炎症抑制脂肪组织中 GPR81 的表达。
Inflammation inhibits GPR81 expression in adipose tissue.
机构信息
Metabolism Section (111F), Department of Veterans Affairs Medical Center, University of California San Francisco, 4150 Clement Street, San Francisco, CA 94121, USA.
出版信息
Inflamm Res. 2011 Oct;60(10):991-5. doi: 10.1007/s00011-011-0361-2. Epub 2011 Jul 13.
OBJECTIVE AND DESIGN
The aim of this study was to examine the expression of G protein-coupled receptor 81 (GPR81) in mouse adipose tissue in response to inflammatory stimuli. GPR81 is activated by lactate resulting in the inhibition of lipolysis.
MATERIALS AND TREATMENT
Mice were injected with saline, lipopolysaccharide (LPS), zymosan, or turpentine, N = 5 per group. 3T3-L1 adipocytes were treated with tumor necrosis factor alpha, interleukin (IL)-l beta, IL-6, or interferon gamma.
METHODS
GPR81 expression levels were measured by real-time PCR and statistical significance was determined by Student's t test.
RESULTS
LPS resulted in a marked decrease in GPR81 mRNA level in mouse adipose tissue in C57BL/6 and OuJ mice, an effect that was not observed in HeJ mice, which have a mutation in TLR4. Zymosan and turpentine also decreased adipose tissue GPR81 expression. Cytokine treatment of 3T3-L1 adipocytes had no effect on GPR81 expression. GPR81 expression was decreased in ob/ob mice, an animal model of type 2 diabetes that is characterized by inflammation.
CONCLUSION
Inflammation decreases the expression of GPR81 in adipose tissue.
目的和设计
本研究旨在检测炎性刺激下小鼠脂肪组织中 G 蛋白偶联受体 81（GPR81）的表达。GPR81 被乳酸激活，导致脂肪分解抑制。
材料和处理
每组 5 只小鼠分别注射盐水、脂多糖（LPS）、酵母聚糖或松节油。用肿瘤坏死因子-α、白细胞介素（IL）-1β、IL-6 或干扰素-γ处理 3T3-L1 脂肪细胞。
方法
实时 PCR 检测 GPR81 表达水平，采用 Student's t 检验确定统计学意义。
结果
LPS 导致 C57BL/6 和 OuJ 小鼠脂肪组织中 GPR81 mRNA 水平显著降低，但 TLR4 突变的 HeJ 小鼠未见此现象。酵母聚糖和松节油也降低脂肪组织 GPR81 表达。3T3-L1 脂肪细胞的细胞因子处理对 GPR81 表达没有影响。肥胖/肥胖（ob/ob）小鼠即 2 型糖尿病的动物模型，其特征为炎症，GPR81 表达降低。
结论
炎症降低脂肪组织中 GPR81 的表达。
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