What is the clinical evidence from this study?

Study design: Observational. Population: Cortisol-producing adenoma. Intervention: Cortisol-producing adenoma vs. Normotension. Primary outcome: Inflammation, fibrosis and oxidative stress markers in perirenal adipose tissue.

January 2, 2019Open Access

Increased oxidative stress, inflammation and fibrosis in perirenal adipose tissue of patients with cortisol-producing adenoma

Key Result

Cortisol-producing adenoma significantly increased perirenal adipose tissue oxidative stress, inflammation, and fibrosis compared to normotensive controls.

Study Design

Type

Observational

Structured PICO

Does chronic exposure to glucocorticoids increase oxidative stress, inflammation, and fibrosis in perirenal adipose tissue?

Population

Perirenal adipose tissue from patients with cortisol-producing adenoma (CPA) and in vitro cell models (predifferentiated stromal vascular fraction cells, 3T3-L1 preadipocytes, and brown preadipocytes)

Exposure

Endogenous glucocorticoids (CPA) or dexamethasone (in vitro)

Comparator

Normotension (NT) group or control cells

Outcome

Levels of oxidative stress, inflammation, and fibrosis markers (TNFα, IL-6, fibronectin, collagen I, Nox4, Nrf2, HO-1)surrogate

Chronic exposure to endogenous glucocorticoids from cortisol-producing adenomas increases oxidative stress, inflammation, and fibrosis in perirenal adipose tissue, potentially contributing to metabolic disturbances.

Abstract

Although much is known about that corticosteroids affect the functions of adipose tissues, little genetic information is available for perirenal adipose tissue (peri-N) from patients with cortisol-producing adenoma (CPA). We conducted microarray analysis of peri-N from patients with CPA by using an Affymetrix human U133 plus 2.0 array. We also analysed the inflammation, fibrosis and oxidative stress in vitro. Compared with normotension (NT) group, CPA group has significantly higher protein levels of TNFα, IL-6, fibronectin (FN) and collagen I (COLI). The protein level of NADPH oxidase 4 (Nox4) significantly increased, while nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) levels were significantly reduced in the CPA group. Dexamethasone markedly induced fibrosis and adipogenesis-related gene expression in predifferentiated stromal vascular fraction (SVF) cells, 3T3-L1 preadipocytes and brown preadipocytes. Chronic exposure to endogenous glucocorticoids due to CPA increases peri-N oxidative stress, inflammation and fibrosis, which may contribute to the metabolic disturbances associated with hypercortisolism in these patients.