Adrenal gland size in obstructive sleep apnea: Morphological assessment of hypothalamic pituitary adrenal axis activity

Abstract Context: Previous studies on the association between the hypothalamic-pituitary-adrenal axis activity and sleep apnea (SA) and obesity are inconsistent and/or limited. Objective: In this study, we evaluated the activity of the hypothalamic-pituitary-adrenal axis in nonpsychologically distressed obese subjects with and without SA and examined the impact of continuous positive airway pressure (CPAP) in SA patients. Design and Participants: In study I, four-night sleep laboratory recordings and serial 24-h plasma measures of cortisol were obtained in 45 obese men with and without apnea and nonobese controls. Sleep apneic patients were reassessed after 3 months of CPAP use. In study II, 38 obese men with and without sleep apnea and nonobese controls were challenged with ovine CRH administration after four nights in the sleep laboratory. Results: The sleep patterns were similar between obese and nonobese controls. Twenty-four-hour plasma cortisol levels were highest in nonobese controls, intermediate in obese apneic patients, and lowest in obese controls (8.8 ± 0.4 vs. 8.1 ± 0.3 vs. 7.5 ± 0.3 μg/dl, P < 0.05). CPAP tended to reduce cortisol levels in the apneic patients (difference −0.7 ± .4 μg/dl, P = 0.1). CRH administration resulted in a higher ACTH response in both obese groups, compared with nonobese controls; the three groups were not different in cortisol response. Conclusions: Nonpsychologically distressed, normally sleeping, obese men had low cortisol secretion. The cortisol secretion was slightly activated by SA and returned to low by CPAP use. The low cortisol secretion in obesity through its inferred hyposecretion of hypothalamic CRH might predispose the obese to sleep apnea.

Download Full-text

Role of the Endothelial-Derived Endogenous Anti-Inflammatory Factor Del-1 in Inflammation-Mediated Adrenal Gland Dysfunction

Endocrinology ◽

10.1210/en.2012-1617 ◽

2013 ◽

Vol 154 (3) ◽

pp. 1181-1189 ◽

Cited By ~ 30

Author(s):

Waldemar Kanczkowski ◽

Antonios Chatzigeorgiou ◽

Sylvia Grossklaus ◽

David Sprott ◽

Stefan R. Bornstein ◽

...

Keyword(s):

Adrenal Gland ◽

Leukocyte Adhesion ◽

Hypothalamic Pituitary Adrenal Axis ◽

Inflammatory Factor ◽

Hypothalamic Pituitary Adrenal ◽

Adrenal Axis ◽

Leukocyte Accumulation ◽

Anti Inflammatory ◽

Underlying Mechanisms ◽

Pituitary Adrenal Axis

Abstract Inflammation in the course of systemic inflammatory response syndrome (SIRS) or sepsis often results in dysregulation of the hypothalamic-pituitary-adrenal axis; however, the underlying mechanisms are not well understood. The adrenal gland is highly vascularized; thus, we hypothesized that endothelial dysfunction may actively participate in inflammation-related adrenal insufficiency. To address this hypothesis, we used the properties of developmental endothelial locus-1 (Del-1), which is an endothelial-derived anti-inflammatory factor that antagonizes integrin-dependent leukocyte adhesion. Here we identified that Del-1 is expressed in the adrenal gland and that its expression was down-regulated upon SIRS induction by systemic lipopolysaccharide administration. Furthermore, we observed increased leukocyte accumulation, inflammation, and higher apoptosis in the adrenal glands of Del-1–deficient mice as compared with wild-type mice. Strikingly, Del-1 deficiency was also associated with reduced corticosterone and ACTH levels 24 hours after lipopolysaccharide administration. Together, these data suggest that Del-1 may act as a gatekeeper of adrenal gland inflammation and may regulate the integrity of the hypothalamic-pituitary-adrenal axis stress response, thereby modulating adrenal (dys)function in the course of SIRS.

Download Full-text