Journal
HORMONE AND METABOLIC RESEARCH
Volume 42, Issue 2, Pages 115-121Publisher
GEORG THIEME VERLAG KG
DOI: 10.1055/s-0029-1241834
Keywords
metabolic syndrome model; liver cells; tissue culture; genomics; insulin; receptor and signaling; phosphorylation; energy utilization; apoptosis
Categories
Funding
- Medical Student Fellowship Training [T35 DK 007405-22-24]
- Merit Review Grant of VA
- NIH [NIH/NIDDK 2R01 DK62103]
Ask authors/readers for more resources
Several studies suggest that TNF-alpha contributes to the development of insulin resistance (IR). We compared transcriptional profiles of rat H-411E liver cells exposed to insulin in the absence or presence of TNF-alpha. We identified 33 genes whose expression was altered by insulin, and then reversed by TNF-alpha. Twenty-six of these 33 genes created a single network centered around: insulin, TNF-alpha, p38-MAPK, TGFb1; SMAD and STAT1; and enzymes and cytokines involved in apoptosis (CASP3, GADD45B, IL2, TNF-alpha, etc.). We analyzed our data together with other data of gene expression in adipocytes and found a number of processes common to both, for example, cell death and inflammation; intercellular signaling and metabolism; G-Protein, IL-10 and PTEN signaling. Moreover, the two datasets combined generated a single molecular network that further identified PTEN (a phosphatase) as a unique new link between insulin signaling, IR, and apoptosis reflecting the pathophysiology of metabolic syndrome .
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available