Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas - UNICAMP, Limeira, São Paulo, Brazil.
Laboratory of Nutrients and Tissue Repair, School of Applied Sciences, University of Campinas - UNICAMP, Limeira, São Paulo, Brazil.
J Dev Orig Health Dis. 2022 Oct;13(5):575-582. doi: 10.1017/S2040174421000659. Epub 2021 Dec 3.
In the last decades, obesity and nonalcoholic fatty liver disease (NAFLD) have become increasingly prevalent in wide world. Fatty liver can be detrimental to liver regeneration (LR) and offspring of obese dams (HFD-O) are susceptible to NAFLD development. Here we evaluated LR capacity in HFD-O after partial hepatectomy (PHx). HFD-O re-exposed or not to HFD in later life were evaluated for metabolic parameters, inflammation, proliferation, tissue repair markers and survival rate after PHx. Increasing adiposity and fatty liver were observed in HFD-O. Despite lower IL-6 levels, Ki67 labeling, cells in S phase and Ciclin D1/PCNA protein content, a lower impact on survival rate was found after PHx, even when re-exposed to HFD. However, no difference was observed between offspring of control dams (SC-O) and HFD-O after surgery. Although LR impairment is dependent of steatosis development, offspring of obese dams are programmed to be protected from the damage promoted by HFD.
在过去的几十年中，肥胖症和非酒精性脂肪性肝病（NAFLD）在世界范围内变得越来越普遍。脂肪肝可能不利于肝再生（LR），并且肥胖母鼠的后代（HFD-O）易患 NAFLD 发展。在这里，我们评估了 PHx 后 HFD-O 的 LR 能力。HFD-O 是否重新暴露于 HFD 或在以后的生活中进行了评估，以评估代谢参数、炎症、增殖、组织修复标志物和 PHx 后的生存率。在 HFD-O 中观察到肥胖和脂肪肝的增加。尽管 IL-6 水平较低，Ki67 标记、S 期细胞和 Ciclin D1/PCNA 蛋白含量较低，但 PHx 后的生存率下降幅度较小，即使重新暴露于 HFD 也是如此。然而，在手术后，对照组母鼠（SC-O）和 HFD-O 的后代之间没有观察到差异。尽管 LR 受损取决于脂肪变性的发展，但肥胖母鼠的后代被编程为免受 HFD 促进的损伤。
