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Diraison, F., Large, V., Brunengraber, H. and Beylot, M. (1998) Non-invasive tracing of liver intermediary metabolism in normal subjects and in moderately hyperglycaemic NIDDM subjects: Evidence against increased gluconeogenesis and hepatic fatty acid oxidation in NIDDM. Diabetologia, 41, 212-220.

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• TITLE: Responses of the perfused liver of neonatal type 2 diabetic rats to gluconeogenic and ammoniogenic substrates

  AUTHORS: Mirian Carvalho-Martini, Fumie Suzuki-Kemmelmeier, Denise Silva de Oliveira, Jurandir Fernando Comar, Adelar Bracht

  KEYWORDS: Type 2 Diabetes; Gluconeogenesis; Ammoniogenesis; Alanine; Lactate

  JOURNAL NAME: Health, Vol.2 No.5, May 27, 2010

  ABSTRACT: The responses of livers from rats with type 2 diabetes to alanine (gluconeogenesis and ammonia detoxification) and other gluconeogenic substrates were investigated. The experimental system was the isolated perfused rat liver. Neonatal type 2 diabetes was induced with streptozotocin. Ammoniogenesis from endogenous substrates was 610% higher in livers from diabetic rats when compared to the control condition. Alanine (2.5 mM) ammoniogenesis was 285% higher in livers of diabetic rats. Gluconeogenesis from the following substrates was smaller in the liver of diabetic rats: Alanine (?43.5%), lactate (?28.3%) and glycerol (?30.5%). Pyruvate gluconeogenesis was normal. The high rate of ammoniogenesis explains the moderate hyperammonemia of type 2 diabetic rats. The enzymatic machinery of the gluconeogenic pathway of type 2 diabetic rats seems to be adapted to low rates of glucose removal by extrahepatic tissues. A significant contribution of gluconeogenesis to the fasting hyperglycemia can be expected only by short-term up-regulation mechanisms.