急性咖啡因暴露对正常和甲状腺切除雄性 Wistar 大鼠血糖和肝糖原含量的影响

Q4 Medicine
Shehu-Tijani Shittu, Grace O Isehunwa, Abdulrasak Akinola Alada
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引用次数: 0

摘要

急性咖啡因暴露可诱发高血糖,但甲状腺激素对咖啡因诱发的高血糖的影响尚未确定。因此,本研究旨在探讨暴露于咖啡因对甲状腺切除大鼠血糖和肝糖原含量的影响。60 只成年雄性 Wistar 大鼠被随机分为 10 组,即 I-X 组(n=6)。 I、III、V、VII和IX组大鼠分别注射正常生理盐水、咖啡因、哌唑嗪+咖啡因、普萘洛尔+咖啡因、哌唑嗪+普萘洛尔+咖啡因联合注射液,II、IV、VI、VIII和X组大鼠切除甲状腺,治疗方法与正常大鼠相似。甲状腺切除组大鼠接受手术切除甲状腺,正常组大鼠接受假手术作为对照。大鼠愈合后禁食一夜,麻醉后分别插入股静脉和颈动脉进行给药和血糖测量。稳定后,在进行基础测量后,给每组大鼠注射生理盐水或咖啡因(6 毫克/千克),而另一组大鼠则在注射咖啡因前预先服用哌唑嗪(0.2 毫克/千克)、普萘洛尔(0.5 毫克/千克)或它们的复方制剂。然后在注射咖啡因后的 60 分钟内监测血糖,每隔 5 分钟监测一次。观察期结束时收集肝脏样本以测定糖原含量。咖啡因导致正常大鼠和甲状腺切除大鼠的血糖水平显著升高,在反应高峰时分别高达210%和180%。甲状腺切除大鼠的肝糖原含量(3.11 ± 0.20 mg/100g组织重量)明显高于正常大鼠(1.91 ± 0.43 mg/100g组织重量)。与对照组相比,正常大鼠(0.25 ± 0.04 mg/100g组织重量)和甲状腺切除大鼠(1.65 ± 0.16 mg/100g组织重量)的糖原含量都因咖啡因而明显降低。使用普萘洛尔或哌唑嗪和普萘洛尔的组合预处理可消除咖啡因对正常大鼠和甲状腺切除大鼠血糖和肝糖原含量的影响,但使用哌唑嗪预处理只能显著降低咖啡因引起的高血糖反应。本研究结果表明,咖啡因诱导的正常大鼠和甲状腺切除大鼠的高血糖反应是通过α和β肾上腺素受体介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Acute Caffeine Exposure on Blood Glucose and Hepatic Glycogen Content in Normal and Thyroidectomized Male Wistar Rats.

Acute caffeine exposure had been shown to induce hyperglycemia however; the influence of thyroid hormones on the caffeine-induced hyperglycemia is yet to be established. The present study was therefore designed to investigate the effect of caffeine exposure on blood glucose and hepatic glycogen content in thyroidectomized rats. Sixty adult male Wistar rats were randomly divided into 10 groups as I-X (n=6).  Rats in groups I, III, V, VII and IX were given normal saline, caffeine, prazosin + caffeine, propranolol +caffeine, combined prazosin+ propranolol+caffeine injections respectively while rats in groups  II, IV, VI, VIII and X were thyroidectomized  and treated in similar manner as the normal rats respectively. Surgical removal of the thyroid gland was done in the thyroidectomised groups while sham-operation was done in Normal group to serve as control. After healing and following an overnight fast, the rats were anaesthetized and the femoral vein and carotid artery were cannulated for drug administration and blood glucose measurement respectively. After stabilization, following basal measurements, rats from each group were injected normal saline or caffeine (6mg/kg) while another sets were pre-treated prazosin (0.2 mg/kg), propanolol (0.5 mg/kg) or their combination before caffeine administration. Blood glucose was then monitored for 60 minutes post-injection of caffeine at 5 minutes interval. Liver samples were collected at the end of the observation period for glycogen content determination. Caffeine caused significant increased blood glucose levels in both normal and thyroidectomized rats which were up to 210% and 180% respectively at the peak of their responses. Liver glycogen content of the thyroidectomized rats (3.11 ± 0.20 mg/100g tissue weight) was significantly higher than the normal rats (1.91 ± 0.43 mg/100g tissue weight). These glycogen contents were significantly reduced by caffeine in both normal (0.25 ± 0.04 mg/100g tissue weight) and thyroidectomized rats (1.65 ± 0.16 mg/100g tissue weight) when compared with their controls. The caffeine effects on blood glucose and hepatic glycogen content were abolished by pretreatment with propanolol or a combination of prazosin and propanolol in both normal and thyroidectomized rats but pretreatment with prazosin caused only significant reduction in hyperglycemic response to caffeine. The findings of this study suggest that caffeine-induced hyperglycemia in both normal and thyroidectomized rats are mediated through both alpha and beta adrenoceptors.

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来源期刊
Nigerian Journal of Physiological Sciences
Nigerian Journal of Physiological Sciences Medicine-Physiology (medical)
CiteScore
0.80
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23
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