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。
基本信息
- 批准号:13680040
- 负责人:
- 金额:$ 1.66万
- 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:2001
- 资助国家:日本
- 起止时间:2001 至 2002
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
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.
在运动训练(跑步9周)的大鼠中,研究了一氧化氮(NO)在脂肪细胞脂肪分解中的可能作用。训练组大鼠脂肪组织中的脂解作用比对照组大鼠更严重。用5 mM N-硝基-L-精氨酸甲酯(L-NAME)处理大鼠脂肪组织,结果表明,训练大鼠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组。相反,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显著高于对照组。训练显著减少了脂肪细胞中亚硝酸盐/硝酸盐的生成,但对组织中的亚硝酸盐/硝酸盐的生成没有影响。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,但不增加诱导型一氧化氮合酶(INOS)的蛋白表达。在组织匀浆中,训练组大鼠eNOS活性显著高于对照组,但iNOS活性不显著。在细胞提取液中,训练显著降低了两种NOS的活性,但两种NOS的mRNA表达在不同组之间没有差异。NO供体S-亚硝基-N-乙酰青霉胺(SNAP)显著抑制异丙肾上腺素引起的脂肪细胞脂肪分解。SNAP对训练大鼠脂肪细胞的这种抑制作用大于对照组大鼠。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,并由于NOSS活性降低而减少了脂肪细胞内亚硝酸盐/硝酸盐的产生。另一方面,运动也可能增加脂肪组织中eNOS的活性或蛋白表达。
项目成果
期刊论文数量(5)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 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)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
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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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- 影响因子:0
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IZAWA Tetsuya其他文献
IZAWA Tetsuya的其他文献
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{{ truncateString('IZAWA Tetsuya', 18)}}的其他基金
Exercise prescription based on the circadian rhythm of adipocyte clock genes : The significance of chrono-exercise prescription
基于脂肪细胞时钟基因昼夜节律的运动处方:计时运动处方的意义
- 批准号:
23300242 - 财政年份:2011
- 资助金额:
$ 1.66万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Clarification of the molecular mechanism(s) behind exercise training-induced suppression of fat mass
阐明运动训练抑制脂肪量背后的分子机制
- 批准号:
15300222 - 财政年份:2003
- 资助金额:
$ 1.66万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
The study of exercise treatment for cardiovascular diseases
运动治疗心血管疾病的研究
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07680102 - 财政年份:1995
- 资助金额:
$ 1.66万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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