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首页> 外文期刊>Brazilian Oral Research >Activity, distribution and regulation of phosphofructokinase in salivary gland of rats with streptozotocin-induced diabetes
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Activity, distribution and regulation of phosphofructokinase in salivary gland of rats with streptozotocin-induced diabetes

机译:链脲佐菌素诱发的糖尿病大鼠唾液腺中果糖磷酸激酶的活性,分布和调节

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摘要

Although the influence of diabetes on salivary glands is well studied, it still presents conflicting results. In this work, the regulation of the phosphofructokinase-1 enzyme (PFK-1) was studied utilizing the salivary glands of rats. Diabetes was induced by a single intraperitoneal injection of streptozotocin (60 mg/Kg of body weight) in rats (180-200 g). The animals were killed 30 days after the induction of diabetes and the submandibular and parotid salivary glands were used. Hyperglycemia was evaluated by blood sugar determination. The distribution of PFK-1 between the soluble and cytoskeleton fractions, the phosphate content of PFK-1, the content of fructose-2,6-bisphosphate and the activity of the PFK-2 enzyme were determined. The calculated relative glandular weight showed a higher value for the parotid gland in comparison with the control, but not for the submandibular gland. The activity of PFK-1 expressed per gland showed no variation between diabetic and control animals. However, considering the specific activity, the soluble enzyme presented a value 50% higher than that of the control and the cytoskeleton bound form increased by 84% compared to the control. For the parotid gland, no difference in the specific activity between diabetic and control animals was observed. On the other hand, the activity per gland of the soluble enzyme increased in the diabetic animals. The phosphate content of PFK-1 increased in the submandibular and parotid glands of diabetic rats. Both the content of fructose-2,6-bisphosphate and the active form of PFK-2 were reduced in the diabetic glands. In conclusion, the increase in the activity of PFK-1 observed in the salivary glands of rats with streptozotocin-induced diabetes does not seem to be due to its modulator fructose-2,6-bisphosphate.
机译:尽管对糖尿病对唾液腺的影响进行了充分的研究,但仍存在矛盾的结果。在这项工作中,利用大鼠唾液腺研究了磷酸果糖激酶-1酶(PFK-1)的调节。通过在大鼠(180-200 g)中腹膜内注射链脲佐菌素(60 mg / Kg体重)诱导糖尿病。在诱发糖尿病后30天将动物处死,并使用颌下和腮腺唾液腺。通过血糖测定评估高血糖症。测定了PFK-1在可溶性部分和细胞骨架部分之间的分布,PFK-1的磷酸盐含量,2,6-二磷酸果糖的含量以及PFK-2酶的活性。与对照相比,腮腺的计算出的相对腺体重量显示出较高的值,但颌下腺却没有。每个腺体表达的PFK-1活性在糖尿病动物和对照动物之间没有变化。然而,考虑到比活性,可溶性酶的值比对照的高50%,并且细胞骨架结合形式与对照相比增加了84%。对于腮腺,在糖尿病动物和对照动物之间没有观察到比活性的差异。另一方面,在糖尿病动物中可溶性酶的每腺活性增加。在糖尿病大鼠的颌下腺和腮腺中,PFK-1的磷酸盐含量增加。糖尿病腺体中的2,6-二磷酸果糖含量和PFK-2活性形式均降低。总之,在链脲佐菌素诱发的糖尿病大鼠的唾液腺中观察到的PFK-1活性的增加似乎不是由于其调节剂果糖2,6-双磷酸酯。

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