Insulin fails to alter plasma LCFA metabolism in muscle perfused at similar glucose uptake.

Insulin fails to alter plasma LCFA metabolism in muscle perfused at similar glucose uptake.
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胰岛素无法改变在类似葡萄糖摄取下灌注的肌肉中的血浆 LCFA 代谢。

DOI:
10.1152/ajpendo.00553.2001
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发表时间:
2002
期刊:
American journal of physiology. Endocrinology and metabolism.
影响因子:
--
通讯作者:
Turcotte,LorraineP
Turcotte,LorraineP
中科院分区:
--
文献类型:
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作者:
Yee,AliceJ;Turcotte,LorraineP

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胰岛素已被证明可以改变肌肉中的长链脂肪酸 (LCFA) 代谢和丙二酰辅酶 A 的产生。然而,这些改变可能部分是由伴随的胰岛素诱导的葡萄糖摄取变化引起的。因此,为了确定独立于葡萄糖摄取变化的胰岛素对 LCFA 代谢的影响,用 600 μM 棕榈酸酯和 [1-14C] 棕榈酸酯以及 20 mM 葡萄糖和无胰岛素 (G) 或 6 mM 葡萄糖和 250 μU/ml 胰岛素 (I) 灌注大鼠后躯。根据我们的方案,G 组和 I 组之间的葡萄糖摄取没有显着差异(10.3 ± 0.6 与 11.0 ± 0.5 μmol·g−1·h−1;P> 0.05)。 G组(10.1±1.0和0.8±0.1nmol·min−1·g−1)和I组(10.2±0.6和1.1±0.2nmol·min−1·g−1)之间总棕榈酸摄取和氧化没有显着差异(P>0.05)。灌注前G组和I组肌肉甘油三酯和丙二酰辅酶A水平无显着差异,灌注过程中也无显着变化(P>0.05)。同样,肌肉甘油三酯合成在各组之间没有显着差异(P>0.05)。这些结果表明,在相似的葡萄糖摄取条件下,胰岛素的存在不会改变 LCFA 代谢,并表明碳水化合物可用性诱导的细胞机制(但不依赖于胰岛素)可能在肌肉 LCFA 代谢的调节中很重要。
Insulin has been shown to alter long-chain fatty acid (LCFA) metabolism and malonyl-CoA production in muscle. However, these alterations may have been induced, in part, by the accompanying insulin-induced changes in glucose uptake. Thus, to determine the effects of insulin on LCFA metabolism independently of changes in glucose uptake, rat hindquarters were perfused with 600 μM palmitate and [1-14C]palmitate and with either 20 mM glucose and no insulin (G) or 6 mM glucose and 250 μU/ml of insulin (I). As dictated by our protocol, glucose uptake was not significantly different between the G and I groups (10.3 ± 0.6 vs. 11.0 ± 0.5 μmol · g−1· h−1;P> 0.05). Total palmitate uptake and oxidation were not significantly different (P> 0.05) between the G (10.1 ± 1.0 and 0.8 ± 0.1 nmol · min−1· g−1) and I (10.2 ± 0.6 and 1.1 ± 0.2 nmol · min−1· g−1) groups. Preperfusion muscle triglyceride and malonyl-CoA levels were not significantly different between the G and I groups and did not change significantly during the perfusion (P> 0.05). Similarly, muscle triglyceride synthesis was not significantly different between groups (P> 0.05). These results demonstrate that the presence of insulin under conditions of similar glucose uptake does not alter LCFA metabolism and suggest that cellular mechanisms induced by carbohydrate availability, but independent of insulin, may be important in the regulation of muscle LCFA metabolism.