The sex specific effect of alcohol consumption on circulating levels of CTRP3.
The sex specific effect of alcohol consumption on circulating levels of CTRP3.
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饮酒对循环水平CTRP3的性别特异性影响。
DOI：
10.1371/journal.pone.0207011
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发表时间：
2018
期刊：
影响因子：
3.7
通讯作者：
Peterson JM
中科院分区：
文献类型：
--
作者：
DeGroat AR;Fleming CK;Dunlay SM;Hagood KL;Moorman JP;Peterson JM
该项目的目的是确定酒精消耗对脂肪组织衍生蛋白C1 q TNF相关蛋白3（CTRP 3）循环水平的影响。脂肪组织分泌脂联素、瘦素等多种脂肪因子，对人体健康具有重要的生物学作用。然而，脂肪组织对酒精消耗极其敏感，不仅导致脂肪储存中断，还导致脂肪因子产生中断。脂肪因子分泌的变化可能具有广泛的生物学效应，并可能导致酒精诱导的疾病，如酒精性脂肪肝（ALD）。CTRP 3先前已被证明可以减轻脂肪肝疾病，并且饮酒抑制CTRP 3可能有助于酒精性脂肪肝疾病的发展和进展。为了检查乙醇消耗对循环脂肪因子水平的影响，向雄性和雌性小鼠饲喂含乙醇的饮食（Lieber-DeCarli 5%（v/v）乙醇饮食）10天，随后单次灌胃5 g/kg乙醇（NIAAA模型），或不添加暴食持续6周（慢性模型）。在雌性小鼠中，在两种乙醇喂养模型中，脂联素水平增加约2倍，但在雄性小鼠中，仅在长期乙醇喂养后观察到脂联素水平增加。另一方面，在雌性小鼠中，循环CTRP 3水平在NIAAA和慢性模型中分别降低了约75%和约50%，而在任一喂养模型中的雄性小鼠中均未观察到变化。无论小鼠的模型或性别如何，乙醇喂养均未改变瘦素水平。最后，长期乙醇喂养导致雌性小鼠死亡率显著增加（约50%），相对乙醇消耗量无差异。这些结果表明，酒精消费可以失调脂肪因子分泌，但影响不同的性别的动物，酒精消费的方法，和脂肪因子检查。这些发现还表明，雌性小鼠对乙醇的慢性影响比雄性小鼠更敏感。值得注意的是，这是第一项记录乙醇消耗对CTRP 3循环水平影响的研究。了解过量饮酒对脂肪因子产生和分泌的影响可以确定酒精诱导人类疾病的新机制。然而，敏感性增加的机制仍然难以捉摸。
The goal of this project was to establish the effect of alcohol consumption on the circulating levels of the adipose tissue derived protein C1q TNF Related Protein 3 (CTRP3). Adipose tissue secretes several adipokines, such as adiponectin and leptin, which exert a multitude of biological effects important for human health. However, adipose tissue is extremely sensitive to alcohol consumption, leading not only to disrupted fat storage, but also to disruptions in adipokine production. Changes to adipokine secretion could have widespread biological effects and potentially contribute to alcohol-induced ailments, such as alcoholic fatty liver disease (ALD). CTRP3 has been previously demonstrated to attenuate fatty liver disease, and suppression of CTRP3 with alcohol consumption could contribute to development of and progression to alcoholic fatty liver disease. To examine the effect of ethanol consumption on circulating adipokine levels, male and female mice were fed an ethanol containing diet (Lieber-DeCarli 5% (v/v) ethanol diet) for 10-days followed by a single gavage of 5 g/kg ethanol (the NIAAA model), or for 6-weeks with no binge added (chronic model). In female mice, adiponectin levels increased ~2-fold in both models of ethanol feeding, but in male mice increased adiponectin levels were only observed after chronic ethanol feeding. On the other hand, in female mice, circulating CTRP3 levels decreased by ~75% and ~50% in the NIAAA and chronic model, respectively, with no changes observed in the male mice in either feeding model. Leptin levels were unchanged with ethanol feeding regardless of model or sex of mice. Lastly, chronic ethanol feeding led to a significant increase in mortality (~50%) in female mice, with no difference in relative ethanol consumption. These findings indicate that ethanol consumption can dysregulate adipokine secretion, but that the effects vary by sex of animal, method of ethanol consumption, and adipokine examined. These findings also indicate that female mice are more sensitive to the chronic effects of ethanol than male mice. Notably, this is the first study to document the effects of ethanol consumption on the circulating levels of CTRP3. Understanding the impact of excessive alcohol consumption on adipokine production and secretion could identify novel mechanisms of alcohol-induced human disease. However, the mechanism responsible for the increased sensitivity remains elusive.
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影响因子：
5.8
作者：
Li Y;Wright GL;Peterson JM
通讯作者：
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5.6
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DOI：
10.1152/ajpendo.00387.2006
发表时间：
2007-02-01
影响因子：
5.1
作者：
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通讯作者：
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作者：
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通讯作者：
RANKIN, JG