Source:http://linkedlifedata.com/resource/pubmed/id/19001546
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2009-1-27
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| pubmed:abstractText |
The current study was undertaken to determine whether Ang-(1-7) is effective in improving metabolic parameters in fructose-fed rats (FFR), a model of metabolic syndrome. Six-week-old male Sprague-Dawley rats were fed either normal rat chow (control) or the same diet plus 10% fructose in drinking water. For the last 2 wk of a 6-wk period of either diet, control and FFR were implanted with subcutaneous osmotic pumps that delivered Ang-(1-7) (100 ng.kg(-1).min(-1)). A subgroup of each group of animals (control or FFR) underwent a sham surgery. We measured systolic blood pressure (SBP) together with plasma levels of insulin, triglycerides, and glucose. A glucose tolerance test (GTT) was performed, with plasma insulin levels determined before and 15 and 120 min after glucose administration. In addition, we evaluated insulin signaling through the IR/IRS-1/PI3K/Akt pathway as well as the phosphorylation levels of IRS-1 at inhibitory site Ser(307) in skeletal muscle and adipose tissue. FFR displayed hypertriglyceridemia, hyperinsulinemia, increased SBP, and an exaggerated release of insulin during a GTT, together with decreased activation of insulin signaling through the IR/IRS-1/PI3K/Akt pathway in skeletal muscle, liver, and adipose tissue, as well as increased levels of IRS-1 phospho-Ser(307) in skeletal muscle and adipose tissue, alterations that correlated with increased activation of the kinases mTOR and JNK. Chronic Ang-(1-7) treatment resulted in normalization of all alterations. These results show that Ang-(1-7) ameliorates insulin resistance in a model of metabolic syndrome via a mechanism that could involve the modulation of insulin signaling.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin I,
http://linkedlifedata.com/resource/pubmed/chemical/Fructose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/angiotensin I (1-7)
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0193-1849
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
296
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
E262-71
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:19001546-Adipose Tissue,
pubmed-meshheading:19001546-Angiotensin I,
pubmed-meshheading:19001546-Animals,
pubmed-meshheading:19001546-Diet,
pubmed-meshheading:19001546-Drug Evaluation, Preclinical,
pubmed-meshheading:19001546-Fructose,
pubmed-meshheading:19001546-Glucose Tolerance Test,
pubmed-meshheading:19001546-Hypertension,
pubmed-meshheading:19001546-Infusion Pumps,
pubmed-meshheading:19001546-Insulin,
pubmed-meshheading:19001546-Insulin Resistance,
pubmed-meshheading:19001546-Liver,
pubmed-meshheading:19001546-Male,
pubmed-meshheading:19001546-Muscle, Skeletal,
pubmed-meshheading:19001546-Peptide Fragments,
pubmed-meshheading:19001546-Rats,
pubmed-meshheading:19001546-Rats, Sprague-Dawley,
pubmed-meshheading:19001546-Signal Transduction,
pubmed-meshheading:19001546-Time Factors
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| pubmed:year |
2009
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| pubmed:articleTitle |
Chronic infusion of angiotensin-(1-7) improves insulin resistance and hypertension induced by a high-fructose diet in rats.
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| pubmed:affiliation |
IQUIFIB, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956, (1113) Buenos Aires, Argentina.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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