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B. B. Fredholm, E. Irenius, B. Kull and G. Schulte, “Comparison of the Potency of Adenosine as an Agonist at Human Adenosine Receptors Expressed in Chinese Hamster Ovary Cells,” Biochemical Pharmacology, Vol. 61, No. 4, 2001, pp. 443-448.
http://dx.doi.org/10.1016/S0006-2952(00)00570-0

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.