Letícia Pazin Bomfim, Maria Stacy Dos Santos Silva, Ivana Regina da Costa, Karen Gomes Luiz, Débora Hipólito Quadreli, Mariana Beirigo Bispo, Paulo Cezar de Freitas Mathias, Glaura Scantamburlo Alves Fernandes
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引用次数: 0
Abstract
Since the 1980s, research has linked environmental factors to adult-onset diseases. The DOHaD theory suggests that exposures during development can permanently affect organ function, predisposing individuals to adult diseases. Studies indicate that protein restriction or a high-fat diet (HFD) during this phase impacts adult metabolism since programmed dysfunctions may depend on changes established during puberty, such as the reproductive system. However, there are no studies on the impact of low-protein (LP) or HFD on male testicles during this phase. For this, Male Wistar rats were categorized into three dietary groups: LP (isocaloric low-protein pelletized); HFD; and Control (balanced commercial) until PND 60. This study was approved by the CEUA-UEM. On postnatal day 61, the animals were euthanized for histopathological, sperm count, and oxidative stress assessments in the testis and epididymis. Statistical analyses were conducted following established ethical principles in animal research. The research revealed significant alterations in daily sperm production and transit through the epididymis. Sperm morphology was affected in the experimental groups. Mitochondrial activity increased in the HFD group. Testicular and epididymal histopathology, seminiferous tubule diameter, and germinal epithelium height, as well as the number of Sertoli and Leydig cells, remained unchanged. Stereological analysis revealed tissue remodeling in the epididymis, particularly in the LP group. LP group showed an increase in lipid peroxidation in the oxidative damage test. In conclusion, low-protein and HFD during peripubertal age did not affect postnatal testicular development in rats. However, they impacted sperm quality, potentially affecting fertility and male reproductive system development.
期刊介绍:
JDOHaD publishes leading research in the field of Developmental Origins of Health and Disease (DOHaD). The Journal focuses on the environment during early pre-natal and post-natal animal and human development, interactions between environmental and genetic factors, including environmental toxicants, and their influence on health and disease risk throughout the lifespan. JDOHaD publishes work on developmental programming, fetal and neonatal biology and physiology, early life nutrition, especially during the first 1,000 days of life, human ecology and evolution and Gene-Environment Interactions.
JDOHaD also accepts manuscripts that address the social determinants or education of health and disease risk as they relate to the early life period, as well as the economic and health care costs of a poor start to life. Accordingly, JDOHaD is multi-disciplinary, with contributions from basic scientists working in the fields of physiology, biochemistry and nutrition, endocrinology and metabolism, developmental biology, molecular biology/ epigenetics, human biology/ anthropology, and evolutionary developmental biology. Moreover clinicians, nutritionists, epidemiologists, social scientists, economists, public health specialists and policy makers are very welcome to submit manuscripts.
The journal includes original research articles, short communications and reviews, and has regular themed issues, with guest editors; it is also a platform for conference/workshop reports, and for opinion, comment and interaction.