首页> 外文期刊>Nigerian Journal of Physiological Sciences >Effect of Cortisol on Plasma Lactate Levels following Cortisolinduced Hyperglycaemia in Common African Toad, Bufo regularis
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Effect of Cortisol on Plasma Lactate Levels following Cortisolinduced Hyperglycaemia in Common African Toad, Bufo regularis

机译:氢化可的松对非洲普通蟾蜍蟾蜍中氢化可的松诱导的高血糖后血浆乳酸水平的影响

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Summary: Previous studies in man have shown that cortisol induces hyperglycemia through gluconeogenesis. However, the metabolic substrates involved in cortisol-induced hyperglycemia and the role of adrenergic receptors in lactate production in toads have not been well studied. This study investigated the effects of adrenergic receptor blockers in cortisol-induced hyperglycemia and blood lactate levels in the common African toad (Bufo regularis). Each toad was fasted and anaesthetized with sodium thiopentone given intraperitoneally (50mg/kg/i.p). The animals (control) received 0.7% amphibian saline while animals (untreated) received cortisol intravenously (50μg/kg/i.v). In pre-treatment groups, animals received propanolol (0.5 mg/kg/i.v), prazosin (0.2 mg/kg/i.v) and combination of propanolol (0.5mg/kg/i.v) and prazosin (0.2 mg/kg/i.v) respectively followed by administration of cortisol 50μg/kg/i.v. Thereafter, blood samples were collected for estimation of glucose and lactate using the modified glucose oxidase method and colorimetric method respectively. Cortisol caused significant increase in blood glucose level ((p<0.05) and reduction in blood lactate levels. Pre-treatment with Prazosin (0.2 mg/kg/i.v) caused significant (p<0.05) increase in blood glucose level and significant reduction in blood lactate levels while pre-treatment with Propanolol (0.5mg/kg/i.v) abolished cortisol-induced hyperglycemia and caused increase in blood lactate levels compared with the untreated group. The combination of both blockers abolished the hyperglycemic effect of cortisol and caused increase in the blood lactate levels. The results of this study show that cortisol-induced hyperglycemia is a consequent of gluconeogenesis and mediated through the beta-adrenergic receptors. The results also show that lactate is produced and used as a gluconeogenic substrate to induce cortisol hyperglycemia in the Common African toad bufo regularis. The beta adrenergic receptors are involved in the use of lactate to induce cortisol hyperglycemia in the Common African toad Bufo-regularis.
机译:摘要:先前在人体中的研究表明,皮质醇可通过糖异生作用诱导高血糖症。然而,尚未充分研究与蟾蜍皮质醇诱导的高血糖有关的代谢底物以及肾上腺素能受体在乳酸产生中的作用。这项研究调查了肾上腺素能受体阻滞剂对普通非洲蟾蜍(大蟾蜍)中皮质醇诱导的高血糖症和血液乳酸水平的影响。将每只蟾蜍禁食并用腹膜内给予的硫代戊酮钠麻醉(50mg / kg / i.p)。动物(对照)接受0.7%的两栖生理盐水,而动物(未处理)接受静脉内皮质醇(50μg/ kg / i.v)。在预处理组中,动物分别接受普萘洛尔(0.5 mg / kg / iv),哌唑嗪(0.2 mg / kg / iv)以及普萘洛尔(0.5mg / kg / iv)和哌唑嗪(0.2 mg / kg / iv)的组合随后服用皮质醇50μg/ kg / iv此后,分别使用改进的葡萄糖氧化酶方法和比色法收集血液样本以评估葡萄糖和乳酸。皮质醇引起血糖水平显着升高(p <0.05)和血乳酸水平降低;普拉唑嗪(0.2 mg / kg / iv)预处理导致血糖水平显着(p <0.05)升高,而血浆乳酸水平降低。与未治疗组相比,丙泊酚(0.5mg / kg / iv)预处理时血乳酸水平消除了皮质醇诱发的高血糖症,并导致血乳酸水平升高;两种阻滞剂的结合消除了皮质醇的高血糖作用,并导致了血浆中的增加。这项研究的结果表明,皮质醇诱导的高血糖是糖异生的结果,并且是通过β-肾上腺素能受体介导的;结果还表明,乳酸盐的产生并用作糖异生的底物,可引起皮质醇的高血糖。非洲蟾蜍蟾蜍:β-肾上腺素能受体参与使用乳酸诱导非洲普通蟾蜍的皮质醇高血糖。 ad Bufo-regularis。

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