ArticleFrontiers in endocrinology2022
Restoring Impaired Fertility Through Diet: Observations of Switching From High-Fat Diet During Puberty to Normal Diet in Adulthood Among Obese Male Mice.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 8 citations in OpenAlex.
- Nicotinamide mononucleotide treatment improves spermatogenesis in obese mice by reducing lysine acetylation of lactate dehydrogenase C.Communications biology · 2025Article
- Integrated Multiomics Analyses Reveal Molecular Insights into How Intermittent Fasting Ameliorates Obesity and Increases Fertility in Male Mice.Nutrients · 2025Article
- Male aging in germ cells: What are we inheriting?Genetics and molecular biology · 2025Article
- Zinc Improves Semen Parameters in High-Fat Diet-Induced Male Rats by Regulating the Expression of LncRNA in Testis Tissue.Biological trace element research · 2023Article
- Wu Zi Yan Zong Wan Improves Triptolide-Induced Testicular Spermatogenic Dysfunction Through the Spermatogenic Microenvironment and the PLCγ/PKC Pathway.American journal of men's healthArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Background: Obesity is associated with a decrease in testicular function, yet the effects and mechanisms relative to different stages of sexual development remain unclear. The aim of this study is to determine whether high-fat diet-induced obesity impairs male fertility during puberty and in adulthood, and to ascertain its underlying mechanisms. This study aims to further reveal whether restoring to a normal diet can improve impaired fertility. Methods: Male mice were divided into 6 groups: the group N and H exposed to a normal diet or high-fat diet during puberty. The group NN or NH were further maintained a normal diet or exposed to high-fat diet in adulthood, the group HH or HN were further maintained high-fat diet or switched to normal diet in adulthood. Metabolic parameters, fertility parameters, testicular function parameters, TUNEL staining and testicular function-related proteins were evaluated, respectively. Results: The fertility of the mice in the high-fat diet group was impaired, which validated by declines in pregnancy rates and litter weight loss. Further analysis demonstrated the increased level of oxidative stress, the increased number of spermatogenic cell apoptosis and decreased number of sperm and decreased acrosome integrity. The expression of steroidogenic acute regulatory (StAR) and spermatogenesis related proteins (WT-1) decreased. Fertility among the HN group recovered, accompanied by the recovery of metabolism, fertility and testicular function parameters, StAR and WT-1 expression. Conclusions: The findings suggest that high-fat diet-induced obesity impairs male fertility during puberty and in adulthood. The loss of acrosome integrity, the increase of oxidative stress, the increase of cells apoptosis and the down-regulation of StAR and WT-1 may be the underlying mechanisms. Switching from high-fat diets during puberty to normal diets in adulthood can improve male fertility.
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