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对短期胰岛素诱导低血糖的糖尿病大鼠灌注肝脏中的生酮作用评估。

Ketogenesis evaluation in perfused liver of diabetic rats submitted to short-term insulin-induced hypoglycemia.

作者信息

Barrena Helenton Cristhian, Gazola Vilma Aparecida Ferreira Godoi, Furlan Maria Montserrat Diaz Pedrosa, Garcia Rosângela Fernandes, de Souza Helenir Medri, Bazotte Roberto Barbosa

机构信息

Department of Morphophysiological Sciences, State University of Maringá, Maringá, PR, Brazil.

出版信息

Cell Biochem Funct. 2009 Aug;27(6):383-7. doi: 10.1002/cbf.1586.

DOI:10.1002/cbf.1586
PMID:19623545
Abstract

Ketogenesis, inferred by the production of acetoacetate plus ss-hydroxybutyrate, in isolated perfused livers from 24-h fasted diabetic rats submitted to short-term insulin-induced hypoglycemia (IIH) was investigated. For this purpose, alloxan-diabetic rats that received intraperitoneal regular insulin (IIH group) or saline (COG group) injection were compared. An additional group of diabetic rats which received oral glucose (gavage) (100 mg kg(-1)) 15 min after insulin administration (IIH + glucose group) was included. The studies were performed 30 min after insulin (1.0 U kg(-1)) or saline injection. The ketogenesis before octanoate infusion was diminished (p < 0.05) in livers from rats which received insulin (COG vs. IIH group) or insulin plus glucose (COG vs. IIH + glucose group). However, the liver ketogenic capacity during the infusion of octanoate (0.3 mM) was maintained (COG vs. IIH group and COG vs. IIH + glucose group). In addition, the blood concentration of ketone bodies was not influenced by the administration of insulin or insulin plus glucose. Taken together, the results showed that inspite the fact that insulin and glucose inhibits ketogenesis, livers from diabetic rats submitted to short-term IIH which received insulin or insulin plus glucose showed maintained capacity to produce acetoacetate and ss-hydroxybutyrate from octanoate.

摘要

通过乙酰乙酸和β-羟基丁酸的生成推断出的生酮作用,在来自禁食24小时的糖尿病大鼠、经受短期胰岛素诱导的低血糖(IIH)的离体灌注肝脏中进行了研究。为此,比较了接受腹腔注射正规胰岛素(IIH组)或生理盐水(COG组)的四氧嘧啶糖尿病大鼠。还纳入了另一组糖尿病大鼠,在胰岛素给药后15分钟给予口服葡萄糖(灌胃)(100 mg kg(-1))(IIH + 葡萄糖组)。在胰岛素(1.0 U kg(-1))或生理盐水注射30分钟后进行研究。在接受胰岛素(COG组与IIH组)或胰岛素加葡萄糖(COG组与IIH + 葡萄糖组)的大鼠肝脏中,辛酸输注前的生酮作用减弱(p < 0.05)。然而,在输注辛酸(0.3 mM)期间肝脏的生酮能力得以维持(COG组与IIH组以及COG组与IIH + 葡萄糖组)。此外,酮体的血浓度不受胰岛素或胰岛素加葡萄糖给药的影响。综上所述,结果表明,尽管胰岛素和葡萄糖抑制生酮作用,但接受胰岛素或胰岛素加葡萄糖的、经受短期IIH的糖尿病大鼠肝脏显示出从辛酸产生乙酰乙酸和β-羟基丁酸的能力得以维持。

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引用本文的文献

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Mol Cell Biochem. 2014 Dec;397(1-2):97-107. doi: 10.1007/s11010-014-2176-2. Epub 2014 Aug 6.
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Oral glutamine is superior than oral glucose to promote glycemia recovery in mice submitted to insulin-induced hypoglycemia.口服谷氨酰胺优于口服葡萄糖,可促进胰岛素诱导低血糖的小鼠血糖恢复。
Int J Endocrinol. 2013;2013:841514. doi: 10.1155/2013/841514. Epub 2013 Aug 24.