Linked Life Data

11723061

Source:http://linkedlifedata.com/resource/pubmed/id/11723061

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-11-27
pubmed:abstractText
Apolipoprotein (APO) C1 is a 6.6-kDa protein present in plasma and associated with lipoproteins. Using hyperinsulinemic-euglycemic clamp tests, we previously found that in APOC1 transgenic mice, the whole-body insulin-mediated glucose uptake is increased concomitant with a decreased fatty acid uptake. These latter results are confirmed in the present study, showing that APOC1 transgenic mice exhibit a 50% reduction in the uptake of the fatty acid analog 15-(p-iodophenyl)-3-(R,S)-methyl pentadecanoic acid in white adipose tissue stores. We next investigated whether APOC1 overexpression can modulate the initiation and/or development of obesity and insulin resistance. When crossbred on the genetically obese ob/ob background, APOC1 transgenic mice were fully protected from the development of obesity compared with ob/ob only mice, as reflected by a strong reduction in body weight (21 +/- 4 vs. 44 +/- 7 g), total adipose tissue stores (15 +/- 3 vs. 25 +/- 3% body wt), and average adipocyte size (7,689 +/- 624 vs. 15,295 +/- 1,289 microm(2)). Although less pronounced, APOC1 overexpression also reduced body weight on a wild-type background, solely due to a reduction in adipose tissue. Furthermore, despite elevated plasma free fatty acid and triglyceride levels, APOC1 overexpression significantly improved insulin sensitivity in ob/ob mice, as demonstrated by a strong reduction in plasma glucose and insulin levels, as well as a better performance in the glucose tolerance test. In conclusion, a marked reduction in the uptake of fatty acids into adipocytes may underlie the protection from obesity and insulin resistance in transgenic mice overexpressing human APOC1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2779-85
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11723061-Adipocytes, pubmed-meshheading:11723061-Adipose Tissue, pubmed-meshheading:11723061-Animals, pubmed-meshheading:11723061-Apolipoprotein C-I, pubmed-meshheading:11723061-Apolipoproteins C, pubmed-meshheading:11723061-Blood Glucose, pubmed-meshheading:11723061-Cell Size, pubmed-meshheading:11723061-Cholesterol, pubmed-meshheading:11723061-Crosses, Genetic, pubmed-meshheading:11723061-Fatty Acids, pubmed-meshheading:11723061-Fatty Acids, Nonesterified, pubmed-meshheading:11723061-Gene Expression, pubmed-meshheading:11723061-Glucose Tolerance Test, pubmed-meshheading:11723061-Humans, pubmed-meshheading:11723061-Insulin, pubmed-meshheading:11723061-Insulin Resistance, pubmed-meshheading:11723061-Iodine Radioisotopes, pubmed-meshheading:11723061-Iodobenzenes, pubmed-meshheading:11723061-Male, pubmed-meshheading:11723061-Mice, pubmed-meshheading:11723061-Mice, Obese, pubmed-meshheading:11723061-Mice, Transgenic, pubmed-meshheading:11723061-Obesity, pubmed-meshheading:11723061-Organ Size, pubmed-meshheading:11723061-Triglycerides, pubmed-meshheading:11723061-Weight Loss
pubmed:year
2001
pubmed:articleTitle
Protection from obesity and insulin resistance in mice overexpressing human apolipoprotein C1.
pubmed:affiliation
TNO-Prevention and Health, Gaubius Laboratory, Leiden, the Netherlands.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't