瘦素的影响在Na (+) - h(+)反向运输(新人道1)活动的肥胖和正常红细胞。
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Konstantinou-Tegou, Kaloyianni M, Bourikas D, Koliakos G
瘦素的影响在Na (+) - h(+)反向运输(新人道1)活动的肥胖和正常红细胞。
摩尔细胞性。2001年10月25日,183 (2):11 - 8。
- PubMed ID
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11604219 (在PubMed]
- 文摘
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肥胖是目前认为是一种慢性代谢性疾病,心血管并发症的风险高。瘦素,一个adipocyte-derived激素多种靶细胞影响广泛的过程。可能的反动hyperleptinaemia目前正在调查中。Na (+) - h(+)换热器(新人道1)参与多种细胞功能和其激活相关的高血压和肥胖。新人道1存在红细胞和各种激素可以刺激。红细胞表面各种受体与基本未知函数。在本文中,瘦素对红细胞的影响新人道1活动调查。出于这个原因,细胞内的pH值和钠大量测量之前和之后的瘦素在红细胞悬浮液从正常和肥胖的人。阿米洛利,特定的新人道1抑制剂,staurosporine蛋白激酶C抑制剂被用来抑制红细胞新人道1。结合研究瘦素与异硫氰酸荧光素标记(FITC)和绑定在红细胞被Scatchard分析估计。 NHE 1 activity increased in the presence of leptin but significantly less in the obese than in the control group. Furthermore the concentrations of leptin binding sites on the surface of erythrocytes were lower in erythrocytes drawn from obese individuals than in erythrocytes drawn from normal subjects. Since NHE 1 activity has been associated with insulin resistance and hypertension, the activation of this antiport by leptin may represent a link between adipose tissue hypertrophy and cardiovascular complications of obesity.