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Phosphoprotein enriched in diabetes gene product (Ped/pea-15) is increased in omental adipose tissue of women with the polycystic ovary syndrome: ex vivo regulation of ped/pea-15 by glucose, insulin and metformin.

Abstract
Polycystic ovary syndrome (PCOS), the commonest endocrine disorder in women, is characterized by an altered steroid milieu and is associated with insulin resistance and type 2 diabetes mellitus (T2DM). Phosphoprotein enriched in diabetes gene product (Ped/pea-15) regulates glucose metabolism and is increased in T2DM. Our novel data indicate that Ped/pea-15 mRNA expression and protein levels are significantly increased in omental adipose tissue (AT) from PCOS women compared to matched controls (p < 0.01); Ped/pea-15 levels in subcutaneous AT were not significantly different. Furthermore, Ped/pea-15 mRNA expression and protein levels were higher in omental compared to subcutaneous AT in PCOS subjects (p < 0.01); however, in control subjects, this was not significant. Glucose was predictive of omental AT Ped/pea-15 mRNA expression (p = 0.045). Importantly, glucose and insulin increased whereas metformin significantly decreased Ped/pea-15 levels in human omental AT explants. Our findings should serve to promote further research on Ped/pea-15 biology.
AuthorsB K Tan, J Chen, R Adya, H S Randeva
JournalDiabetes, obesity & metabolism (Diabetes Obes Metab) Vol. 13 Issue 2 Pg. 181-4 (Feb 2011) ISSN: 1463-1326 [Electronic] England
PMID21199270 (Publication Type: Letter, Research Support, Non-U.S. Gov't)
Chemical References
  • Apoptosis Regulatory Proteins
  • Biomarkers
  • Insulin
  • Intracellular Signaling Peptides and Proteins
  • PEA15 protein, human
  • Phosphoproteins
  • Metformin
  • Glucose
Topics
  • Adipose Tissue (metabolism)
  • Adult
  • Apoptosis Regulatory Proteins
  • Biomarkers (metabolism)
  • Female
  • Glucose (metabolism)
  • Humans
  • Insulin (metabolism)
  • Insulin Resistance (genetics)
  • Intracellular Signaling Peptides and Proteins (genetics)
  • Metformin (metabolism)
  • Phosphoproteins (genetics)
  • Polycystic Ovary Syndrome (drug therapy, genetics, metabolism)

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