Diet-induced obese mice are leptin insufficient after weight reduction.
Diet-induced obese mice are leptin insufficient after weight reduction.
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减轻体重后，饮食引起的肥胖小鼠是瘦素不足。
DOI：
10.1038/oby.2009.106
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Reizes O
中科院分区：
文献类型：
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作者：
Shi H;Akunuru S;Bierman JC;Hodge KM;Mitchell MC;Foster MT;Seeley RJ;Reizes O
旨在减少多余身体脂肪的行为疗法导致节食后脂肪损失有限。为了了解维持肥胖的原因，将高脂肪（HF）饮食诱导的肥胖（DIO）小鼠转换为低脂食物饮食，并检查食物对脂肪组织和代谢参数的组织学和分子学改变的影响。DIO小鼠在转换为食物（HF-食物）后降低并稳定了它们的体重，但比食物喂养的小鼠保留了更大量的肥胖。脂肪细胞体积的减少，而不是数量的减少，导致了脂肪量的减少。HF-chow小鼠显示正常化的循环胰岛素和瘦素水平，改善的葡萄糖耐量，和减少的炎症状态在白色脂肪组织（WAT）。HF-chow小鼠的循环瘦素水平经脂肪量校正后较低。瘦素施用用于测试HF-食物小鼠的瘦素水平降低是否抑制进一步的脂肪损失。瘦素治疗导致肥胖症的额外减少。最后，HF-HF小鼠附睾WAT中β3-肾上腺素能受体（β3-AR）的mRNA水平低于普通饲料喂养小鼠，饮食改变导致WAT β3-AR mRNA水平增加，与普通饲料喂养小鼠的水平相似，表明相对于HF-HF小鼠，饮食改变期间WAT的交感神经激活升高，导致瘦素水平和促炎细胞因子含量降低。总之，由于瘦素不足，HF-chow小鼠对进一步的脂肪减少具有抵抗力。饮食从HF到低脂的改变改善了DIO小鼠的代谢状态，尽管它们的肥胖在更高的水平上得到了保护。
Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high-fat (HF) diet-induced obese (DIO) mice were switched to a low-fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF-chow), but retained a greater amount of adiposity than chow-fed mice. Reduction in adipocyte volume, not number, caused the decrease in fat mass. HF-chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF-chow mice. Leptin administration was used to test whether reduced leptin level of HF-chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF-HF mice had lower mRNA levels of β3- adrenergic receptor (β3-AR) in epididymal WAT compared to chow-fed mice, and diet change led to an increase in the WAT β3-AR mRNA levels that were similar to the levels of chow-fed mice, suggesting an elevation in sympathetic activation of WAT during diet-switch relative to HF-HF mice leading to the reduced leptin level and pro-inflammatory cytokine content. In summary, HF-chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low-fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level.