Article citationsMore>>
N. Yasuda, T. Inoue, T. Horizoe, K. Nagata, H. Minami, T. Kawata, Y. Hoshino, H. Harada, S. Yoshikawa, O. Asano, J. Nagaoka, M. Murakami, S. Abe, S. Kobayashi and I. Tanaka, “Functional Characterization of the Adenosine Receptor Contributing to Glycogenolysis and Gluconeogenesis in Rat Hepatocytes,” European Journal of Pharmacology, Vol. 459, No. 2-3, 2003, pp. 159-166.
http://dx.doi.org/10.1016/S0014-2999(02)02832-7
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.
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