Kiss G, Somogyi J, Csermely P, Szelényi J, Vér A
Semmelweis University, Department of Conservative Dentistry, Budapest, Hungary.
Diabetologia. 2001 Feb;44(2):220-3. doi: 10.1007/s001250051602.
AIMS/HYPOTHESIS: Diabetes mellitus has a serious effect on most of the properties of skeletal muscles. Changes in neuromuscular transmission are also involved in propagating the disease.
In our experiments, acetylcholinesterase was extracted from the fast extensor digitorum longus and slow soleus muscles of control, non-treated 6-week-diabetic and insulin-treated diabetic rats. The extracts were applied to velocity sedimentation and acetylcholinesterase activity was determined.
We observed considerable differences in the distribution of individual acetylcholinesterase molecular forms in diabetic fast muscles. This included a 59% decline in G4 content together with a fivefold increase in A8 and a 53 % increase in A12 activity resulting in a shift of acetylcholinesterase profile characteristically towards slow muscles. These alterations were partly reversed by insulin treatment.
CONCLUSION/INTERPRETATION: In slow muscles diabetes caused an increase in G4 activity without affecting the sedimentation profile. Decline in G4 content in fast muscles could contribute to enhanced desensitization of acetylcholine receptors in diabetes.
目的/假设:糖尿病对骨骼肌的大多数特性都有严重影响。神经肌肉传递的变化也与该疾病的传播有关。
在我们的实验中,从对照、未经治疗的6周糖尿病大鼠和胰岛素治疗的糖尿病大鼠的快肌趾长伸肌和慢肌比目鱼肌中提取乙酰胆碱酯酶。将提取物进行速度沉降并测定乙酰胆碱酯酶活性。
我们观察到糖尿病快肌中单个乙酰胆碱酯酶分子形式的分布存在显著差异。这包括G4含量下降59%,同时A8增加五倍,A12活性增加53%,导致乙酰胆碱酯酶谱特征性地向慢肌转移。胰岛素治疗部分逆转了这些改变。
结论/解读:在慢肌中,糖尿病导致G4活性增加,而不影响沉降谱。快肌中G4含量的下降可能导致糖尿病中乙酰胆碱受体脱敏增强。