Role of VEGFA in type 2 diabetes mellitus rats subjected to partial hepatectomy

npj Gut and Liver Pub Date : 2024-12-04 DOI:10.1038/s44355-024-00013-9

Carlos Rojano-Alfonso, Marc Micó-Carnero, Cristina Maroto-Serrat, Araní Casillas-Ramírez, Carmen Peralta

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Abstract

The crucial role of vascular endothelial growth Factor A (VEGFA) in healthy rat livers undergoing partial hepatectomy under vascular occlusion (PH + I/R) has been demonstrated. This study evaluates whether this observation can be extrapolated to the presence of type 2 diabetes mellitus (T2DM). VEGFA was pharmacologically modulated and its effects during liver surgery were evaluated. Exogenous VEGFA exacerbated necrosis, with no changes in inflammation, apoptosis, or regeneration compared to PH + I/R. Endogenous VEGFA inhibition led to damage and inflammation similar to PH + I/R but promoted regeneration via PI3K/AKT. VEGFA did not affect hepatic VEGFB. VEGFB administration increased necrosis without affecting apoptosis or regeneration. Low hepatic VEGFA and VEGFB in PH + I/R may be influenced by intestine and adipose tissue. Detrimental effects of exogenous VEGFA could be due to exacerbated hepatic necrosis, while endogenous VEGFA inhibition improved regeneration via PI3K/AKT. Therefore, endogenous VEGFA inhibition is a protective strategy promoting liver regeneration in PH + I/R with T2DM.

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VEGFA在2型糖尿病肝部分切除大鼠中的作用

血管内皮生长因子A （VEGFA）在血管闭塞（PH + I/R）下接受部分肝切除术的健康大鼠肝脏中的重要作用已经得到证实。本研究评估这一观察结果是否可以推断为2型糖尿病（T2DM）的存在。对VEGFA进行药理学调节，并评估其在肝脏手术中的作用。与PH + I/R相比，外源性VEGFA加重了坏死，炎症、凋亡或再生没有变化。内源性VEGFA抑制导致类似于PH + I/R的损伤和炎症，但通过PI3K/AKT促进再生。VEGFA对肝脏VEGFB无影响。给药vegf可增加坏死，但不影响细胞凋亡或再生。PH + I/R低肝VEGFA和VEGFB可能受到肠道和脂肪组织的影响。外源性VEGFA的有害影响可能是由于肝坏死加剧，而内源性VEGFA抑制通过PI3K/AKT促进再生。因此，内源性VEGFA抑制是促进PH + I/R T2DM患者肝脏再生的保护策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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npj Gut and Liver

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