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长期链脲佐菌素诱导糖尿病对大鼠肌肉收缩及组织化学特性的影响。

Effects of long-term streptozotocin diabetes on the contractile and histochemical properties of rat muscles.

作者信息

Cotter M, Cameron N E, Lean D R, Robertson S

机构信息

Department of Physiology, Marischal College, University of Aberdeen.

出版信息

Q J Exp Physiol. 1989 Jan;74(1):65-74. doi: 10.1113/expphysiol.1989.sp003240.

Abstract

Contractile and histochemical properties of soleus (a slow-twitch muscle) and extensor digitorum longus (EDL, a fast-twitch muscle) were studied in mature rats after 3 months of streptozotocin-induced diabetes. Results were compared with age- and weight-matched controls. Diabetes produced profound wasting of fast muscles and particularly of the fast glycolytic (FG) fibres. Slow muscle fibres, both within the mixed EDL and in soleus, were less atrophied. Strength performance of EDL was reduced by diabetes, but maintained in soleus. Diabetes was without effect on the time to peak tension (TTP) and half-relaxation time (HRT) of EDL. However it produced profound slowing of soleus muscles, particularly of the relaxation phase. Part of the slowing effect of diabetes may be related to a histochemically demonstrable loss of fast oxidative glycolytic (FOG) fibres in soleus. Histochemical staining for the oxidative marker succinic dehydrogenase (SDH) revealed marked disruption of reaction product distribution in soleus, indicating an impairment of oxidative capacity.

摘要

在链脲佐菌素诱导的糖尿病3个月后,对成年大鼠比目鱼肌(一种慢肌)和趾长伸肌(EDL,一种快肌)的收缩和组织化学特性进行了研究。将结果与年龄和体重匹配的对照组进行比较。糖尿病导致快肌尤其是快速糖酵解(FG)纤维严重萎缩。混合的EDL和比目鱼肌内的慢肌纤维萎缩程度较小。糖尿病使EDL的力量表现降低,但比目鱼肌的力量表现保持不变。糖尿病对EDL的峰值张力时间(TTP)和半松弛时间(HRT)没有影响。然而,它使比目鱼肌明显减慢,尤其是在松弛阶段。糖尿病的部分减慢作用可能与比目鱼肌中组织化学可证实的快速氧化糖酵解(FOG)纤维的丧失有关。氧化标记琥珀酸脱氢酶(SDH)的组织化学染色显示比目鱼肌中反应产物分布明显紊乱,表明氧化能力受损。

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