Glucocorticoids and Brown Adipose Tissue: Do glucocorticoids really inhibit thermogenesis?. (August 2019)

• Record Type: Journal Article
• Authors: Luijten, Ineke H.N.; Cannon, Barbara; Nedergaard, Jan
• Is Part Of: Molecular aspects of medicine. Volume 68(2019)
• Page Start: 42
• Page End: 59
• Publication Date: 2019-08
• Subjects: Glucocorticoids -- Brown adipose tissue -- Thermogenesis -- Thermoneutrality -- Obesity -- Cushing's; Pathology, Molecular -- Periodicals; Medicine -- Periodicals; Biochemistry -- Periodicals; Medicine -- Periodicals; Molecular Biology -- Periodicals; Pathologie moléculaire -- Périodiques; Médecine -- Périodiques; Electronic journals; 612.015
• DOI: 10.1016/j.mam.2019.07.002
• Languages: English
• ISSNs: 0098-2997

Abstract

Abstract: A reduction in the thermogenic activity of brown adipose tissue (BAT) is presently discussed as a possible determinant for the development of obesity in humans. One group of endogenous factors that could potentially affect BAT activity is the glucocorticoids (e.g. cortisol). We analyse here studies examining the effects of alterations in glucocorticoid signaling on BAT recruitment and thermogenic capacity. We find that irrespective of which manipulation of glucocorticoid signaling is examined, a seemingly homogeneous picture of lowered thermogenic capacity due to glucocorticoid stimulation is apparently obtained: e.g. lowered uncoupling protein 1 (UCP1) protein levels per mg protein, and an increased lipid accumulation in BAT. However, further analyses generally indicate that these effects result from a dilution effect rather than a true decrease in total capacity; the tissue may thus be said to be in a state of pseudo-atrophy . However, under conditions of very low physiological stimulation of BAT, glucocorticoids may truly inhibit Ucp1 gene expression and consequently lower total UCP1 protein levels, but the metabolic effects of this reduction are probably minor. It is thus unlikely that glucocorticoids affect organismal metabolism and induce the development of obesity through alterations of BAT activity.