Article citationsMore>>

R. A. Figler, G. Wang, S. Srinivasan, D. Y. Jung, Z. Zhang, J. S. Pankow, K. Ravid, B. Fredholm, C. C. Hedrick, S. S. Rich, J. K. Kim, K. F. LaNoue and J. Linden, “Links between Insulin Resistance, Adenosine A2B Receptors, and Inflammatory Markers in Mice and Humans,” Diabetes, Vol. 60, No. 2, 2011, pp. 669-679.
http://dx.doi.org/10.2337/db10-1070

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.