| EGF Receptor (ERBB1) Abundance in Adipose Tissue Is Reduced in Insulin-Resistant and Type 2 Diabetic Women. | |
| | |
MedLine Citation:
|
PMID: 22238402 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
|
Context:Indications of adipose tissue dysfunction correlate with systemic insulin resistance and type 2 diabetes. It has been suggested that a defect in adipose tissue turnover may be involved in the development of these disorders. Whether this dysfunction causes or exacerbates systemic insulin resistance is not fully understood.Objectives, Participants, and Measures:We tested whether the expression of members of the mitogenic ErbB family was reduced in adipose tissue of insulin-resistant individuals and whether ErbB1 and ErbB2 were involved in adipogenesis. Thirty-two women covering a wide range of body mass index values and insulin sensitivity participated in the cross-sectional portion of this study. We also studied preadipocytes isolated from 12 insulin-sensitive individuals to evaluate the impact of ErbB1 or ErbB2 inhibition on adipogenesis in vitro. For this purpose, we measured phospho-ErbB1 and phospho-ErbB2 levels using ELISA and the expression of peroxisome proliferator-activated receptor γ (PPARγ) and PPARγ-regulated genes by real-time PCR.Results:Among the ErbB family members, only ErbB1 expression was correlated with insulin sensitivity. Additionally, ErbB1 levels correlated positively with PPARγ and several PPARγ-regulated genes including acyl-coenzyme A synthetase long-chain family member 1 (ACSL1), adiponectin, adipose tissue triacylglycerol lipase (ATGL), diacylglycerol acyl transferase 1 (DGAT1), glycerol-3-phosphate dehydrogenase 1 (GPD1), and lipoprotein lipase (LPL), but negatively with CD36 and fatty acid-binding protein 4 (FABP4). In preadipocyte culture, ErbB1, but not ErbB2, inhibition was associated with a reduction in the expression of all the above-mentioned genes.Conclusion:These findings demonstrate a key role for ErbB1 in adipogenesis and suggest that lower ErbB1 protein abundance may lead to adipose tissue dysfunction. |
| | |
Authors:
|
Carlyle Rogers; Fatiha Moukdar; Marie A McGee; Barbara Davis; Benjamin M Buehrer; Kiefer W Daniel; Sheila Collins; Hisham Barakat; Jacques Robidoux |
Publication Detail:
|
Type: JOURNAL ARTICLE Date: 2012-1-11 |
Journal Detail:
|
Title: The Journal of clinical endocrinology and metabolism Volume: - ISSN: 1945-7197 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
|
Created Date: 2012-1-12 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: - |
Other Details:
|
Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
|
Departments of Pharmacology and Toxicology (C.R., M.A.M., B.D., J.R.), Physiology (F.M.), and Internal Medicine (H.B.), Brody School of Medicine, and East Carolina Diabetes and Obesity Institute (H.B., J.R.), East Carolina University, Greenville, North Carolina 27834; Zen-Bio, Inc. (B.B., K.W.D.), Research Triangle Park, North Carolina 27709; and Sanford Burnham Institute for Medical Research (S.C.), Orlando, Florida 32827. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Clinical review: Regulation of food intake, energy balance, and body fat mass: implications for the ...
Next Document: Loss of WT1 Expression in the Endometrium of Infertile PCOS Patients: A Hyperandrogenic Effect?