RGD Reference Report - Chronic 17beta-estradiol treatment improves skeletal muscle insulin signaling pathway components in insulin resistance associated with aging. - Rat Genome Database

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Chronic 17beta-estradiol treatment improves skeletal muscle insulin signaling pathway components in insulin resistance associated with aging.

Authors: Moreno, M  Ordonez, P  Alonso, A  Diaz, F  Tolivia, J  Gonzalez, C 
Citation: Moreno M, etal., Age (Dordr). 2010 Mar;32(1):1-13. Epub 2009 May 22.
RGD ID: 4108478
Pubmed: PMID:19462258   (View Abstract at PubMed)
PMCID: PMC2829641   (View Article at PubMed Central)
DOI: DOI:10.1007/s11357-009-9095-2   (Journal Full-text)

Insulin resistance is a common feature of aging in both humans and rats. In the case of females, it seems to be related to loss of gonadal function, due mainly due to a decrease in plasma estrogen levels. Several causes have been postulated for this insulin resistance, among them changes in several steps of the insulin pathway. In view of these findings, the purpose of the present study was to examine the role of chronic 17beta-estradiol treatment on insulin sensitivity during the aging process, and its effects on levels of the insulin-sensitive glucose transporter Glut4 (both total and plasma membrane localized), the interaction between p85alpha subunit of PI3-k and IRS-1, Tyr- and Ser-612 phosphorylation of IRS-1 levels, and Ser-473 phosphorylation of Akt. The present findings indicate that 17beta-estradiol treatment is able to minimize the deleterious effect of aging on insulin sensitivity, at least at the level of plasma membrane localized Glut4. Nevertheless further research is needed to determine this conclusively.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to estradiol  IEP 4108478 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Pik3r1  (phosphoinositide-3-kinase regulatory subunit 1)


Additional Information