Linked Life Data

18042832

Source:http://linkedlifedata.com/resource/pubmed/id/18042832

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-2-20
pubmed:abstractText
We evaluated the effect of skeletal muscle mitochondrial uncoupling on energy and glucose metabolism under different diets. For 3 mo, transgenic HSA-mUCP1 mice with ectopic expression of uncoupling protein 1 in skeletal muscle and wild-type littermates were fed semisynthetic diets with varying macronutrient ratios (energy % carbohydrate-protein-fat): HCLF (41:42:17), HCHF (41:16:43); LCHF (11:45:44). Body composition, energy metabolism, and insulin resistance were assessed by NMR, indirect calorimetry, and insulin tolerance test, respectively. Gene expression in different organs was determined by real-time PCR. In wild type, both high-fat diets led to an increase in body weight and fat. HSA-mUCP1 mice considerably increased body fat on HCHF but stayed lean on the other diets. Irrespective of differences in body fat content, HSA-mUCP1 mice showed higher insulin sensitivity and decreased plasma insulin and liver triglycerides. Respiratory quotient and gene expression indicated overall increased carbohydrate oxidation of HSA-mUCP1 but a preferential channeling of fatty acids into muscle rather than liver with high-fat diets. Evidence for increased lipogenesis in white fat of HSA-mUCP1 mice suggests increased energy dissipating substrate cycling. Retinol binding protein 4 expression in white fat was increased in HSA-mUCP1 mice despite increased insulin sensitivity, excluding a causal role in the development of insulin resistance. We conclude that skeletal muscle mitochondrial uncoupling does not protect from the development of obesity in all circumstances. Rather it can lead to a "healthy" obese phenotype by preserving insulin sensitivity and a high metabolic flexibility, thus protecting from the development of obesity associated disturbances of glucose homeostasis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1531-2267
pubmed:author
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
352-9
pubmed:meshHeading
pubmed-meshheading:18042832-Adipose Tissue, pubmed-meshheading:18042832-Animals, pubmed-meshheading:18042832-Body Composition, pubmed-meshheading:18042832-Body Weight, pubmed-meshheading:18042832-Dietary Carbohydrates, pubmed-meshheading:18042832-Dietary Fats, pubmed-meshheading:18042832-Dietary Proteins, pubmed-meshheading:18042832-Energy Intake, pubmed-meshheading:18042832-Energy Metabolism, pubmed-meshheading:18042832-Gene Expression Profiling, pubmed-meshheading:18042832-Glucose, pubmed-meshheading:18042832-Insulin Resistance, pubmed-meshheading:18042832-Ion Channels, pubmed-meshheading:18042832-Liver, pubmed-meshheading:18042832-Male, pubmed-meshheading:18042832-Mice, pubmed-meshheading:18042832-Mice, Transgenic, pubmed-meshheading:18042832-Mitochondrial Proteins, pubmed-meshheading:18042832-Muscle, Skeletal, pubmed-meshheading:18042832-Obesity, pubmed-meshheading:18042832-Organ Size, pubmed-meshheading:18042832-Random Allocation, pubmed-meshheading:18042832-Triglycerides
pubmed:year
2008
pubmed:articleTitle
Dissociation of obesity and insulin resistance in transgenic mice with skeletal muscle expression of uncoupling protein 1.
pubmed:affiliation
German Institute of Human Nutrition in Potsdam-Rehbruecke, Group of Energy Metabolism, Nuthetal, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't