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Photoperiod Regulates Lean Mass Accretion but Not Adiposity in Growing F344 Rats Fed a High Fat Diet

机译:光周期调节成长中的F344大鼠高脂饮食的瘦体重增加但不是脂肪。

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摘要

In this study the effects of photoperiod and diet, and their interaction, were examined for their effects on growth and body composition in juvenile F344 rats over a 4-week period. On long (16L:8D), relative to short (8L:16D), photoperiod food intake and growth rate were increased, but percentage adiposity remained constant (ca 3-4%). On a high fat diet (HFD), containing 22.8% fat (45% energy as fat), food intake was reduced, but energy intake increased on both photoperiods. This led to a small increase in adiposity (up to 10%) without overt change in body weight. These changes were also reflected in plasma leptin and lipid levels. Importantly while both lean and adipose tissue were strongly regulated by photoperiod on a chow diet, this regulation was lost for adipose, but not lean tissue, on HFD. This implies that a primary effect of photoperiod is the regulation of growth and lean mass accretion. Consistent with this both hypothalamic GHRH gene expression and serum IGF-1 levels were photoperiod dependent. As for other animals and humans, there was evidence of central hyposomatotropism in response to obesity, as GHRH gene expression was suppressed by the HFD. Gene expression of hypothalamic AgRP and CRH, but not NPY nor POMC, accorded with the energy balance status on long and short photoperiod. However, there was a general dissociation between plasma leptin levels and expression of these hypothalamic energy balance genes. Similarly there was no interaction between the HFD and photoperiod at the level of the genes involved in thyroid hormone metabolism (Dio2, Dio3, TSHβ or NMU), which are important mediators of the photoperiodic response. These data suggest that photoperiod and HFD influence body weight and body composition through independent mechanisms but in each case the role of the hypothalamic energy balance genes is not predictable based on their known function.
机译:在这项研究中,研究了光周期和饮食的影响及其相互作用,研究了它们在4周内对F344幼鼠生长和身体组成的影响。在长期(16L:8D)上,相对于短期(8L:16D),光周期食物摄入量和生长速率增加,但脂肪百分比保持恒定(大约3-4%)。在高脂肪饮食(HFD)中,脂肪含量为22.8%(能量中脂肪含量为45%)时,食物摄入量减少,但两种光周期中的能量摄入量均增加。这导致肥胖症小幅增加(最高10%)而体重没有明显变化。这些变化也反映在血浆瘦素和脂质水平上。重要的是,尽管瘦肉和脂肪组织都受到光饮食对光周期的强烈调节,但脂肪对HFD的脂肪而非脂肪组织却失去了这种调节作用。这意味着光周期的主要作用是调节生长和瘦肉积聚。与此一致的是,下丘脑GHRH基因表达和血清IGF-1水平都是光周期依赖性的。与其他动物和人类一样,有证据表明,肥胖对中枢性躯体营养不良的影响很大,因为HFD抑制了GHRH基因的表达。下丘脑AgRP和CRH的基因表达,而不是NPY或POMC,与长短光周期的能量平衡状态一致。但是,血浆瘦素水平与这些下丘脑能量平衡基因的表达之间普遍存在分离。同样,在甲状腺激素代谢相关基因(Dio2,Dio3,TSHβ或NMU)的水平上,HFD和光周期之间也没有相互作用,而这些基因是光周期反应的重要介体。这些数据表明光周期和HFD通过独立的机制影响体重和身体组成,但是在每种情况下,基于它们的已知功能,下丘脑能量平衡基因的作用是不可预测的。

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