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Article Abstract
Investigating the principles of fish fat deposition and conducting related research are current focal points in fish nutrition. This study explores the endocrine regulation of LEAP2 and GHSR1a in zebrafish by constructing mutantmodels andexamining the effects of the endocrine factors LEAP2 and its receptor GHSR1a on zebrafish growth, feeding, and liver fat deposition. Compared to the wild type (WT), the mutation of LEAP2 results in increased feeding and decreased swimming in zebrafish. The impact is more pronounced in adult female zebrafish, characterized by increased weight, length, width, and accumulation of lipid droplets in the liver.Incontrast, deficiency in GHSR1a significantly reduces the growth of male zebrafish and markedly decreases liver fat deposition.These research findings indicate the crucial roles of LEAP2 and GHSR1a in zebrafish feeding, growth, and intracellular fat metabolism. This study, for the first time, investigated the endocrine metabolic regulation functions of LEAP2 and GHSR1a in the model organism zebrafish, providing initial insights into their effects and potential mechanisms on zebrafish fat metabolism.
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| http://dx.doi.org/10.1016/j.ygcen.2024.114563 | DOI Listing |
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Article Synopsis
- - LEAP2 acts as a natural inhibitor of the growth hormone secretagogue receptor, countering the effects of ghrelin, which boosts growth hormone secretion; previous studies show that knocking out LEAP2 leads to increased GH levels.
- - Researchers used mutant zebrafish created via CRISPR-Cas9 to study LEAP2's role in early development, employing various molecular techniques to measure GH expression during embryonic development.
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