Orozco-Arguelles Leticia, De Los Santos Sergio, Coral-Vázquez Ramón M, Vega-García Claudia Cecilia, Zambrano Elena, Canto Patricia
Unidad de Investigación en Obesidad, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, México.
Subdirección de Investigación Clínica, Dirección de Investigación, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", Ciudad de México, México.
J Dev Orig Health Dis. 2025 Aug 6;16:e31. doi: 10.1017/S204017442510010X.
The obesogenic maternal environment can lead to cardiac hypertrophy in the offspring. The aim of this study was to investigate whether (-)-epicatechin (Epi) modify the expression of genes related to pathological cardiac hypertrophy (CH), and its physiological pathway, in offspring obese by programing. Four groups of eight male offspring Wistar rats of 110 days were randomly selected to control groups [C and offspring of maternal obesity (MO)] or to Epi groups (C + Epi or MO + Epi). In heart tissue, we evaluated the size of the ventricular walls and cavities, presence of fibrosis, mRNA and protein of Myh6, Myh7, Anp, Bnp, Acta 1, Col1a1, Akt, and Mtor. We observed an increase of the heart weight/body ratio in groups treated with Epi. Only in MO group, heart area and its perimeter were increased, as well as and mRNA. We found a significant decrease of fibrosis area in male offspring treatment with Epi. In Epi group mRNA was decreased whilst Anp protein in MO group was increased; further, a decrease in Col1a1 protein was found in MO group. In conclusion, the maternal obesity activates pathological CH markers reactivating fetal cardiac genes involved in histological changes observed in cardiac tissue. Epi treatment decreased the and expression of some fetal cardiac genes participating in this pathway in offspring of maternal obesity.
致肥胖的母体环境可导致子代心脏肥大。本研究旨在调查（-）-表儿茶素（Epi）是否能通过编程改变肥胖子代中与病理性心脏肥大（CH）相关基因的表达及其生理途径。随机选择四组，每组8只110日龄的雄性Wistar大鼠，分为对照组[C和母体肥胖（MO）的子代]或Epi组（C + Epi或MO + Epi）。在心脏组织中，我们评估了心室壁和腔的大小、纤维化的存在、Myh6、Myh7、Anp、Bnp、Acta 1、Col1a1、Akt和Mtor的mRNA和蛋白质。我们观察到用Epi处理的组中心脏重量/体重比增加。仅在MO组中，心脏面积及其周长增加，以及 和 mRNA增加。我们发现用Epi处理的雄性子代中纤维化面积显著减少。在Epi组中 mRNA减少，而MO组中Anp蛋白增加；此外，在MO组中发现Col1a1蛋白减少。总之，母体肥胖激活了病理性CH标志物，重新激活了参与心脏组织中观察到的组织学变化的胎儿心脏基因。Epi处理降低了母体肥胖子代中参与该途径的一些胎儿心脏基因的 和表达。
