Format

Send to

Choose Destination
See comment in PubMed Commons below
Biochim Biophys Acta. 2008 Sep;1782(9):532-41. doi: 10.1016/j.bbadis.2008.06.002. Epub 2008 Jun 13.

Influence of increased adiposity on mitochondrial-associated proteins of the rat colon: a proteomic and transcriptomic analysis.

Author information

1
Molecular Nutrition, Greenburn Road, Bucksburn, Aberdeen, AB21 9SB, Scotland, UK.

Abstract

Epidemiological studies report obesity to be an important risk factor influencing colon pathologies, yet mechanism(s) are unknown. Recent studies have shown significant elevation of insulin, leptin and triglycerides associated with increased adipose tissue. In situ hybridisation studies have located insulin, leptin and adiponectin receptor expression in the colon epithelia. The influence of increased adiposity and associated deregulation of insulin and adipokines on regulation of the colon epithelium is unknown. Altered adipokine and insulin signalling associated with obesity has an impact on mitochondrial function and mitochondrial dysfunction is increasingly recognised as a contributing factor in many diseases. Proteomics and transcriptomics are potentially powerful methods useful in elucidating the mechanisms whereby obesity increases risk of colon diseases as observed epidemiologically. This study investigated colon mitochondrial-associated protein profiles and corresponding gene expression in colon in response to increased adiposity in a rat model of diet induced obesity. Increased adiposity in diet-induced obese sensitive rats was found to be associated with altered protein expression of 69 mitochondrial-associated proteins involved in processes associated with calcium binding, protein folding, energy metabolism, electron transport chain, structural proteins, protein synthesis and degradation, redox regulation, and transport. The changes in these mitochondrial protein profiles were not correlated with changes at the gene expression level assessed using real-time PCR arrays.

PMID:
18598761
DOI:
10.1016/j.bbadis.2008.06.002
[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center