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创伤大鼠骨骼肌中葡萄糖摄取及通过磷酸果糖激酶的通量

Glucose uptake and flux through phosphofructokinase in wounded rat skeletal muscle.

作者信息

Forster J, Morris A S, Shearer J D, Mastrofrancesco B, Inman K C, Lawler R G, Bowen W, Caldwell M D

机构信息

Department of Surgery, Brown University, Providence, Rhode Island 02902.

出版信息

Am J Physiol. 1989 Jun;256(6 Pt 1):E788-97. doi: 10.1152/ajpendo.1989.256.6.E788.

DOI:10.1152/ajpendo.1989.256.6.E788
PMID:2525343
Abstract

Skeletal muscle injured with lambda-carrageenan has increased aerobic glycolysis. To assess the regulation of this process, the tissue concentrations of glycolytic intermediates, the flux through phosphofructokinase (PFK), and the intracellular concentrations of PFK effectors were examined in wounded rat skeletal muscle and in macrophages, the predominant inflammatory cell in the early stages of this wound model. Autoradiography demonstrated increased 2-deoxy-D-glucose uptake in wounded tissue compared with nonwounded muscle. 2-Deoxy-D-glucose was localized to the cellular infiltrate. The glycolytic intermediate concentrations demonstrated a facilitation of PFK in macrophages and wounded tissue as compared with nonwounded muscle. Wounded tissue had twice the flux through PFK compared with nonwounded muscle (10.0 +/- 0.6 wounded vs. 4.9 +/- 0.4 mumol.h-1.g-1 nonwounded). Macrophages had the highest flux through PFK (63.7 +/- 5.7 mumol.h-1.g-1) and when coincubated with muscle, the combined flux through PFK was equal to that of wounded muscle. The increase in glycolysis associated with wounded tissue may be explained by increased glucose uptake and increased flux through PFK by the inflammatory cells present in wounded tissue.

摘要

用λ-角叉菜胶损伤的骨骼肌有氧糖酵解增加。为了评估这一过程的调节机制,我们检测了受伤大鼠骨骼肌和巨噬细胞(此伤口模型早期主要的炎症细胞)中糖酵解中间产物的组织浓度、通过磷酸果糖激酶(PFK)的通量以及PFK效应物的细胞内浓度。放射自显影显示,与未受伤的肌肉相比,受伤组织对2-脱氧-D-葡萄糖的摄取增加。2-脱氧-D-葡萄糖定位于细胞浸润处。与未受伤的肌肉相比,糖酵解中间产物浓度表明巨噬细胞和受伤组织中的PFK活性增强。与未受伤的肌肉相比,受伤组织通过PFK的通量是其两倍(受伤组织为10.0±0.6 μmol·h⁻¹·g⁻¹,未受伤组织为4.9±0.4 μmol·h⁻¹·g⁻¹)。巨噬细胞通过PFK的通量最高(63.7±5.7 μmol·h⁻¹·g⁻¹),当与肌肉共同孵育时,通过PFK的总通量与受伤肌肉相等。受伤组织中糖酵解的增加可能是由于受伤组织中存在的炎症细胞增加了葡萄糖摄取以及通过PFK的通量。

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