[HTML][HTML] Energy metabolism in the liver

L Rui - Comprehensive physiology, 2014 - ncbi.nlm.nih.gov
Comprehensive physiology, 2014ncbi.nlm.nih.gov
The liver is an essential metabolic organ, and its metabolic activity is tightly controlled by
insulin and other metabolic hormones. Glucose is metabolized into pyruvate through
glycolysis in the cytoplasm, and pyruvate is completely oxidized to generate ATP through the
TCA cycle and oxidative phosphorylation in the mitochondria. In the fed state, glycolytic
products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty
acids are incorporated into triacylglycerol, phospholipids, and cholesterol esters in …
Abstract
The liver is an essential metabolic organ, and its metabolic activity is tightly controlled by insulin and other metabolic hormones. Glucose is metabolized into pyruvate through glycolysis in the cytoplasm, and pyruvate is completely oxidized to generate ATP through the TCA cycle and oxidative phosphorylation in the mitochondria. In the fed state, glycolytic products are used to synthesize fatty acids through de novo lipogenesis. Long-chain fatty acids are incorporated into triacylglycerol, phospholipids, and cholesterol esters in hepatocytes, and these complex lipids are stored in lipid droplets and membrane structures, or secreted into the circulation as VLDL particles. In the fasted state, the liver secretes glucose through both breakdown of glycogen (glycogenolysis) and de novo glucose synthesis (gluconeogenesis). During pronged fasting, hepatic gluconeogenesis is the primary source of endogenous glucose production. Fasting also promotes lipolysis in adipose tissue to release nonesterified fatty acids which are converted into ketone bodies in the liver though mitochondrial β oxidation and ketogenesis. Ketone bodies provide a metabolic fuel for extrahepatic tissues. Liver metabolic processes are tightly regulated by neuronal and hormonal systems. The sympathetic system stimulates, whereas the parasympathetic system suppresses, hepatic gluconeogenesis. Insulin stimulates glycolysis and lipogenesis, but suppresses gluconeogenesis; glucagon counteracts insulin action. Numerous transcription factors and coactivators, including CREB, FOXO1, ChREBP, SREBP, PGC-1α, and CRTC2, control the expression of the enzymes which catalyze the rate-limiting steps of liver metabolic processes, thus controlling liver energy metabolism. Aberrant energy metabolism in the liver promotes insulin resistance, diabetes, and nonalcoholic fatty liver diseases (NAFLD).
ncbi.nlm.nih.gov