Impact of diet-induced maternal obesity on the reproductive capacity of F1 female offspring and the early development of the second generation

IF 4.8 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Nutritional Biochemistry Pub Date : 2024-07-15 DOI:10.1016/j.jnutbio.2024.109700
María Agustina Meneghini, Jeremías Pablo Flores Quiroga, Florencia Heinecke, Rocío Alejandra Galarza, Verónica White, Alicia Graciela Faletti
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Abstract

The aim of this study was to examine the impact of maternal obesity on the reproductive capacity of the female offspring (F1) and on the early development of the second generation (F2). To this end, rats were fed either standard (SD) or cafeteria (CD) diet. CD rats and their offspring were divided into 2 groups: rats with 18% and ≥25% overweight (CD18 and CD25, respectively) and offspring from CD18 and CD25 rats (OCD18 and OCD25, respectively). Both OCD groups achieved greater weight gain than controls, without changes in the serum levels of glucose, cholesterol or triglycerides. However, they showed increased gonadal cholesterol concentration and fat content compared to controls. Female OCD groups showed a slight prolongation of the estrous cycle and different pattern of changes in the weight gain during pregnancy. The OCD25 group displayed an increased fertility index and preimplantation losses, and changes in some fetal measurements. Some OCD25 dams gave birth to a larger litter of pups and displayed a lower viability index and lactation rate than controls. OCD25 dams also showed an increase in estradiol and a decrease in testosterone and anti-Müllerian hormone. OCD25 rats showed increased mRNA levels of steroidogenenic enzymes. The offspring from OCD25 females (F2OCD25 offspring) showed early vaginal opening and higher ovulation rate in females, and lower ano-genital distances in males, compared to controls. In conclusion, these results reflect that maternal obesity impacts on the reproductive health of successive generations, probably as a result of epigenetic changes in different systems, including germ cells.

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饮食引起的母体肥胖对第一代雌性后代生殖能力和第二代早期发育的影响。
本研究旨在探讨母体肥胖对雌性后代(F1)生殖能力和第二代(F2)早期发育的影响。为此,给大鼠喂食标准(SD)或自助餐(CD)饮食。CD大鼠及其后代被分为两组:超重18%和≥25%的大鼠(分别为CD18和CD25)以及CD18和CD25大鼠的后代(分别为OCD18和OCD25)。与对照组相比,强迫症组的体重增加幅度更大,但血清中的葡萄糖、胆固醇或甘油三酯水平没有发生变化。不过,与对照组相比,它们的性腺胆固醇浓度和脂肪含量都有所增加。雌性 OCD 组的发情周期略有延长,孕期体重增加的变化模式也有所不同。OCD25 组的受孕指数和胚胎植入前损失增加,胎儿的某些测量值也发生了变化。与对照组相比,一些 OCD25 母鼠产下的幼崽较多,但存活指数和泌乳率较低。OCD25 母鼠的雌二醇也有所增加,而睾酮和抗缪勒氏管激素则有所减少。OCD25 大鼠体内类固醇生成酶的 mRNA 水平升高。与对照组相比,OCD25雌性大鼠的后代(F2OCD25后代)表现出较早的阴道开放和较高的排卵率,而雄性大鼠的生殖器外距离较低。总之,这些结果表明,母体肥胖会影响后代的生殖健康,这可能是包括生殖细胞在内的不同系统发生表观遗传变化的结果。
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来源期刊
Journal of Nutritional Biochemistry
Journal of Nutritional Biochemistry 医学-生化与分子生物学
CiteScore
9.50
自引率
3.60%
发文量
237
审稿时长
68 days
期刊介绍: Devoted to advancements in nutritional sciences, The Journal of Nutritional Biochemistry presents experimental nutrition research as it relates to: biochemistry, molecular biology, toxicology, or physiology. Rigorous reviews by an international editorial board of distinguished scientists ensure publication of the most current and key research being conducted in nutrition at the cellular, animal and human level. In addition to its monthly features of critical reviews and research articles, The Journal of Nutritional Biochemistry also periodically publishes emerging issues, experimental methods, and other types of articles.
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