Epigenetic Regulation of Hepatic Lipogenesis: Role in Hepatosteatosis and Diabetes.
Jose ViscarraHei Sook SulPublished in: Diabetes (2020)
Hepatosteatosis, which is frequently associated with development of metabolic syndrome and insulin resistance, manifests when triglyceride (TG) input in the liver is greater than TG output, resulting in the excess accumulation of TG. Dysregulation of lipogenesis therefore has the potential to increase lipid accumulation in the liver, leading to insulin resistance and type 2 diabetes. Recently, efforts have been made to examine the epigenetic regulation of metabolism by histone-modifying enzymes that alter chromatin accessibility for activation or repression of transcription. For regulation of lipogenic gene transcription, various known lipogenic transcription factors, such as USF1, ChREBP, and LXR, interact with and recruit specific histone modifiers, directing specificity toward lipogenesis. Alteration or impairment of the functions of these histone modifiers can lead to dysregulation of lipogenesis and thus hepatosteatosis leading to insulin resistance and type 2 diabetes.
Keyphrases
- insulin resistance
- high fat diet induced
- type diabetes
- transcription factor
- metabolic syndrome
- glycemic control
- dna methylation
- high fat diet
- adipose tissue
- polycystic ovary syndrome
- skeletal muscle
- genome wide
- genome wide identification
- cardiovascular disease
- gene expression
- dna binding
- dna damage
- uric acid
- quality improvement
- cardiovascular risk factors
- climate change
- structural basis