Abstract | AIMS: MAIN METHODS: KEY FINDINGS: Non-obese, diabetic GK rats exhibited a decrease in their hepatic and pancreatic PRMT1 activity, as compared to the control Wistar rats, which was associated with the impaired arginine methylation of several proteins in the tissues. Transfection of PRMT1-siRNA diminished the agonist-induced activation of insulin signaling and the subsequent suppression of gluconeogenic genes expression in the liver-derived cells. Pretreatment with MTA attenuated the glucose-stimulated insulin secretion, but not glucose utilization, in isolated pancreatic islets of Wistar controls, and its pattern was comparable to that of the GK rats undergoing similar modulation. SIGNIFICANCE: The present data demonstrates that the impaired PRMT1 activity may be implicated in glucose intolerance in GK rats through the disturbed hepatic glucose metabolism and insulin secretion.
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Authors | Hiroaki Iwasaki |
Journal | Life sciences
(Life Sci)
Vol. 85
Issue 3-4
Pg. 161-6
(Jul 17 2009)
ISSN: 1879-0631 [Electronic] Netherlands |
PMID | 19467247
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Insulin
- RNA, Small Interfering
- Arginine
- PRMT1 protein, rat
- Protein-Arginine N-Methyltransferases
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Topics |
- Animals
- Arginine
(metabolism)
- Diabetes Mellitus, Type 2
(enzymology)
- Gene Deletion
- Gene Expression
- Gluconeogenesis
(genetics)
- Insulin
(metabolism)
- Insulin Secretion
- Insulin-Secreting Cells
(metabolism)
- Liver
(enzymology)
- Methylation
- Pancreas
(enzymology)
- Protein-Arginine N-Methyltransferases
(genetics, metabolism)
- RNA, Small Interfering
(genetics)
- Rats
- Rats, Mutant Strains
- Rats, Wistar
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