞功能的潜在增强剂。用腺病毒载体将人 PAX4 cDNA 递送至 T2D 人胰岛中，并检测其对β细胞的作用。PAX4 基因传递显著提高了β细胞的存活率，并增加了 T2D 人胰岛中的β细胞组成。表达 PAX4 的胰岛中的基础胰岛素和葡萄糖刺激的胰岛素分泌明显高于未处理或对照处理的 T2D 人胰岛。在 T2D 人胰岛中引入 PAX4 表达可改善β细胞功能，因此可能为 T2D 治疗提供治疗益处。
