Expression of UCP-2 and UCP-3 genes in obese type 2 diabetes mellitus and its modification by a cytokine inducer

UCP-2和UCP-3基因在肥胖2型糖尿病中的表达及其细胞因子诱导剂的修饰

基本信息

  • 批准号:
    10671053
  • 负责人:
  • 金额:
    $ 2.11万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1998
  • 资助国家:
    日本
  • 起止时间:
    1998 至 1999
  • 项目状态:
    已结题

项目摘要

Expression of UCP-2 and UCP-3 genes in obese type 2 diabetes mellitus and its modification by a cytokine inducerKK-Ay mouse is a model of obese type 2 diabetes mellitus. Glucose intolerance of KK-Ay mice was significantly improved by CFA treatment and the improvement was medicated by IL-1. CFA-treated KK-Ay mice lost body weight as compared to saline-treated control mice even though food intake was not changed, suggesting increase of energy expenditure in CFA-treated KK-Ay mice. To observe the increase of energy expenditure, body temperature, oxygen consumption and heart rate were measured in CFA-treated and control mice. However, there was no significant different in these measurements between both groups. mRNA expression of UCP-2 and UCP-3 was examined in C57/BL mice and KK-Ay mice. There was a tendency that expression of UCP-2 mRNA in the spleen, white adipose tissue and muscle were lower in KK-Ay mice than those in C57/BL mice and these were increased by CFA treatment. Further experiments were in progress to confirm these results. Finally, to screen obese patients with type 2 diabetes mellitus for abnormal energy metabolism, we measured temperature of tympanitic membrane before and after meals. However, we could not find obviously abnormal patients in the temperature change, because of unstable changes with wide range.
肥胖2型糖尿病中UCP-2和UCP-3基因的表达及细胞因子诱导的修饰KK-Ay小鼠是一种肥胖型2型糖尿病模型。CFA可明显改善KK-Ay小鼠的糖耐量,这种改善作用可被IL-1拮抗。尽管食物摄入量没有改变,但与生理盐水对照组相比,CFA处理的KK-Ay小鼠体重减轻,这表明CFA处理的KK-Ay小鼠的能量消耗增加。为了观察能量消耗的增加,测定了CFA治疗组和对照组小鼠的体温、耗氧量和心率。然而,在这些测量中,两组之间没有显著差异。检测C57/BL小鼠和KK-Ay小鼠UCP-2和UCP-3的mRNA表达。KK-Ay小鼠的脾、白色脂肪组织和肌肉中UCP-2mRNA的表达有低于C57/BL小鼠的趋势,经CFA治疗后,这些表达均有增加的趋势。进一步的实验正在进行中,以证实这些结果。最后,为了筛查肥胖2型糖尿病患者的能量代谢异常,我们测量了餐前和餐后鼓膜温度。但由于温度变化范围大,变化不稳定,我们在体温变化中没有发现明显的异常。

项目成果

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SATOH Jo其他文献

SATOH Jo的其他文献

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{{ truncateString('SATOH Jo', 18)}}的其他基金

Screening of clinical medicines for effects on gene expressions and protein productions of adipocytokines by using a newly-isolated preadipocyte line
利用新分离的前脂肪细胞系筛选影响脂肪细胞因子基因表达和蛋白质产生的临床药物
  • 批准号:
    15590926
  • 财政年份:
    2003
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Study on associations of novel TNF-α promoter polymorphisms with diabetes and diabetic complications
新型TNF-α启动子多态性与糖尿病及糖尿病并发症的相关性研究
  • 批准号:
    12671095
  • 财政年份:
    2000
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Abnomal cytokine expression in diabetes mellitus and diabetic complications, and their treatment by cytokine control
糖尿病和糖尿病并发症中细胞因子的异常表达及其细胞因子控制的治疗
  • 批准号:
    06670997
  • 财政年份:
    1994
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
Study on mechanism of action of biological response modifier (BRM) in prevention of type 1 diabetes mellitus.
生物反应调节剂(BRM)预防1型糖尿病的作用机制研究。
  • 批准号:
    63570520
  • 财政年份:
    1988
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
Screening of biological response modifiers (BRMs) for preventive effects on type 1 diabetes mellitus in animal models.
在动物模型中筛选生物反应调节剂 (BRM) 对 1 型糖尿病的预防作用。
  • 批准号:
    62870046
  • 财政年份:
    1987
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for Developmental Scientific Research
Basic study on prevention and treatment of type 1 diabetes mellitus with biological respomse modifiers.
生物反应调节剂防治1型糖尿病的基础研究。
  • 批准号:
    61570536
  • 财政年份:
    1986
  • 资助金额:
    $ 2.11万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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    2321818
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    2024
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Determinants of Longitudinal Progression of Adipose Tissue Inflammation in Individuals at High-Risk for Type 2 Diabetes: Novel Insights from Metabolomic Profiling
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确定青年发病 2 型糖尿病 (IMPACT DM) 的代谢和心理社会因素和特征
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