Leptin-independent programming of adult body weight and adiposity in mice.
Leptin-independent programming of adult body weight and adiposity in mice.
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DOI：
10.1210/en.2010-0911
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发表时间：
2011-02
期刊：
影响因子：
4.8
通讯作者：
Ozanne SE
中科院分区：
文献类型：
--
作者：
Cottrell EC;Martin-Gronert MS;Fernandez-Twinn DS;Luan J;Berends LM;Ozanne SE
低出生体重和出生后体重快速增加是随后发生代谢性疾病的独立和叠加风险因素。尽管有大量的证据表明这些关联，但缺乏机制数据。激素瘦素作为一种潜在的编程因子已经受到了极大的关注，因为早期生命中瘦素谱的差异与肥胖易感性的改变有关。到目前为止，瘦素本身是否是编程肥胖的关键因素仍不清楚。使用瘦素缺乏的ob/ob小鼠，我们表明，低出生体重，然后在哺乳期（恢复后代）的快速追赶增长，导致持续增加体重的成年生活中，无论是在野生型和ob/ob动物。此外，恢复的后代是贪食和附睾脂肪垫重量显着增加，反映了更大的肥胖。这些结果明确表明，瘦素以外的因素是至关重要的，在这个模型中的能量稳态的编程，并强大到足以改变肥胖的遗传菌株。
Low birth weight and rapid postnatal weight gain are independent and additive risk factors for the subsequent development of metabolic disease. Despite an abundance of evidence for these associations, mechanistic data are lacking. The hormone leptin has received significant interest as a potential programming factor, because differences in the profile of leptin in early life have been associated with altered susceptibility to obesity. Whether leptin alone is a critical factor for programming obesity has, until now, remained unclear. Using the leptin-deficient ob/ob mouse, we show that low birth weight followed by rapid catch-up growth during lactation (recuperated offspring) leads to a persistent increase in body weight in adult life, both in wild-type and ob/ob animals. Furthermore, recuperated offspring are hyperphagic and epididymal fat pad weights are significantly increased, reflecting greater adiposity. These results show definitively that factors other than leptin are crucial in the programming of energy homeostasis in this model and are powerful enough to alter adiposity in a genetically obese strain.
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影响因子：
7.7
作者：
Butler AA;Kozak LP
通讯作者：
Kozak LP
DOI：
10.1152/ajpregu.90497.2008
发表时间：
2009-08-01
影响因子：
2.8
作者：
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通讯作者：
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作者：
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通讯作者：
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影响因子：
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作者：
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