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首页> 外文期刊>Life sciences >Decreased responsiveness of gluconeogenesis to the modulation by sulfonylureas in hepatocytes isolated from obese (fa/fa) Zucker rats.
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Decreased responsiveness of gluconeogenesis to the modulation by sulfonylureas in hepatocytes isolated from obese (fa/fa) Zucker rats.

机译：肥胖（fa / fa）祖克大鼠分离的肝细胞中糖异生对磺酰脲类药物调节的反应性降低。

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摘要

The influence of the hypoglycemic agent glipizide (0-100 microM) on the rate of gluconeogenesis from lactate, as well as on the levels of fructose 2,6-bisphosphate, has been investigated in hepatocytes isolated from genetically obese (fa/fa) Zucker rats and from their corresponding lean (Fa/-) littermates. As compared to lean rat hepatocytes, liver cells isolated from obese animals showed a lower rate of basal gluconeogenesis (0.9 +/- 0.2 vs 5.4 +/- 0.5 micromol of lactate converted to glucose/g cell x 30 min, n=4) and higher levels of fructose 2,6-bisphosphate (11.5 +/- 1.0 vs 5.9 +/- 0.4 nmol/g cell, n=8-9). In lean rat hepatocytes, the presence of glipizide in the incubation medium caused a dose-dependent inhibition of the rate of lactate conversion to glucose (maximal inhibition=46%; EC50 value=26 microM), and simultaneously raised the cellular content of fructose-2,6-bisphosphate (maximal increment=40%; EC50 value=10 microM). In contrast, in hepatocytes isolated from obese rats, the inhibition of gluconeogenesis and the increment in fructose-2,6-bisphosphate levels elicited by glipizide were significantly reduced (maximal effects of 22 and 13%, respectively). Similarly, the activation of glycogen phosphorylase and the increase in hexose 6-phosphate levels in response to glipizide were less marked in obese rat hepatocytes than in liver cells isolated from lean animals. These results demonstrate that the efficacy of sulfonylureas as inhibitors of hepatic gluconeogenesis is reduced in the genetically obese (fa/fa) Zucker rat.
机译：在从遗传性肥胖（fa / fa）Zucker分离的肝细胞中，已经研究了降糖药格列吡嗪（0-100 microM）对乳酸糖异生率以及果糖2,6-二磷酸水平的影响。大鼠及其相应的瘦肉（Fa /-）同窝仔。与瘦大鼠肝细胞相比，从肥胖动物中分离出的肝细胞显示出较低的基础糖异生率（0.9 +/- 0.2 vs 5.4 +/- 0.5 micromol乳酸转化为葡萄糖/ g细胞x 30分钟，n = 4），并且高水平的果糖2,6-二磷酸酯（11.5 +/- 1.0与5.9 +/- 0.4 nmol / g细胞，n = 8-9）。在瘦大鼠肝细胞中，温育培养基中格列吡嗪的存在导致乳酸转化为葡萄糖的速率呈剂量依赖性抑制（最大抑制率= 46％; EC50值= 26 microM），同时增加了果糖- 2,6-二磷酸酯（最大增量= 40％; EC50值= 10 microM）。相反，在从肥胖大鼠分离的肝细胞中，格列吡嗪引起的糖原异生抑制作用和果糖2,6-二磷酸水平的增加显着降低（最大作用分别为22％和13％）。类似地，肥胖大鼠肝细胞中糖原磷酸化酶的激活和响应格列吡嗪的6-磷酸己糖水平的增加在肥胖大鼠肝细胞中的特征要比从瘦动物分离的肝细胞中的特征少。这些结果证明，在遗传性肥胖（fa / fa）的祖克大鼠中，磺酰脲类作为肝糖异生的抑制剂的功效降低。

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