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早期生活食物限制对遗传性多食雄性 OLETF 大鼠肥胖的抑制作用:外周机制。

Attenuation of obesity by early-life food restriction in genetically hyperphagic male OLETF rats: peripheral mechanisms.

机构信息

Life Sciences Faculty, Bar Ilan University, Ramat Gan 52900, Israel.

出版信息

Horm Behav. 2010 Apr;57(4-5):455-62. doi: 10.1016/j.yhbeh.2010.02.002. Epub 2010 Feb 13.

Abstract

The alarming increase in childhood, adolescent and adult obesity has exposed the need for understanding early factors affecting obesity and for treatments that may help prevent or moderate its development. In the present study, we used the OLETF rat model of early-onset hyperphagia induced obesity, which become obese as a result of the absence of CCK(1) receptors, to examine the influence of partial food restriction on peripheral adiposity-related parameters during and after chronic and early short-term food restriction. Pair feeding (to the amount of food eaten by control, LETO rats) took place from weaning until postnatal day (PND) 45 (early) or from weaning until PND90 (chronic). We examined fat pad weight (brown, retroperitoneal, inguinal and epididymal); inguinal adipocyte size and number; and plasma leptin, oxytocin and creatinine levels. We also examined body weight, feeding efficiency and spontaneous intake after release from food-restriction. The results showed that chronic food restriction produced significant reductions in adiposity parameters, hormones and body weight, while early food restriction successfully reduced long-term body weight, intake and adiposity, without affecting plasma measurements. Early (and chronic) dieting produced promising long-term effects that may imply the reorganization of both peripheral and central mechanisms that determine energy balance and further support the theory suggesting that early interventions may effectively moderate obesity, even in the presence of a genetic tendency.

摘要

儿童、青少年和成年肥胖症的惊人增长暴露了人们对了解影响肥胖的早期因素以及可能有助于预防或缓解肥胖发展的治疗方法的需求。在本研究中,我们使用了 OLETF 大鼠模型,该模型具有由于 CCK(1)受体缺失而导致的早期过度摄食诱导肥胖,以研究在慢性和早期短期食物限制期间和之后,部分食物限制对周围肥胖相关参数的影响。从断奶到产后第 45 天(早期)或从断奶到产后第 90 天(慢性)进行配对喂养(喂给 LETO 大鼠的食物量)。我们检查了脂肪垫重量(棕色、腹膜后、腹股沟和附睾);腹股沟脂肪细胞大小和数量;以及血浆瘦素、催产素和肌酐水平。我们还检查了释放食物限制后的体重、进食效率和自发摄入。结果表明,慢性食物限制可显著降低肥胖参数、激素和体重,而早期食物限制可成功降低长期体重、摄入和肥胖,而不影响血浆测量。早期(和慢性)节食产生了有希望的长期效果,这可能意味着外周和中枢机制的重新组织,这些机制决定了能量平衡,并进一步支持了早期干预可能有效缓解肥胖的理论,即使存在遗传倾向也是如此。

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本文引用的文献

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Development of obesity in the Otsuka Long-Evans Tokushima Fatty rat.大冢长- Evans 德岛肥胖大鼠肥胖症的发展
Am J Physiol Regul Integr Comp Physiol. 2009 Dec;297(6):R1749-60. doi: 10.1152/ajpregu.00461.2009. Epub 2009 Sep 30.
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Inflammation and impaired adipogenesis in hypertrophic obesity in man.人类肥胖症中肥大与脂肪生成受损相关的炎症反应。
Am J Physiol Endocrinol Metab. 2009 Nov;297(5):E999-E1003. doi: 10.1152/ajpendo.00377.2009. Epub 2009 Jul 21.
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Early life origins of obesity: role of hypothalamic programming.肥胖的早期生活起源:下丘脑编程的作用。
J Pediatr Gastroenterol Nutr. 2009 Mar;48 Suppl 1:S31-8. doi: 10.1097/MPG.0b013e3181977375.
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Unraveling the obesity of OLETF rats.解析OLETF大鼠的肥胖问题。
Physiol Behav. 2008 Apr 22;94(1):71-8. doi: 10.1016/j.physbeh.2007.11.035. Epub 2007 Nov 29.
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Altered dopamine D2 receptor function and binding in obese OLETF rat.肥胖的OLETF大鼠中多巴胺D2受体功能和结合的改变。
Brain Res Bull. 2008 Jan 31;75(1):70-6. doi: 10.1016/j.brainresbull.2007.07.019. Epub 2007 Aug 8.

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