Linked Life Data

12351432

Source:http://linkedlifedata.com/resource/pubmed/id/12351432

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2002-9-27
pubmed:abstractText
Age-dependent changes in insulin action and body fat distribution are risk factors for the development of type 2 diabetes. To examine whether the accumulation of visceral fat (VF) could play a direct role in the pathophysiology of insulin resistance and type 2 diabetes, we monitored insulin action, glucose tolerance, and the expression of adipo-derived peptides after surgical removal of VF in aging (20-month-old) F344/Brown Norway (FBN) and in Zucker Diabetic Fatty (ZDF) rats. As expected, peripheral and hepatic insulin action were markedly impaired in aging FBN rats, and extraction of VF (accounting for approximately 18% of their total body fat) was sufficient to restore peripheral and hepatic insulin action to the levels of young rats. When examined at the mechanistic level, removal of VF in ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels. However, the expression of tumor necrosis factor-alpha and leptin in subcutaneous (SC) adipose tissue were markedly decreased after VF removal (by approximately three- and twofold, respectively). Finally, extracted VF retained approximately 15-fold higher resistin mRNA compared with SC fat. Our data suggest that insulin resistance and the development of diabetes can be significantly reduced in aging rats by preventing the age-dependent accumulation of VF. This study documents a cause-and-effect relationship between VF and major components of the metabolic syndrome.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2951-8
pubmed:dateRevised
2008-6-13
pubmed:meshHeading
pubmed-meshheading:12351432-Abdomen, pubmed-meshheading:12351432-Adipose Tissue, pubmed-meshheading:12351432-Aging, pubmed-meshheading:12351432-Animals, pubmed-meshheading:12351432-Body Composition, pubmed-meshheading:12351432-Diabetes Mellitus, Type 2, pubmed-meshheading:12351432-Fatty Acids, Nonesterified, pubmed-meshheading:12351432-Gene Expression, pubmed-meshheading:12351432-Glucose, pubmed-meshheading:12351432-Hormones, Ectopic, pubmed-meshheading:12351432-Insulin Resistance, pubmed-meshheading:12351432-Leptin, pubmed-meshheading:12351432-Nerve Growth Factor, pubmed-meshheading:12351432-Obesity, pubmed-meshheading:12351432-Proteins, pubmed-meshheading:12351432-Rats, pubmed-meshheading:12351432-Rats, Inbred BN, pubmed-meshheading:12351432-Rats, Inbred F344, pubmed-meshheading:12351432-Rats, Zucker, pubmed-meshheading:12351432-Resistin, pubmed-meshheading:12351432-Tumor Necrosis Factor-alpha
pubmed:year
2002
pubmed:articleTitle
Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process?
pubmed:affiliation
Diabetes Research and Training Center and Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't