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长链多不饱和欧米伽3脂肪酸缺乏的大鼠胰岛中L-谷氨酰胺和棕榈酸的分解代谢

L-glutamine and palmitate catabolism in pancreatic islets from rats depleted in long-chain polyunsaturated omega 3 fatty acids.

作者信息

Zhang Ying, Louchami Karim, Carpentier Yvon A, Malaisse Willy J, Sener Abdullah

机构信息

Laboratory of Experimental Hormonology, Brussels Free University, Belgium.

出版信息

Cell Biochem Funct. 2008 Jan-Feb;26(1):82-6. doi: 10.1002/cbf.1403.

DOI:10.1002/cbf.1403
PMID:17299809
Abstract

The catabolism of D-glucose was recently found to be impaired in pancreatic islets from rats depleted in long-chain polyunsaturated omega3 fatty acids. The specificity of this alteration was now investigated by characterizing the oxidative fate of endogenous nutrients in islets preincubated with either L-[U-14C]glutamine or [U-14C]palmitate and then incubated variously in the absence of D-glucose, presence of the hexose or presence of metabolic poisons. Relative to their radioactive content after preincubation, the production of 14CO2 by islets prelabelled with [U-14C]glutamine was higher in omega3-depleted rats than control animals. The enhancing action of D-glucose upon such production was impaired, however, in the omega3-depleted rats. The net uptake of 14C-palmitate and absolute value for 14CO2 output were both increased in omega3-depleted rats, whilst the ratio between 14CO2 output and islet radioactive content was decreased in the same animals. The inhibition of 14CO2 production by metabolic poisons was comparable in all cases. These results are consistent with recent findings on such items as the availability of endogenous amino acids and uptake of unesterified fatty acids in extrapancreatic sites of the omega3-depleted rats. They also support the view that the alteration of D-glucose metabolism in the islets of the latter animals may be attributable, in part at least, to alteration of glucokinase kinetics by high intracellular acyl-CoA levels.

摘要

最近发现,在长链多不饱和ω-3脂肪酸缺乏的大鼠胰岛中,D-葡萄糖的分解代谢受损。现在通过表征预先用L-[U-14C]谷氨酰胺或[U-14C]棕榈酸酯预孵育,然后在无D-葡萄糖、有己糖或有代谢毒物的情况下进行不同孵育的胰岛中内源性营养物质的氧化命运,来研究这种改变的特异性。相对于预孵育后的放射性含量,用[U-14C]谷氨酰胺预标记的胰岛产生的14CO2在ω-3缺乏的大鼠中比对照动物更高。然而,在ω-3缺乏的大鼠中,D-葡萄糖对这种产生的增强作用受损。在ω-3缺乏的大鼠中,14C-棕榈酸酯的净摄取和14CO2输出的绝对值均增加,而在相同动物中14CO2输出与胰岛放射性含量之间的比率降低。在所有情况下,代谢毒物对14CO2产生的抑制作用相当。这些结果与最近关于ω-3缺乏大鼠胰腺外部位内源性氨基酸的可用性和未酯化脂肪酸摄取等项目的发现一致。它们还支持这样一种观点,即后一种动物胰岛中D-葡萄糖代谢的改变可能至少部分归因于细胞内高酰基辅酶A水平对葡萄糖激酶动力学的改变。

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