链脲佐菌素诱导的糖尿病增加大鼠巨噬细胞中果糖2,6-二磷酸水平和葡萄糖代谢

Bustos R., Morenoaurioles V.R., Conde M., Montano R., Sobrino F.
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引用次数: 3

摘要

研究了链脲佐菌素诱导的糖尿病对大鼠腹膜巨噬细胞糖代谢的影响。在葡萄糖浓度增加的情况下,这些细胞在体外积累的果糖2,6-二磷酸大约是正常大鼠细胞的两倍,并且观察到乳酸的产生增加。与正常大鼠相比,糖尿病大鼠细胞中磷酸果糖激酶-1、磷酸果糖激酶-2、己糖激酶和丙酮酸激酶活性增加。糖尿病大鼠细胞中2-脱氧-d -葡萄糖的转运增加。[U-14C]糖尿病细胞中葡萄糖与糖原的结合也增加,而14CO2的释放量比正常动物细胞少。此外,与正常动物细胞相比,糖尿病患者的巨噬细胞没有更活跃的戊糖磷酸途径(用[1-14C]葡萄糖氧化测量),也没有产生更多的超氧阴离子(巨噬细胞激活的指标)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Streptozotocin-Induced Diabetes Increases Fructose 2,6-Bisphosphate Levels and Glucose Metabolism in Rat Macrophages

The acute effects of streptozotocin-induced diabetes on several parameters of glucose metabolism were investigated in rat peritoneal macrophages. These cells accumulated in vitro about twofold more fructose 2,6-bisphosphate in the presence of increasing glucose concentration than cells from normal rats, and an increased production of lactate was observed. Phosphofructokinase-1, phosphofructokinase-2, hexokinase, and pyruvate kinase activities were increased in cells from diabetic rats compared with those from normal rats. Transport of 2-deoxy-D-glucose was increased in cells from diabetic rats. [U-14C]Glucose incorporation into glycogen was also increased in cells from diabetics and the 14CO2 liberation was less than in cells from normal animals. Moreover, macrophages from diabetics did not possess a more active pentose phosphate pathway (measure with [1-14C]glucose oxidation) nor a greater production of superoxide anion (index of activation of macrophages) than in cells from normal animals.

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