Glucocorticoid Influence on Hepatic Lipid Metabolism
Summary
Glucocorticoids are steroid hormones that modulate energy metabolism by acting on the glucocorticoid receptor in hepatocytes. In the liver, they stimulate gluconeogenesis, promote lipolysis in adipose tissue and increase delivery of free fatty acids to the liver. Under acute stress or fasting, this mechanism ensures adequate energy supply. However, chronic or excess glucocorticoid exposure shifts the balance towards enhanced hepatic de novo lipogenesis and impaired fatty acid oxidation, leading to hepatic steatosis. Local regeneration of active glucocorticoids by 11β-hydroxysteroid dehydrogenase type 1 further amplifies receptor signalling within the liver, with downstream effects on key transcriptional regulators such as peroxisome proliferator-activated receptor α. Prolonged lipid accumulation can progress to non-alcoholic steatohepatitis and fibrosis, highlighting the clinical significance of targeting glucocorticoid action and its downstream metabolic pathways for the treatment of fatty liver disease.
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Glucocorticoid Influence on Hepatic Lipid Metabolism publication trend
The graph below shows the total number of articles in glucocorticoid influence on hepatic lipid metabolism across all publications each year (not limited to Nature Index journals).
Technical terms
Glucocorticoid: A class of steroid hormones that regulate metabolism, inflammation and stress responses.
Glucocorticoid receptor (GR): An intracellular transcription factor activated by glucocorticoids to regulate gene expression.
Hepatic steatosis: Accumulation of lipid droplets within liver cells, often referred to as fatty liver.
De novo lipogenesis: The metabolic process by which fatty acids are synthesised from non-lipid precursors in the liver.
11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1): An enzyme that converts inactive cortisone to active cortisol, amplifying local glucocorticoid action.
AMPK: AMP-activated protein kinase, a cellular energy sensor that promotes catabolic pathways under low energy states.
SIRT1: A nicotinamide adenine dinucleotide-dependent deacetylase involved in metabolic regulation and stress responses.
References
- Glucocorticoid receptor modulator CORT125385 alleviates diet-induced hepatosteatosis in male and female mice. European Journal of Pharmacology (2023).
- Regulation of triglyceride metabolism by glucocorticoid receptor. Cell & Bioscience (2012).
- 11β-HSD1 Inhibitor Alleviates Non-Alcoholic Fatty Liver Disease by Activating the AMPK/SIRT1 Signaling Pathway. Nutrients (2022).
- Inhibition of 11β-hydroxysteroid dehydrogenase 1 relieves fibrosis through depolarizing of hepatic stellate cell in NASH. Cell Death & Disease (2022).
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