
SREBP family have been recently established as bHLH type transcription factors governing lipid synthesis. While SREBP-2 regulates expression of genes involved in cholesterol biosynthesis and LDL receptor, SREBP-1c controls fatty acid synthesis. Cellular cholesterol is regulated by feedback system where SCAP/Insig system regulates cleavage of SREBP-2 for its activation depending upon cellular cholesterol demand. Meanwhile, SREBP-1c is nutritionally regulated, excess energy intake could activate hepatic SREBP-1c expression leading to formation of remnant lipoproteins and hepatic insulin resistance through suppression of IRS-2 expression. Hepatic SREBP-1c could be deeply involved in metabolic syndrome. Thus, SREBP-1c could be a therapeutic target to treat metabolic syndrome. Polyunsaturated fatty acids suppress SREBP-1c and suppress lipogenesis.
Metabolic Syndrome, Arteriosclerosis, Intracellular Signaling Peptides and Proteins, Membrane Proteins, Phosphoproteins, Lipids, DNA-Binding Proteins, Gene Expression Regulation, Liver, Receptors, LDL, CCAAT-Enhancer-Binding Proteins, Fatty Acids, Unsaturated, Insulin Receptor Substrate Proteins, Animals, Humans, Insulin Resistance, Energy Intake, Sterol Regulatory Element Binding Protein 1, Sterol Regulatory Element Binding Protein 2, Transcription Factors
Metabolic Syndrome, Arteriosclerosis, Intracellular Signaling Peptides and Proteins, Membrane Proteins, Phosphoproteins, Lipids, DNA-Binding Proteins, Gene Expression Regulation, Liver, Receptors, LDL, CCAAT-Enhancer-Binding Proteins, Fatty Acids, Unsaturated, Insulin Receptor Substrate Proteins, Animals, Humans, Insulin Resistance, Energy Intake, Sterol Regulatory Element Binding Protein 1, Sterol Regulatory Element Binding Protein 2, Transcription Factors
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