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McClellanville Library
Closed for renovations
Phone: (843) 887-3699
Miss Jane's Building (Edisto Library Temporary Location)
9 a.m. - 4 p.m.
Phone: (843) 869-2355
Main Library
9 a.m. - 8 p.m.
Phone: (843) 805-6930
West Ashley Library
9 a.m. - 7 p.m.
Phone: (843) 766-6635
Folly Beach Library
Closed for renovations
Phone: (843) 588-2001
John L. Dart Library
9 a.m. - 7 p.m.
Phone: (843) 722-7550
St. Paul's/Hollywood Library
9 a.m. - 8 p.m.
Phone: (843) 889-3300
Mt. Pleasant Library
9 a.m. – 8 p.m.
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Dorchester Road Library
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Edgar Allan Poe/Sullivan's Island Library
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John's Island Library
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Wando Mount Pleasant Library
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Phone: (843) 805-6892
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Phone: (843) 884-9741
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Metformin enhances insulin signalling in insulin-dependent and-independent pathways in insulin resistant muscle cells.
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- Author(s): Kumar, N.; Dey, C.S.; Kumar, Naresh; Dey, Chinmoy S
- Source:
British Journal of Pharmacology; Oct2002, Vol. 137 Issue 3, p329-336, 8p- Subject Terms:
BLOOD sugar; TYPE 2 diabetes; MUSCLE cells; TYROSINE metabolism; ANIMAL experimentation; CARRIER proteins; CELL culture; CELL receptors; CELLULAR signal transduction; COMPARATIVE studies; DEOXY sugars; HYPOGLYCEMIC agents; IMIDAZOLES; INSULIN; INSULIN resistance; RESEARCH methodology; MEDICAL cooperation; MICE; PHOSPHOPROTEINS; PHOSPHORYLATION; PHOSPHOTRANSFERASES; PYRIDINE; RESEARCH; TRANSFERASES; EVALUATION research; METFORMIN; SKELETAL muscle; PHARMACODYNAMICS - Source:
- Additional Information
- Abstract: 1 Metformin lowers blood glucose levels in type 2 diabetic patients. To evaluate the insulin sensitizing action of metformin on skeletal muscle cells, we have used C2C12 skeletal muscle cells differentiated in chronic presence or absence of insulin. 2 Metformin was added during the last 24 h of differentiation of the C2C12 myotubes. Insulin-stimulated tyrosine phosphorylation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) was determined. 3 Chronic insulin treatment resulted in 60 and 40% reduction in insulin-stimulated tyrosine phosphorylation of IR and IRS-1, respectively. Treatment with metformin was able to increase the tyrosine phosphorylation of IR and IRS-1 by 100 and 90% respectively. 4 Chronic insulin treatment drastically reduced (45%) insulin-stimulated phosphatidyl inositol 3-kinase (PI 3-kinase) activity. Metformin treatment restored PI 3-kinase activity in insulin-resistant myotubes. 5 Insulin-stimulated glucose uptake was impaired in chronically insulin-treated myotubes. Metformin increased basal glucose uptake to significant levels (P<0.05), but metformin did not increase insulin-stimulated glucose transport. 6 All the three mitogen-activated protein kinases (MAPK) were activated by insulin in sensitive myotubes. The activation of p38 MAPK was impaired in resistant myotubes, while ERK and JNK were unaffected. Treatment with metformin enhanced the basal activation levels of p38 in both sensitive and resistant myotubes, but insulin did not further stimulate p38 activation in metformin treated cells. 7 Treatment of cells with p38 inhibitor, SB203580, blocked insulin- and metformin-stimulated glucose uptake as well as p38 activation. 8 Since the effect of metformin on glucose uptake corresponded to p38 MAPK activation, this suggests the potential role p38 in glucose uptake. 9 These data demonstrate the direct insulin sensitizing action of metformin on skeletal muscle cells. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of British Journal of Pharmacology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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