Growth hormone and insulin-like growth factors I and II produce distinct alterations in glucose metabolism in 3T3-F442A adipocytes.

Growth hormone and insulin-like growth factors I and II produce distinct alterations in glucose metabolism in 3T3-F442A adipocytes.
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生长激素和胰岛素样生长因子 I 和 II 对 3T3-F442A 脂肪细胞中的葡萄糖代谢产生明显的改变。

DOI:
10.1073/pnas.82.24.8724
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发表时间:
1985
影响因子:
11.1
通讯作者:
Satin,MS
Satin,MS
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Schwartz,J;Foster,CM;Satin,MS

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在3T3-F442A脂肪细胞中,人生长激素(hGH)在4小时内刺激葡萄糖氧化。生长激素浓度在50-100 ng/ml时显著增加,很少超过对照的50%。刺激是短暂的;生长激素孵育48小时后,葡萄糖氧化被显著抑制到比控制值低35%。鉴于胰岛素样生长因子(IGF)可能介导生长激素的作用,我们比较了hGH (500 ng/ml)和几种IGF制剂对3T3脂肪细胞糖代谢的影响。孵育4小时后,来自人血浆的igf - 1以剂量相关的方式刺激葡萄糖氧化,在50 ng/ml时产生10倍的增加。重组DNA技术制备的甲硫基IGF-I的有效性为IGF-I的85-88%。IGF-II在50 ng/ml孵育4小时后刺激葡萄糖氧化3倍。与hGH在48小时后观察到的抑制相反,所有三种IGF制剂在孵育48小时后都刺激了葡萄糖氧化,并且与4小时后一样有效。当每一种IGF制剂(浓度为5 ng/ml)与生长激素联合测试时,生长激素的刺激和抑制作用叠加在IGF的刺激上。因此,IGF的刺激特性与生长激素的不同之处在于,与生长激素相比,IGF增加葡萄糖氧化的最大程度是生长激素的20倍。此外,在生长激素抑制葡萄糖代谢的条件下,所有IGF制剂在48小时后都刺激了葡萄糖氧化。因此,细胞外IGFs不太可能介导hGH对3T3-F442A脂肪细胞葡萄糖代谢的影响。
In 3T3-F442A adipocytes, human growth hormone (hGH) stimulates glucose oxidation in 4 hr. A maximal increase is evident at hGH concentrations of 50-100 ng/ml and rarely exceeds 50% above control. The stimulation is transient; after 48 hr of incubation with GH, glucose oxidation is significantly suppressed to 35% below control values. In view of the concept that insulin-like growth factors (IGF) may mediate the effects of GH, we compared the effects of hGH (500 ng/ml) and several preparations of IGF on glucose metabolism in 3T3 adipocytes. After 4 hr of incubation, IGF-I from human plasma stimulated glucose oxidation in a dose-related manner, producing a 10-fold increase at 50 ng/ml. Methionyl-IGF-I produced by recombinant DNA techniques was 85-88% as effective as IGF-I. IGF-II stimulated glucose oxidation 3-fold at 50 ng/ml after 4 hr of incubation. In contrast to the suppression observed with hGH after 48 hr, all three of the IGF preparations stimulated glucose oxidation after 48 hr of incubation and were as effective as they were after 4 hr. When each of the IGF preparations was tested (at 5 ng/ml) in combination with hGH, both the stimulatory and suppressive effects of GH were superimposed on the stimulation by the IGFs. Thus, the stimulatory properties of IGF differed from those of GH in that the maximum extent to which IGF increased glucose oxidation, compared with hGH, was as much as 20-fold greater. Furthermore, all of the IGF preparations stimulated glucose oxidation after 48 hr under conditions in which hGH suppressed glucose metabolism. Thus, it is unlikely that extracellular IGFs mediate the effects of hGH on glucose metabolism in 3T3-F442A adipocytes.