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胰岛素和去甲肾上腺素对大鼠棕色脂肪细胞葡萄糖转运及代谢的影响。胰岛素对去甲肾上腺素诱导的葡萄糖氧化的增强作用。

Effects of insulin and norepinephrine on glucose transport and metabolism in rat brown adipocytes. Potentiation by insulin of norepinephrine-induced glucose oxidation.

作者信息

Ebner S, Burnol A F, Ferre P, de Saintaurin M A, Girard J

机构信息

Centre de Recherches sur la Nutrition du Centre National de la Recherche Scientifique, Meudon-Bellevue, France.

出版信息

Eur J Biochem. 1987 Dec 30;170(1-2):469-74. doi: 10.1111/j.1432-1033.1987.tb13723.x.

DOI:10.1111/j.1432-1033.1987.tb13723.x
PMID:3319619
Abstract

Glucose is an important fuel for rat brown adipose tissue in vivo and its utilization is highly sensitive to insulin. In this study, the different glucose metabolic pathways and their regulation by insulin and norepinephrine were examined in isolated rat brown adipocytes, using [6-14C]glucose as a tracer. Glucose utilization was stimulated for insulin concentrations in the range of 40-1000 microU/ml. Furthermore, the addition of adenosine deaminase (200 mU/ml) or adenosine (10 microM) did not alter insulin sensitivity of glucose metabolism. The major effect of insulin (1 mU/ml) was a respective 7-fold and 5-fold stimulation of lipogenesis and lactate synthesis, whereas glucose oxidation remained very low. The 5-fold stimulation of total glucose metabolism by 1 mU/ml of insulin was accompanied by an 8-fold increase in glucose transport. In the presence of norepinephrine (8 microM), total glucose metabolism was increased 2-fold. This was linked to a 7-fold increase of glucose oxidation, whereas lipogenesis was greatly inhibited (by 72%). In addition, norepinephrine alone did not modify glucose transport. The addition of insulin to adipocytes incubated with norepinephrine, induced a potentiation of glucose oxidation, while lipogenesis remained very low. In conclusion, in the presence of insulin and norepinephrine glucose is a oxidative substrate for brown adipose tissue. However the quantitative importance of glucose as oxidative fuel remains to be determined.

摘要

葡萄糖是大鼠体内棕色脂肪组织的重要燃料,其利用对胰岛素高度敏感。在本研究中,以[6-¹⁴C]葡萄糖作为示踪剂,在分离的大鼠棕色脂肪细胞中检测了不同的葡萄糖代谢途径及其受胰岛素和去甲肾上腺素的调节情况。胰岛素浓度在40 - 1000微单位/毫升范围内时可刺激葡萄糖利用。此外,添加腺苷脱氨酶(200毫单位/毫升)或腺苷(10微摩尔)不会改变葡萄糖代谢的胰岛素敏感性。胰岛素(1微单位/毫升)的主要作用是分别使脂肪生成和乳酸合成增加7倍和5倍,而葡萄糖氧化仍然很低。1微单位/毫升胰岛素对总葡萄糖代谢的5倍刺激伴随着葡萄糖转运增加8倍。在去甲肾上腺素(8微摩尔)存在的情况下,总葡萄糖代谢增加了2倍。这与葡萄糖氧化增加7倍有关,而脂肪生成受到极大抑制(抑制72%)。此外,单独的去甲肾上腺素不会改变葡萄糖转运。向与去甲肾上腺素一起孵育的脂肪细胞中添加胰岛素,可增强葡萄糖氧化,而脂肪生成仍然很低。总之,在胰岛素和去甲肾上腺素存在的情况下,葡萄糖是棕色脂肪组织的氧化底物。然而,葡萄糖作为氧化燃料的定量重要性仍有待确定。

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