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Possible role of nitric oxide in lipolysis in exercise-trained rats.

Possible role of nitric oxide in lipolysis in exercise-trained rats.
一氧化氮在运动训练大鼠脂肪分解中的可能作用。
批准号:
13680040
负责人:
IZAWA Tetsuya
金额:
$1.66万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2002

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中文摘要
翻译
在运动训练大鼠(跑步9周)中,研究了一氧化氮(NO)对脂肪细胞脂解的可能作用。经过训练的大鼠脂肪组织中的脂肪分解往往比对照组大。用5 mM N^G -硝基- l-精氨酸甲酯(L-NAME)处理脂肪组织表明,训练大鼠的基础脂肪分解和异丙肾上腺素刺激的脂肪分解均显著高于对照大鼠。相比之下,在分离的脂肪细胞中,L-NAME对两组大鼠的脂肪分解都没有影响,尽管训练大鼠的分离脂肪细胞的脂肪分解明显高于对照组大鼠。训练显著减少脂肪细胞中亚硝酸盐/硝酸盐的产生,但组织中没有。另一方面,训练增加了组织匀浆提取物中内皮型一氧化氮合酶(eNOS)的蛋白表达,但没有增加诱导型一氧化氮合酶(iNOS)的蛋白表达。在组织匀浆中,训练大鼠的eNOS活性明显高于对照组大鼠,而iNOS活性不显著高于对照组大鼠。在细胞提取物中,训练显著降低了两种NOSs的活性,但两种NOSs的mRNA表达量在组间无显著差异。一氧化氮供体s -亚硝基-n -乙酰-青霉胺(SNAP)在两组对异丙肾上腺素的反应中均显著抑制脂肪细胞的脂肪分解。SNAP对训练大鼠脂肪细胞的抑制作用大于对照大鼠。因此,NO可能参与了脂肪分解的调节,运动训练增强了脂肪细胞对细胞外NO的反应性,由于NOSs活性的降低,脂肪细胞中亚硝酸盐/硝酸盐的产生减少。另一方面,运动也可能增加脂肪组织中eNOS的活性或蛋白质表达。
英文摘要
A possible role of nitric oxide (NO) on adipocyte lipolysis was studied in exercise-trained (9 weeks of running) rats. Lipolysis in adipose tissue tended to be greater in trained rats than in control rats. Treatment of adipose tissue with 5 mM N^G -nitro-L-arginine methyl ester (L-NAME) showed that both basal and isoproterenol-stimulated lipolysis were significantly greater in trained rats than in control rats. In contrast, in isolated adipocytes, L-NAME had no effect on lipolysis in either group of rats, although the lipolysis of isolated adipocytes was significantly greater in trained rats than in control rats. Training significantly reduced nitrite/nitrate production in adipocytes but not in tissue. On the other hand, training increased the protein expression of endothelial nitric oxide synthase (eNOS) but not that of inducible NOS (iNOS) in the extracts of tissue homogenates. In tissue homogenates, eNOS activity but not iNOS activity was significantly greater in trained rats than in control rats. In cellular extracts, training significantly reduced the activites of both NOSs, but the mRNA expressions of both NOSs were not different between groups. The NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), significantly inhibited adipocyte lipolysis in response to isoproterenol in both groups. This inhibitory effect of SNAP was greater in the adipocytes of trained rats than in those of the control rats. Thus, it is possible that NO is involved in the regulation of lipolysis and that exercise training enhances the responsiveness of adipocytes to extracellular NO with the reduced production of nitrite/nitrate in adipocytes due to decreased activites of NOSs. On the other hand, it is also possible that exercise increases either the activity or protein expression of eNOS in adipose tissue.
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会议论文
Kawanami, Hitomi, et al.: "Possible role of nitric oxide on adipocyte lipolysis in exercise-trained rats."Japanese Journal of Physiology. 52(4). 343-352 (2002)
Kawanami、Hitomi 等人:“一氧化氮对运动训练大鼠脂肪细胞脂肪分解的可能作用。”日本生理学杂志。
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通讯作者:
Kawanami, Hitomi et al.: "Possible role of nitric oxide on adipocyte lipolysis in exercise-trained rats"Japanese Journal of Physioloy. 52・4. 343-352 (2002)
Kawanami, Hitomi 等:“一氧化氮对运动训练大鼠脂肪细胞脂肪分解的可能作用”日本生理学杂志 52・4 (2002)。
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通讯作者:
Nomura, Sachiko, et al.: "Possible mechanisms by which adipocyte lipolysis is enhanced in exercise-trained rats."Biochemical and Biophysical Research Communications. 295(2). 236-242 (2002)
Nomura、Sachiko 等人:“运动训练大鼠脂肪细胞脂肪分解增强的可能机制。”生物化学和生物物理研究通讯。
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通讯作者:
Exercise prescription based on the circadian rhythm of adipocyte clock genes : The significance of chrono-exercise prescription
  • 批准号:
    23300242
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $12.4万
  • 财政年份:
    2011
  • 负责人:
    IZAWA Tetsuya
  • 依托单位:
Clarification of the molecular mechanism(s) behind exercise training-induced suppression of fat mass
  • 批准号:
    15300222
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $10.62万
  • 财政年份:
    2003
  • 负责人:
    IZAWA Tetsuya
  • 依托单位:
The study of exercise treatment for cardiovascular diseases
国内基金
海外基金
支链氨基酸代谢紊乱调控“Adipocytes - Macrophages Crosstalk”诱发2型糖尿病脂肪组织功能和结构障碍的作用及机制