Ornellas Fernanda, Carapeto Priscila V, Mandarim-de-Lacerda Carlos A, Aguila Marcia B
Universidade do Estado do Rio de Janeiro (UERJ), Centro Biomédico, Laboratório de Morfometria, Metabolismo e Doenças Cardiovasculares, Rio de Janeiro, RJ, Brazil.
Universidade do Estado do Rio de Janeiro (UERJ), Centro Biomédico, Laboratório de Morfometria, Metabolismo e Doenças Cardiovasculares, Rio de Janeiro, RJ, Brazil.
J Pediatr (Rio J). 2017 Nov-Dec;93(6):551-559. doi: 10.1016/j.jped.2017.02.004. Epub 2017 Aug 17.
To discuss the recent literature on paternal obesity, focusing on the possible mechanisms of transmission of the phenotypes from the father to the children.
A non-systematic review in the PubMed database found few publications in which paternal obesity was implicated in the adverse transmission of characteristics to offspring. Specific articles on epigenetics were also evaluated. As the subject is recent and still controversial, all articles were considered regardless of year of publication.
Studies in humans and animals have established that paternal obesity impairs their hormones, metabolism, and sperm function, which can be transmitted to their offspring. In humans, paternal obesity results in insulin resistance/type 2 diabetes and increased levels of cortisol in umbilical cord blood, which increases the risk factors for cardiovascular disease. Notably, there is an association between body fat in parents and the prevalence of obesity in their daughters. In animals, paternal obesity led to offspring alterations on glucose-insulin homeostasis, hepatic lipogenesis, hypothalamus/feeding behavior, kidney of the offspring; it also impairs the reproductive potential of male offspring with sperm oxidative stress and mitochondrial dysfunction. An explanation for these observations (human and animal) is epigenetics, considered the primary tool for the transmission of phenotypes from the father to offspring, such as DNA methylation, histone modifications, and non-coding RNA.
Paternal obesity can induce programmed phenotypes in offspring through epigenetics. Therefore, it can be considered a public health problem, affecting the children's future life.
探讨近期关于父亲肥胖的文献，重点关注从父亲到子女的表型传递的可能机制。
在PubMed数据库中进行的非系统综述发现，很少有出版物表明父亲肥胖与特征向后代的不良传递有关。还评估了关于表观遗传学的具体文章。由于该主题较新且仍存在争议，所有文章均被纳入考虑，无论其发表年份。
对人类和动物的研究已证实，父亲肥胖会损害其激素、代谢和精子功能，这些都可能传递给后代。在人类中，父亲肥胖会导致胰岛素抵抗/2型糖尿病以及脐带血中皮质醇水平升高，这会增加心血管疾病的风险因素。值得注意的是，父母的体脂与女儿肥胖的患病率之间存在关联。在动物中，父亲肥胖会导致后代在葡萄糖-胰岛素稳态、肝脏脂肪生成、下丘脑/进食行为、后代肾脏方面出现改变；还会因精子氧化应激和线粒体功能障碍损害雄性后代的生殖潜力。对这些观察结果（人类和动物）的一种解释是表观遗传学，它被认为是从父亲到后代传递表型的主要工具，如DNA甲基化、组蛋白修饰和非编码RNA。
父亲肥胖可通过表观遗传学在后代中诱导程序性表型。因此，它可被视为一个公共卫生问题，影响儿童的未来生活。
