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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Gene expression changes in subcutaneous adipose tissue due to Cushing's disease
Irit Hochberg1, Innocence Harvey2, Quynh T Tran2
1Institute 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.
Abstract:
Glucocorticoids have major effects on adipose tissue metabolism. To study tissue mRNA expression changes induced by chronic elevated endogenous glucocorticoids, we performed RNA sequencing on the subcutaneous adipose tissue from patients with Cushing's disease (n=5) compared to patients with nonfunctioning pituitary adenomas (n=11). 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. To further study this in a model system, we subjected mice to dexamethasone treatment for 12 weeks and analyzed their inguinal (subcutaneous) fat pads, which led to similar findings. Additionally, mice treated with dexamethasone showed drastic decreases in lean body mass as well as increased fat mass, further supporting the human transcriptomic data. These data provide insight to transcriptional changes that may be responsible for the comorbidities associated with chronic elevations of glucocorticoids.
