lipidsyntese

Lipidsyntese, commonly called lipogenesis, is the cellular process of producing lipids from smaller building blocks. In animals, the liver and adipose tissue are the primary sites, with most activity in the cytosol and endoplasmic reticulum. The process uses NADPH as reducing power and is driven by surplus energy, especially from carbohydrates, which increases the supply of acetyl-CoA and reducing equivalents.

A central step is fatty acid synthesis. Acetyl-CoA carboxylase (ACC) converts acetyl-CoA to malonyl-CoA, the rate-limiting step of fatty acid formation. Fatty acid synthase (FAS) then elongates the chain to palmitate (C16:0). Desaturation and further elongation can generate other fatty acids. ACC activity is stimulated by insulin and inhibited by glucagon/epinephrine and by AMPK, and malonyl-CoA also inhibits fatty acid oxidation by blocking carnitine palmitoyltransferase 1.

Cytosolic acetyl-CoA is mainly derived from citrate exported from mitochondria, with NADPH supplied by the pentose phosphate pathway, malic enzyme, and isocitrate dehydrogenase. Glycerolipid synthesis follows: glycerol-3-phosphate is acylated to form phosphatidic acid, which is dephosphorylated to diacylglycerol (DAG) and then esterified with another acyl-CoA to yield triglycerides, stored in lipid droplets. DAG also serves as a precursor for phospholipid synthesis in membranes.

Sterol synthesis proceeds via the mevalonate pathway to cholesterol, regulated by HMG-CoA reductase and transcription factors such as SREBP. Overall, lipidsyntese provides fatty acids, triglycerides, phospholipids, and sterols for energy storage, membrane construction, and signaling, and is tightly regulated by hormonal and nutritional status. Dysregulation can contribute to metabolic diseases such as hepatic steatosis and obesity.