Glucocorticoid-Induced Fatty Liver Disease
Leili Rahimi,1 Aman Rajpal,1,2 Faramarz Ismail-Beigi1,2 1Department of Medicine, Case Western Reserve University, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; 2Cleveland VA Medical Center, Cleveland, OH, USACorrespondence: Faramarz Ismail-BeigiDepartment of Medicine, Case Weste...
Guardado en:
| Autores principales: | , , |
|---|---|
| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Dove Medical Press
2020
|
| Materias: | |
| Acceso en línea: | https://doaj.org/article/c82fe6d3d6a24257a465929983374ba5 |
| Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | Leili Rahimi,1 Aman Rajpal,1,2 Faramarz Ismail-Beigi1,2 1Department of Medicine, Case Western Reserve University, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; 2Cleveland VA Medical Center, Cleveland, OH, USACorrespondence: Faramarz Ismail-BeigiDepartment of Medicine, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH 44106, USATel + 12163686122Fax +12163685824Email fxi2@case.eduAbstract: Glucocorticoids (GCs) are commonly used at high doses and for prolonged periods (weeks to months) in the treatment of a variety of diseases. Among the many side effects are increased insulin resistance with disturbances in glucose/insulin homeostasis and increased deposition of lipids (mostly triglycerides) in the liver. Here, we review the metabolic pathways of lipid deposition and removal from the liver that become altered by excess glucocorticoids. Pathways of lipid deposition stimulated by excess glucocorticoids include 1) increase in appetite and high caloric intake; 2) increased blood glucose levels due to GC-induced stimulation of gluconeogenesis; 3) stimulation of de novo lipogenesis that is augmented by the high glucose and insulin levels and by GC itself; and 4) increased release of free fatty acids from adipose stores and stimulation of their uptake by the liver. Pathways that decrease hepatic lipids affected by glucocorticoids include a modest stimulation of very-low-density lipoprotein synthesis and secretion into the circulation and inhibition of β-oxidation of fatty acids. Role of 11β-hydroxysteroid dehydrogenases-1 and -2 and the reversible conversion of cortisol to cortisone on intracellular levels of cortisol is examined. In addition, GC control of osteocalcin expression and the effect of this bone-derived hormone in increasing insulin sensitivity are discussed. Finally, research focused on gaining a better understanding of the dose and duration of treatment with glucocorticoids, which leads to increased triglyceride deposition in the liver, and the reversibility of the condition is highlighted.Keywords: obesity, Cushing’s disease, fatty liver, metabolic syndrome, hyperphagia, LPL, hormone-sensitive lipase |
|---|