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RESEARCH PAPER / 2024-08-18

Leptin A deficiency affecting the mitochondrial dynamics of aged oocytes in medaka (Oryzias latipes).

Jihui Yang, Ying Wang, Guangxing Wang, Zhenhua Guo, Xinwen Li, Jigang Lu, Huaming Tu, Shilin Li, Jinming Wan, Guijun Guan, Liangbiao Chen

Key Laboratory of Freshwater Aquatic Genetic Resources, Ministry of Agriculture and Rural Affairs, Shanghai Ocean University, PR China; International Research Center for Marine Biosciences, Ministry of Science and Technology, Shanghai Ocean University, PR China; Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, PR China. · pubmed

Abstract

Mitochondrial dysfunction and metabolic disorder have been associated to age-related subfertility, however, the precise molecular mechanism controlling the development of fertile oocytes in aging females remains elusive. Leptin plays an important role in the maintenance of energy homeostasis, as both excessive or insufficient levels can affect the body weight and fertility of mice. Here, we report that leptin A deficiency affects growth and shortens reproductive lifespan by reducing fertility in medaka (Oryzias latipes). Targeted disruption of lepa (lepa

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of leptin A deficiency in mitochondrial dynamics and fertility in aged medaka, which touches on mechanisms related to aging and reproductive lifespan. However, while it contributes to understanding the biological processes involved in age-related subfertility, it does not address broader mechanisms of aging or lifespan extension. The findings are solid but represent a limited advance in the field of longevity research.

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