Neuropeptide FF Receptor 2 Overexpression Aggravates Lipid Accumulation and Metabolic Dysfunction in Mice with Diet-Induced Metabolic Stress.

IF 4.4 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Hsiang-Ting Hsu, Chun-Chun Hsu, Yun-Jou Liao, Hui-Yun Li, Yao-Chang Chiang, Ya-Tin Lin
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引用次数: 0

Abstract

Background: Obesity is a major contributor to metabolic dysfunction and is driven by complex genetic, behavioral, and physiological factors. Neuropeptide FF receptor 2 (NPFFR2) has been implicated in regulating feeding behavior, as well as energy and glucose homeostasis. However, its precise role in obesity and metabolic disorders remains unclear. This study aimed to investigate the systemic role of NPFFR2 in obesity-induced metabolic dysfunction.

Material and methods: The role of NPFFR2 was examined using wild-type and Npffr2-overexpressing transgenic mice subjected to 15 weeks of high-fat high-sucrose diet to induce obesity. Systemic, tissue-specific, and serum metabolic profiles were analyzed, with a particular focus on lipid abnormalities in the liver and adipose tissues.

Results: Npffr2 overexpression exacerbated obesity-induced metabolic dysfunction, including accelerated body weight gain, impaired glucose homeostasis, altered fat composition, adipose tissue inflammation, and dysregulated lipid metabolism. In addition, hypertrophy of both hepatocytes and adipocytes was aggravated in Npffr2-overexpressing mice, collectively contributing to excessive energy storage and reduced metabolic efficiency.

Conclusions: These findings suggest that NPFFR2 may contribute to the regulation of energy balance and lipid metabolism, potentially via central regulatory pathways. These findings highlight the need for mechanistic studies to clarify its region-specific roles and therapeutic potential in metabolic disorders.

神经肽FF受体2过表达加重饮食诱导代谢应激小鼠的脂质积累和代谢功能障碍。
背景:肥胖是代谢功能障碍的主要原因,受复杂的遗传、行为和生理因素的影响。神经肽FF受体2 (NPFFR2)参与调节摄食行为以及能量和葡萄糖稳态。然而,它在肥胖和代谢紊乱中的确切作用尚不清楚。本研究旨在探讨NPFFR2在肥胖诱导的代谢功能障碍中的全系统作用。材料和方法:采用野生型和过表达NPFFR2的转基因小鼠,经15周高脂高糖饮食诱导肥胖,检测NPFFR2的作用。分析了全身、组织特异性和血清代谢谱,特别关注肝脏和脂肪组织中的脂质异常。结果:Npffr2过表达加剧了肥胖诱导的代谢功能障碍,包括体重增加加速、葡萄糖稳态受损、脂肪成分改变、脂肪组织炎症和脂质代谢失调。此外,npffr2过表达小鼠的肝细胞和脂肪细胞肥大加剧,共同导致能量储存过度和代谢效率降低。结论:这些发现表明NPFFR2可能通过中枢调控途径参与能量平衡和脂质代谢的调节。这些发现强调需要进行机制研究,以阐明其在代谢紊乱中的区域特异性作用和治疗潜力。
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来源期刊
Biomedical Journal
Biomedical Journal Medicine-General Medicine
CiteScore
11.60
自引率
1.80%
发文量
128
审稿时长
42 days
期刊介绍: Biomedical Journal publishes 6 peer-reviewed issues per year in all fields of clinical and biomedical sciences for an internationally diverse authorship. Unlike most open access journals, which are free to readers but not authors, Biomedical Journal does not charge for subscription, submission, processing or publication of manuscripts, nor for color reproduction of photographs. Clinical studies, accounts of clinical trials, biomarker studies, and characterization of human pathogens are within the scope of the journal, as well as basic studies in model species such as Escherichia coli, Caenorhabditis elegans, Drosophila melanogaster, and Mus musculus revealing the function of molecules, cells, and tissues relevant for human health. However, articles on other species can be published if they contribute to our understanding of basic mechanisms of biology. A highly-cited international editorial board assures timely publication of manuscripts. Reviews on recent progress in biomedical sciences are commissioned by the editors.
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