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Gene expression changes in subcutaneous adipose tissue due to Cushing's disease.

Hochberg I, Harvey I, Tran QT, Stephenson EJ, Barkan AL, Saltiel AR, Chandler WF, Bridges D - J. Mol. Endocrinol. (2015)

Bottom Line: Glucocorticoids have major effects on adipose tissue metabolism.We found a higher expression of transcripts involved in several metabolic pathways, including lipogenesis, proteolysis and glucose oxidation as well as a decreased expression of transcripts involved in inflammation and protein synthesis.These data provide insight to transcriptional changes that may be responsible for the comorbidities associated with chronic elevations of glucocorticoids.

View Article: PubMed Central - PubMed

Affiliation: Institute of EndocrinologyDiabetes and Metabolism, Rambam Health Care Campus, Haifa, IsraelLife Science InstituteUniversity of Michigan, Ann Arbor, MI, USAPhysiologyUTHSC, Memphis, TN, USAPreventive MedicineUTHSC, Memphis, TN, USAInternal MedicineUniversity of Michigan, Ann Arbor, MI USANeurosurgeryUniversity of Michigan, Ann Arbor, MI USAPediatricsUTHSC, Memphis, TN, USA Institute of EndocrinologyDiabetes and Metabolism, Rambam Health Care Campus, Haifa, IsraelLife Science InstituteUniversity of Michigan, Ann Arbor, MI, USAPhysiologyUTHSC, Memphis, TN, USAPreventive MedicineUTHSC, Memphis, TN, USAInternal MedicineUniversity of Michigan, Ann Arbor, MI USANeurosurgeryUniversity of Michigan, Ann Arbor, MI USAPediatricsUTHSC, Memphis, TN, USA i_hochberg@rambam.health.gov.il dbridge9@uthsc.edu.

No MeSH data available.


Related in: MedlinePlus

Expression of insulin signaling transcripts, ceramides and inflammatory transcripts in control vs Cushing's disease subjects. (A) Insulin signaling transcript expression levels. (B) Ceramide levels. (C) MHC complex transcript expression levels.
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fig7: Expression of insulin signaling transcripts, ceramides and inflammatory transcripts in control vs Cushing's disease subjects. (A) Insulin signaling transcript expression levels. (B) Ceramide levels. (C) MHC complex transcript expression levels.

Mentions: As described in Figs 1B and 2F, we observed insulin resistance in concert with elevated glucocorticoid levels in both mice and humans. Several mechanisms have been proposed linking glucocorticoids to insulin sensitivity including elevated lipolysis. As shown in Fig. 7A, there was a slightly higher expression of insulin pathway transcripts including FOXO1, the insulin receptor (INSR), the insulin receptor substrates IRS1 or IRS2 and the p85 regulatory subunit of phosphoinositide-3-kinase (PIK3R1), consistent with previous studies (Gathercole et al. 2007, Tomlinson et al. 2010, Hazlehurst et al. 2013), though in our hands none of these genes reached statistical significance. The insulin pathway was generally expressed at significantly higher levels in the Cushing's disease patients compared to controls (KEGG pathway, net enrichment score 1.84, Padj=0.006). These data do not support transcriptional downregulation of proximal insulin signaling genes as mediating insulin resistance in subcutaneous adipose tissue.


Gene expression changes in subcutaneous adipose tissue due to Cushing's disease.

Hochberg I, Harvey I, Tran QT, Stephenson EJ, Barkan AL, Saltiel AR, Chandler WF, Bridges D - J. Mol. Endocrinol. (2015)

Expression of insulin signaling transcripts, ceramides and inflammatory transcripts in control vs Cushing's disease subjects. (A) Insulin signaling transcript expression levels. (B) Ceramide levels. (C) MHC complex transcript expression levels.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4543687&req=5

fig7: Expression of insulin signaling transcripts, ceramides and inflammatory transcripts in control vs Cushing's disease subjects. (A) Insulin signaling transcript expression levels. (B) Ceramide levels. (C) MHC complex transcript expression levels.
Mentions: As described in Figs 1B and 2F, we observed insulin resistance in concert with elevated glucocorticoid levels in both mice and humans. Several mechanisms have been proposed linking glucocorticoids to insulin sensitivity including elevated lipolysis. As shown in Fig. 7A, there was a slightly higher expression of insulin pathway transcripts including FOXO1, the insulin receptor (INSR), the insulin receptor substrates IRS1 or IRS2 and the p85 regulatory subunit of phosphoinositide-3-kinase (PIK3R1), consistent with previous studies (Gathercole et al. 2007, Tomlinson et al. 2010, Hazlehurst et al. 2013), though in our hands none of these genes reached statistical significance. The insulin pathway was generally expressed at significantly higher levels in the Cushing's disease patients compared to controls (KEGG pathway, net enrichment score 1.84, Padj=0.006). These data do not support transcriptional downregulation of proximal insulin signaling genes as mediating insulin resistance in subcutaneous adipose tissue.

Bottom Line: Glucocorticoids have major effects on adipose tissue metabolism.We found a higher expression of transcripts involved in several metabolic pathways, including lipogenesis, proteolysis and glucose oxidation as well as a decreased expression of transcripts involved in inflammation and protein synthesis.These data provide insight to transcriptional changes that may be responsible for the comorbidities associated with chronic elevations of glucocorticoids.

View Article: PubMed Central - PubMed

Affiliation: Institute of EndocrinologyDiabetes and Metabolism, Rambam Health Care Campus, Haifa, IsraelLife Science InstituteUniversity of Michigan, Ann Arbor, MI, USAPhysiologyUTHSC, Memphis, TN, USAPreventive MedicineUTHSC, Memphis, TN, USAInternal MedicineUniversity of Michigan, Ann Arbor, MI USANeurosurgeryUniversity of Michigan, Ann Arbor, MI USAPediatricsUTHSC, Memphis, TN, USA Institute of EndocrinologyDiabetes and Metabolism, Rambam Health Care Campus, Haifa, IsraelLife Science InstituteUniversity of Michigan, Ann Arbor, MI, USAPhysiologyUTHSC, Memphis, TN, USAPreventive MedicineUTHSC, Memphis, TN, USAInternal MedicineUniversity of Michigan, Ann Arbor, MI USANeurosurgeryUniversity of Michigan, Ann Arbor, MI USAPediatricsUTHSC, Memphis, TN, USA i_hochberg@rambam.health.gov.il dbridge9@uthsc.edu.

No MeSH data available.


Related in: MedlinePlus