Abstract
The liver is the principal organ responsible for conversion of excess dietary carbohydrate to storage fat. Glucose, a major source of energy in mammals, provides pyruvate, which is either oxidized to generate ATP or converted into triglycerides for storage. The coordinated control of the metabolic pathways that direct the fate of glucose allows for the efficient use of dietary carbohydrate. Key enzymes in these pathways, including pyruvate kinase, acetyl-CoA carboxylase, and fatty acid synthase complex, are regulated by allosteric, post-translational mechanisms that are triggered by increased insulin secretion or nutrient levels. Insulin-induced expression of the steroid response element binding protein (SREBP)-1c, which mediates insulin-dependent activation of lipogenic gene transcription, contributes up to 40% of the triglycerides in liver. The other half of fat synthesis in liver is regulated by the carbohydrate response element binding protein (ChREBP), which operates independently of insulin. ChREBP induces the expression of liver pyruvate kinase (LPK) gene as well as all the lipogenic enzyme-encoding genes.
Original language | English (US) |
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Title of host publication | Encyclopedia of Biological Chemistry |
Subtitle of host publication | Second Edition |
Publisher | Elsevier Inc. |
Pages | 374-378 |
Number of pages | 5 |
ISBN (Electronic) | 9780123786319 |
ISBN (Print) | 9780123786302 |
DOIs | |
State | Published - Feb 15 2013 |
Keywords
- AMP-activated protein kinase
- CAMP-activated protein kinase
- Carbohydrate metabolism
- Carbohydrate responsive element
- Diabetes
- Glucose signaling
- Lipogenesis
- Liver pyruvate kinase
- Obesity
- Polyunsaturated fatty acids
- Protein phosphatase 2A
- Regulation of fat synthesis
- Triglycerides synthesis
- Xylulose-5-phsophate
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology