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正常、脂肪组织量增加及减少的人体血液中脂联素浓度和脂肪组织脂联素分泌率。

Concentrations of adipsin in blood and rates of adipsin secretion by adipose tissue in humans with normal, elevated and diminished adipose tissue mass.

作者信息

Napolitano A, Lowell B B, Damm D, Leibel R L, Ravussin E, Jimerson D C, Lesem M D, Van Dyke D C, Daly P A, Chatis P

机构信息

Division of Endocrinology, Beth Israel Hospital, Boston, Massachusetts.

出版信息

Int J Obes Relat Metab Disord. 1994 Apr;18(4):213-8.

PMID:8044195
Abstract

Adipsin, which is identical to complement factor D, is synthesized by fat cells, circulates in the bloodstream and is profoundly deficient in mice with genetic and hypothalamic obesity. With the recent cloning of human adipsin, a quantitative human immunoassay has been developed. In the present study, we measured adipsin blood concentrations in humans with increased and decreased adipose stores as well as adipsin secretion by adipose tissue obtained from lean and obese individuals. The results demonstrate that adipsin is released by human adipose tissue fragments as has previously been shown in mice, and that, in contrast to obese mice, blood adipsin concentrations were not reduced in the obese humans tested in this study. We also observed that blood adipsin concentrations can vary as a function of feeding or adiposity, in that they tend to be mildly elevated in obese individuals or mildly reduced in individuals with total lipo-atrophy, cachexia related to AIDS and anorexia nervosa. Thus, the circulating concentration of adipsin tends to correlate positively with degree of adiposity. Clearly, no deficiency in blood adipsin concentrations or adipsin secretion by adipose tissue was observed in the obese individuals studied.

摘要

脂联素与补体因子D相同,由脂肪细胞合成,在血液循环中流动,在患有遗传性和下丘脑性肥胖的小鼠中严重缺乏。随着人类脂联素的近期克隆,已开发出一种定量的人类免疫测定法。在本研究中,我们测量了脂肪储存增加和减少的人类的脂联素血浓度,以及从瘦人和肥胖个体获得的脂肪组织分泌的脂联素。结果表明,脂联素由人类脂肪组织碎片释放,正如先前在小鼠中所显示的那样,并且与肥胖小鼠不同,在本研究中测试的肥胖人类中血脂联素浓度并未降低。我们还观察到血脂联素浓度可随进食或肥胖程度而变化,即它们在肥胖个体中往往轻度升高,而在全脂肪萎缩、与艾滋病相关的恶病质和神经性厌食症患者中则轻度降低。因此,脂联素的循环浓度往往与肥胖程度呈正相关。显然,在所研究的肥胖个体中未观察到血脂联素浓度或脂肪组织分泌脂联素的缺乏。

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