lipidsynthese

Lipidsynthese, or lipid synthesis, refers to the cellular processes that generate lipids from smaller carbon sources. In eukaryotic cells, the major sites are the cytosol and the endoplasmic reticulum, with the liver and adipose tissue playing central roles in whole-organism lipid production and storage. The process yields fatty acids, triglycerides, phospholipids, and sterols that are used for energy storage, membrane formation, and signaling.

Fatty acid synthesis begins in the cytosol from acetyl-CoA. Acetyl-CoA is produced in mitochondria and exported to the cytosol as citrate, which is cleaved by ATP citrate lyase to regenerate acetyl-CoA. Acetyl-CoA carboxylase converts acetyl-CoA to malonyl-CoA, the committed step of fatty acid synthesis. Fatty acid synthase then elongates the growing chain by two-carbon units, typically producing palmitate (C16:0). Desaturation and further elongation occur mainly in the endoplasmic reticulum, giving rise to a range of saturated and unsaturated fatty acids.

Glycerolipid biosynthesis uses the glycerol-3-phosphate pathway. Enzymes such as GPAT and AGPAT assemble fatty acyl chains onto glycerol-3-phosphate to form phosphatidic acid, which can be dephosphorylated to diacylglycerol and further acylated by DGAT to yield triglycerides. Phospholipid synthesis proceeds via the Kennedy pathway, generating phosphatidylcholine, phosphatidylethanolamine, and related lipids that are essential components of cellular membranes.

Sterol synthesis follows the mevalonate pathway, producing cholesterol and other isoprenoids. HMG-CoA reductase is the key rate-limiting enzyme and a major target of statin drugs.

Regulation integrates hormonal and nutritional signals. Insulin promotes lipogenesis, while glucagon and AMP-activated protein kinase inhibit key enzymes such as acetyl-CoA carboxylase. Transcription factors SREBP-1c and ChREBP adjust gene expression in response to diet.