ESPEYB19 8. Adrenals New Paradigms (1 abstracts)
8.12. Glucocorticoid-induced fingerprints on visceral adipose tissue transcriptome and epigenome
García-Eguren G , González-Ramírez M , Vizán P , Giró O , Vega-Beyhart A , Boswell L , Mora M , Halperin I , Carmona F , Gracia M , Casals G , Squarcia M , Enseñat J , Vidal O , Di Croce L & Hanzu FA
J Clin Endocrinol Metab. 2022; 107(1): 150-166. PMID: 34487152https://pubmed.ncbi.nlm.nih.gov/34487152/
Brief Summary: This translational study determined the persistent visceral adipose tissue (VAT) transcriptomic alterations and epigenetic fingerprints induced by chronic hypercortisolism in patients with Cushing’s syndrome (CS) and in a reversible CS mouse model.
Excessive and prolonged glucocorticoid (GC) exposure may result in diverse and long-term adverse outcomes. Patients with Cushing’s Syndrome (CS, endogenous GC excess) have persistently increased cardiometabolic risk, with abdominal fat accumulation and systemic low-grade inflammation. GCs play an important role in adipose tissue metabolism, however, the effects on transcriptomic and epigenomic changes have not been studied extensively in this patient group.
These authors described these effects using a translational approach, including both visceral adipose tissue (VAT) biopsies from patients with active CS and matched controls, and a mouse model of reversible hypercortisolism. The authors performed RNA sequencing and chromatin immunoprecipitation sequencing on the histone modifications H3K4me3, H3K27ac, and H3K27me3 to identify persistent transcriptional and epigenetic signatures in VAT produced during active CS and after remission. They found similar transcriptomic changes in both humans and mice with differentially expressed genes being related to inflammation and regulation of transcription. More importantly, GC exposure altered the expression of genes associated with controlling circadian rhythm or disrupting it. Furthermore, the results regarding histone modifications were different from controls in both mice and humans, showing opposite effects, with mice showing increased signals from all three modifications and humans showing the opposite effect. Observed changes in both H3K4me3 and H3K27ac, histone modifications that are markers for gene-activation, correlated with the differences observed in gene expression in active CS and after remission, indicating that chronic GC exposure alters the epigenetic profile of VAT that persists through time with important implications for gene expression and downstream biological functions.
In summary, the article explores and describes the effects of GCs on VAT both during and after hypercortisolism. Hypercortisolism has numerous and various adverse effects depending on time and the magnitude of the exposure. Understanding the biological effects of excess GC exposure in different tissues and the underlying mechanisms of these effects may be helpful in the future clinical management.
Volume 19
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ESPE Yearbook of Paediatric Endocrinology
ISSN 1662-4009 (Online)
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