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影响易发生或抵抗饮食诱导肥胖的小鼠能量调节的行为机制。

Behavioural mechanisms affecting energy regulation in mice prone or resistant to diet- induced obesity.

机构信息

Philipps-Universität Marburg, Faculty of Biology, Department of Animal Physiology, Karl-von-Frisch-Strasse 8, 35043 Marburg, Germany.

出版信息

Physiol Behav. 2010 Mar 3;99(3):370-80. doi: 10.1016/j.physbeh.2009.12.001. Epub 2009 Dec 16.

Abstract

We investigated inbred SWR/J and AKR/J mice, two established models for different susceptibility to diet-induced obesity (DIO), to scrutinize the contribution of physical activity and energy assimilation to the etiology of developing obesity. Body mass gain and body composition of mice fed a high-energy (HE) or a low caloric control diet were monitored. In parallel, assimilated energy, locomotor activity and thermoregulatory behaviour were measured. Activity was continuously registered by radio telemetry and, in addition, Open Field (OF) behaviour was used as a quick screening tool for spontaneous activity before and after the feeding trial. Energy assimilation was increased in both strains on HE (AKR/J: +60.7% and SWR/J: +42.8%) but only in AKR/J, body mass (+8.1%) and fat mass (+40.7%) were significantly elevated. As a trend, total home cage activity was increased and was more scattered in SWR/J. Interestingly, HE stimulated OF activity only in SWR/J in the second trial at the end of the feeding experiment. The spatial pattern of OF activity also differed between strains with obese mice avoiding the core area. Under housing conditions, nest building behaviour was more pronounced in AKR/J. To further evaluate OF behaviour as a marker for spontaneous activity an obese mouse line was investigated. Mice lacking the leptin receptor (db/db) showed already before the onset of obesity lowest activity levels in OF. Adjustment of energy intake, higher activity levels and energy consuming thermoregulatory behaviour are mechanisms employed by SWR/J mice to dissipate excess energy as a defence against the onset of obesity. Therefore our results deciphering mechanisms of DIO-sensitivity in mice contribute to the understanding of inter-individual differences in body weight development in an adipogenic environment.

摘要

我们研究了近交 SWR/J 和 AKR/J 小鼠,这两种小鼠是研究饮食诱导肥胖(DIO)易感性差异的成熟模型,以仔细研究体力活动和能量同化对肥胖发生的病因学的影响。监测喂食高能(HE)或低热量控制饮食的小鼠的体重增加和身体成分。同时,测量同化的能量、运动活性和体温调节行为。活动通过无线电遥测连续记录,此外,在喂养试验前后,还使用开放式场(OF)行为作为自发性活动的快速筛选工具。两种品系在 HE 时能量同化增加(AKR/J:+60.7%,SWR/J:+42.8%),但仅在 AKR/J 中,体重(+8.1%)和脂肪量(+40.7%)显著升高。趋势是,SWR/J 的总笼内活动增加,且更加分散。有趣的是,HE 仅在第二次试验中在 SWR/J 中刺激 OF 活动。OF 活动的空间模式也因品系而异,肥胖小鼠避开了核心区域。在饲养条件下,AKR/J 的筑巢行为更为明显。为了进一步评估 OF 行为作为自发性活动的标志物,研究了一种肥胖小鼠品系。瘦素受体缺失(db/db)的小鼠在肥胖发生之前就已经表现出最低的 OF 活动水平。SWR/J 小鼠通过调整能量摄入、提高活动水平和消耗能量的体温调节行为来消耗多余的能量,作为防止肥胖发生的防御机制。因此,我们的研究结果阐明了小鼠 DIO 敏感性的机制,有助于理解在致肥胖环境中个体间体重发育差异的机制。

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