Insulin-like growth factor 1 promotes the proliferation and adipogenesis of orbital adipose-derived stromal cells in thyroid-associated ophthalmopathy.
Zhao P., Deng Y., Gu P., Wang Y., Zhou H., Hu Y.
Prospective Study, published in Exp Eye Res (2012) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Exp Eye Res (2012)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 23219871
- DOI
- 10.1016/j.exer.2012.11.014
- Citations
- 51
Abstract (original English)
Thyroid-associated ophthalmopathy (TAO) is characterised by increased volume of the orbital contents involving adipose tissue, but the factors responsible for stimulation of orbital adipogenesis remain uncertain. Previous studies have shown that insulin-like growth factor 1 (IGF-1) is increased in the orbital fatty connective tissues of patients with TAO. The present study was conducted to investigate the effects of IGF-1 on orbital adipose-derived stromal cells (OADSCs) derived from TAO patients and to identify the signalling mechanisms involved. Our results showed that IGF-1 significantly promoted the cell proliferation and lipid accumulation of TAO OADSCs. The mRNA expression of adipogenic markers (adiponectin, leptin, adipocyte fatty acid binding protein [AP2] and fatty acid synthase [FAS]) was increased in TAO cultures treated with IGF-1. Further research demonstrated that the protein levels of peroxisome proliferator-activated receptor-γ (PPARγ) were up-regulated when OADSCs were treated with IGF-1. We also found that the inhibition of either IGF-1 receptor (IGF-1R) or phosphoinositide 3-kinase (PI3K) activity decreased the levels of IGF-1-stimulated mRNA encoding adiponectin, leptin, AP2, and FAS, as well as PPARγ protein levels. Moreover, the expression of phosphorylated Akt (p-Akt) protein in TAO cells was up-regulated by IGF-1, while a specific PI3K inhibitor (LY29400
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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