Linked Life Data

18846047

Source:http://linkedlifedata.com/resource/pubmed/id/18846047

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2009-3-12
pubmed:abstractText
Obesity is a major cause of insulin resistance and contributes to the development of type 2 diabetes. The altered expression of genes involved in mitochondrial oxidative phosphorylation (OXPHOS) has been regarded as a key change in insulin-sensitive organs of patients with type 2 diabetes. This study explores possible molecular signatures of obesity and examines the clinical significance of OXPHOS gene expression in the livers of patients with type 2 diabetes. We analyzed gene expression in the livers of 21 patients with type 2 diabetes (10 obese and 11 nonobese patients; age, 53.0 +/- 2.1 years; BMI, 24.4 +/- 0.9 kg/m(2); fasting plasma glucose, 143.0 +/- 10.6 mg/dl) using a DNA chip. We screened 535 human pathways and extracted those metabolic pathways significantly altered by obesity. Genes involved in the OXPHOS pathway, together with glucose and lipid metabolism pathways, were coordinately upregulated in the liver in association with obesity. The mean centroid of OXPHOS gene expression was significantly correlated with insulin resistance indices and the hepatic expression of genes involved in gluconeogenesis, reactive oxygen species (ROS) generation, and transcriptional factors and nuclear co-activators associated with energy homeostasis. In conclusion, obesity may affect the pathophysiology of type 2 diabetes by upregulating genes involved in OXPHOS in association with insulin resistance markers and the expression of genes involved in hepatic gluconeogenesis and ROS generation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1930-7381
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2601-9
pubmed:meshHeading
pubmed-meshheading:18846047-Alanine Transaminase, pubmed-meshheading:18846047-Body Mass Index, pubmed-meshheading:18846047-Diabetes Mellitus, Type 2, pubmed-meshheading:18846047-Energy Metabolism, pubmed-meshheading:18846047-Fatty Acids, pubmed-meshheading:18846047-Fatty Liver, pubmed-meshheading:18846047-Female, pubmed-meshheading:18846047-Gene Expression Regulation, pubmed-meshheading:18846047-Gluconeogenesis, pubmed-meshheading:18846047-Glucose, pubmed-meshheading:18846047-Homeostasis, pubmed-meshheading:18846047-Humans, pubmed-meshheading:18846047-Insulin Resistance, pubmed-meshheading:18846047-Liver, pubmed-meshheading:18846047-Male, pubmed-meshheading:18846047-Metabolic Networks and Pathways, pubmed-meshheading:18846047-Middle Aged, pubmed-meshheading:18846047-Mitochondria, pubmed-meshheading:18846047-Obesity, pubmed-meshheading:18846047-Oxidative Phosphorylation, pubmed-meshheading:18846047-Reactive Oxygen Species, pubmed-meshheading:18846047-Transcription Factors, pubmed-meshheading:18846047-Up-Regulation
pubmed:year
2008
pubmed:articleTitle
Obesity upregulates genes involved in oxidative phosphorylation in livers of diabetic patients.
pubmed:affiliation
Department of Disease Control and Homeostasis, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan. ttakamura@m-kanazawa.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't