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R. C. Garland, “Induction of Glucose 6-Phosphatase in Cultured Hepatoma Cells by Dexamethasone,” Biochemical Biophysical Research Communications, Vol. 139, No. 3, 1986, pp. 1130-1134.
http://dx.doi.org/10.1016/S0006-291X(86)80295-9

has been cited by the following article:

• TITLE: The Adenosine Receptor Agonist 5’-N-Ethylcarboxamide-Adenosine Increases Glucose 6-Phosphatase Expression and Gluconeogenesis

  AUTHORS: Koichi Matsuda, Yoko Horikawa, Yasuto Sasaki, Shigeko F. Sakata

  KEYWORDS: 5’-N-Ethylcarboxamide-Adenosine; Glucose 6-Phosphatase; Gluconeogenesis

  JOURNAL NAME: Pharmacology & Pharmacy, Vol.5 No.1, January 8, 2014

  ABSTRACT: Intraperitoneal administration of the non-selective adenosine receptor agonist 5’-N-ethylcarboxamide-adenosine (NECA) (0.1 or 0.3 mg/kg) increased fasting serum glucose levels in mice. To clarify the mechanism responsible for this, the expression of liver glucose 6-phosphatase (G6Pase: a gluconeogenic enzyme) was analyzed, and it was found that G6Pase mRNA was increased by NECA treatment. Administration of 0.3 mg/kg NECA resulted in elevated serum glucose levels at 1 h and were further elevated at 6 h. Administration of 0.1 mg/kg NECA increased serum glucose levels at 1 h and had returned to control levels by 6 h. The increase in fasting serum glucose levels induced by NECA are thought to be caused, in part, by elevated G6Pase expression.