Abstract
Glucocorticoids (GCs) are hormones that aid the body under stress by regulating glucose and free fatty acids. GCs maintain energy homeostasis in multiple tissues, including those in the liver and skeletal muscle, white adipose tissue (WAT), and brown adipose tissue (BAT). WAT stores energy as triglycerides, while BAT uses fatty acids for heat generation. The multiple genomic and non-genomic pathways in GC signaling vary with exposure duration, location (adipose tissue depot), and species. Genomic effects occur directly through the cytosolic GC receptor (GR), regulating the expression of proteins related to lipid metabolism, such as ATGL and HSL. Non-genomic effects act through mechanisms often independent of the cytosolic GR and happen shortly after GC exposure. Studying the effects of GCs on adipose tissue breakdown and generation (lipolysis and adipogenesis) leads to insights for treatment of adipose-related diseases, such as obesity, coronary disease, and cancer, but has led to controversy among researchers, largely due to the complexity of the process. This paper reviews the recent literature on the genomic and non-genomic effects of GCs on WAT and BAT lipolysis and proposes research to address the many gaps in knowledge related to GC activity and its effects on disease.
Highlights
Glucocorticoids (GCs) are potent regulators of whole-body energy metabolism, elevating circulating glucose and free fatty acid (FFA) levels in times of stress
These results suggest that DEX and growth hormone (GH) are both required to alter the lipolytic rate, through a synergic mechanism [68]
In addition to the studies in which GCs are introduced to the environment, there are loss of function genomic studies that focus on the lipolytic actions of GCs by eliminating the 11β-HSD1 or the GC receptor (GR)
Summary
Glucocorticoids (GCs) are potent regulators of whole-body energy metabolism, elevating circulating glucose and free fatty acid (FFA) levels in times of stress. They are steroid hormones that include active cortisol (human) and corticosterone (CORT; rodent) hormones and their inactive counterparts, cortisone and 11-dehydrocorticosterone [1]. MR activation increases in the visceral adipose of obese mouse models [16]; MR overexpression in mice adipocytes induces a phenotype resembling the metabolic syndrome This involves increased fat mass and dyslipidemia [17], which increases the risk of coronary disease and stroke. The non-genomic mechanisms of action of GCs can affect various tissue types, including those in the central nervous system and AT. The AT, remains a major site of GC action, largely regulating lipid metabolism through genomic and non-genomic signaling on several key features of adipogenesis, body adiposity, and lipolysis, as described below
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