Albuquerque G G, Gazola V A F G, Garcia R F, Souza K L A, Barrena H C, Curi R, Bazotte R B
Department of Morphophysiological Sciences, State University of Maringá, Maringá, PR, Brazil.
Cell Biochem Funct. 2008 Mar-Apr;26(2):228-32. doi: 10.1002/cbf.1440.
Gluconeogenesis and ketogenesis of in situ rat perfused liver submitted to short-term insulin-induced hypoglycaemia (IIH) were investigated. For this purpose, 24-h fasted rats that received intraperitoneal (ip) regular insulin (1.0 U kg(-1)) or saline were compared. The studies were performed 30 min after insulin (IIH group) or saline (COG group) injection. For gluconeogenesis studies, livers from the IIH and COG groups were perfused with increasing concentrations (from basal blood concentrations until saturating concentration) of glycerol, L-lactate (Lac) or pyruvate (Pyr). Livers of the IIH group showed maintained efficiency to produce glucose from glycerol and higher efficiency to produce glucose from Lac and Pyr. In agreement with these results the oral administration of glycerol (100 mg kg(-1)), Lac (100 mg kg(-1)), Pyr (100 mg kg(-1)) or glycerol (100 mg kg(-1)) + Lac (100 mg kg(-1)) + Pyr (100 mg kg(-1)) promoted glycaemia recovery. It can be inferred that the increased portal availability of Lac, Pyr and glycerol could help glycaemia recovery by a mechanism mediated, partly at least, by a maintained (glycerol) or increased (Lac and Pyr) hepatic efficiency to produce glucose. Moreover, in spite of the fact that insulin inhibits ketogenesis, the capacity of the liver to produce ketone bodies from octanoate during IIH was maintained.
研究了原位大鼠灌注肝脏在短期胰岛素诱导低血糖（IIH）情况下的糖异生和酮体生成。为此，对禁食24小时后腹腔注射（ip）正规胰岛素（1.0 U kg⁻¹）或生理盐水的大鼠进行了比较。在注射胰岛素（IIH组）或生理盐水（COG组）30分钟后进行研究。对于糖异生研究，用甘油、L-乳酸（Lac）或丙酮酸（Pyr）浓度递增（从基础血液浓度直至饱和浓度）的溶液灌注IIH组和COG组大鼠的肝脏。IIH组肝脏从甘油生成葡萄糖的效率保持不变，从Lac和Pyr生成葡萄糖的效率更高。与这些结果一致，口服甘油（100 mg kg⁻¹）、Lac（100 mg kg⁻¹）、Pyr（100 mg kg⁻¹）或甘油（100 mg kg⁻¹）+Lac（100 mg kg⁻¹）+Pyr（100 mg kg⁻¹）可促进血糖恢复。可以推断，Lac、Pyr和甘油门静脉可用性的增加可能通过至少部分由维持（甘油）或增加（Lac和Pyr）肝脏生成葡萄糖的效率介导的机制来帮助血糖恢复。此外，尽管胰岛素抑制酮体生成，但在IIH期间肝脏从辛酸生成酮体的能力仍得以维持。
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