Article citationsMore>>
H. Hagberg, P. Andersson, J. Lacarewicz, I. Jacobson, S. Butcher and M. Sandberg, “Extracellular Adenosine, Inosine, Hypoxanthine, and Xanthine in Relation to Tissue Nucleotides and Purines in Rat Striatum during Transient Ischemia,” Journal of Neurochemistry, Vol. 49, No. 1, 1987, pp. 227-231.
http://dx.doi.org/10.1111/j.1471-4159.1987.tb03419.x
has been cited by the following article:
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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.