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目的研究血糖波动对糖尿病(DM)大鼠甲状腺组织的损伤程度。方法将30只雄性大鼠随机分为模型组20只,对照组10只,模型组采用高糖高脂饲料叠加腹腔注射链脲佐菌素(STZ)构建DM大鼠模型。将模型组随机分为持续性高血糖组和血糖波动组,每组10只;血糖波动组每天注射优泌乐注射液,高血糖组和对照组每天腹腔注射等量生理盐水,分析3组大鼠每日血糖水平标准差(SDBG)、平均血糖水平(MBG)和最大血糖波动幅度(LAGE)。12周后处死大鼠,采心脏血检测生化指标和甲状腺功能三项,观察甲状腺组织超微结构。结果血糖波动组和持续高血糖组大鼠MBG、SDBG和LAGE均高于对照组(P<0.05);血糖波动组MBG低于持续高血糖组(P<0.05),SDBG和LAGE高于持续高血糖组(P<0.05)。血糖波动组总胆固醇(TC)、空腹血糖(FPG)和糖化血红蛋白(Hb A1c)均高于对照组(P<0.05);TC、FPG和三酰甘油(TG)均低于持续高血糖组(P<0.05)。持续高血糖和血糖波动组游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)均低于对照组(P<0.05)。持续高血糖组与血糖波动组甲状腺滤泡上皮细胞损伤,微绒毛缺失。结论持续的高血糖或血糖波动均可导致DM大鼠甲状腺激素合成和释放功能下降;持续高血糖组和血糖波动组DM大鼠甲状腺的超微结构均有变化,但两组差异不明显。
Objective To investigate the degree of damage of thyroid tissue induced by blood glucose in diabetic rats. Methods Thirty male rats were randomly divided into model group (n = 20) and control group (n = 10). The model group was induced by intraperitoneal injection of streptozotocin (STZ). The model group was randomly divided into persistent hyperglycemia group and blood glucose fluctuation group, with 10 rats in each group. The blood glucose fluctuation group was given intragastric injection of the same amount of saline every day. The rats in the hyperglycemia group and the control group were given intraperitoneal injection of normal saline. Daily SDGG, MBG, and LAGE. After 12 weeks, the rats were sacrificed and the biochemical indexes and thyroid function of the blood were collected to observe the ultrastructure of thyroid tissue. Results The MBG, SDBG and LAGE in hyperglycemia group and hyperglycemia group were significantly higher than those in control group (P <0.05). MBG in hyperglycemia group was lower than that in hyperglycemia group (P <0.05), while SDBG and LAGE were higher than those in hyperglycemia group Blood glucose group (P <0.05). TC, FPG and Hb A1c in blood glucose fluctuation group were higher than those in control group (P <0.05); TC, FPG and triglyceride (TG) were lower than those in continuous hyperglycemia group P <0.05). The levels of free triiodothyronine (FT3) and free thyroxine (FT4) in hyperglycemia and glycemic group were lower than those in control group (P <0.05). Sustained hyperglycemia and blood glucose fluctuations in thyroid follicular epithelial cell damage, lack of microvilli. Conclusions Continuous hyperglycemia or fluctuation of blood glucose can lead to the decrease of thyroid hormone synthesis and release in diabetic rats. The ultrastructures of thyroid in DM rats with persistent hyperglycemia and hyperglycemia were all changed, but the difference was not obvious between the two groups.