Table of Contents
- What is Lipogenesis?
- Role of Carbohydrates in Lipogenesis
- Function of Lipogenesis
- Process of Lipogenesis
- Lesson Summary
Lipogenesis is the synthesis of acetyl-coenzyme A (acetyl-CoA) subunits into triglycerides. Lipogenesis consists of fatty acid synthesis followed by triglyceride synthesis. The triglycerides formed in lipogenesis are stored in the adipocytes of adipose tissue. Acetyl-CoA is the building block of fatty acids, and consists of an acetyl group bonded to the nucleotide coenzyme A. It is generated and used in different metabolic pathways, including the citric acid cycle and amino acid synthesis. Fatty acids consist of a carboxylic head group bonded to a long hydrocarbon chain. Triglycerides consist of three fatty acid residues esterified to glycerol, a three-carbon alcohol.
Lipogenesis occurs mainly in the liver, adipose tissue, and small intestine, but it also occurs in other cells such as the kidneys and mammary glands. Fatty acid synthesis occurs mainly in the cytosol. Elongation of fatty acids occurs in the endoplasmic reticulum or mitochondrion. Desaturation of fatty acids occurs in the endoplasmic reticulum. Triglyceride synthesis takes place in the endoplasmic reticulum. In contrast, beta-oxidation, the degradation of fatty acids into acetyl-CoA subunits, occurs in the mitochondrion and peroxisome in animals. Lipolysis, the hydrolysis of triglycerides into fatty acids and glycerol, occurs on the surface of lipid droplets in adipocytes. It also occurs in the gastrointestinal system and in lipoproteins in the blood.
Cells can convert molecules from other metabolic pathways into triglycerides. First, the starting molecule is degraded to one of the starting materials for lipogenesis, and then lipogenesis forms triglycerides. Excess carbohydrates in the body are commonly converted into triglycerides. Polysaccharides used for lipolysis are first broken down into monosaccharides. Polysaccharides either come directly from food or are stored as glycogen in the liver and muscle tissue. Glycogenolysis is responsible for degrading glycogen to glucose (in the liver) or glucose-6-phosphate (in muscle). Polysaccharides from the diet are broken down into monosaccharides including glucose, fructose, and galactose. These monosaccharides enter glycolysis at different steps, where they are degraded to different intermediates and ultimately pyruvate. Pyruvate can then be decarboxylated to form acetyl-CoA, one of the starting materials for fatty acid synthesis. Glycolysis intermediates dihydroxyacetone phosphate and pyruvate can also be converted to glycerol-3-phosphate, one of the starting materials for triglyceride synthesis.
The purpose of lipogenesis is to synthesize triglycerides that will be stored as energy in adipose tissue. These triglycerides can later be broken down via beta-oxidation to generate adenosine triphosphate (ATP). Triglycerides are the preferred energy storage molecule because the highly reduced fatty acid tails have high energy potential when oxidized. In fact, fatty acids produce over twice as much energy per gram as polysaccharides during oxidation. Triglycerides can be synthesized via lipogenesis from various starting materials, including carbohydrates, amino acids, and other lipids. These molecules are degraded through different metabolic pathways to produce the starting materials for lipogenesis, including acetyl-CoA and glycerol-3-phosphate.
Lipogenesis involves fatty acid synthesis followed by triglyceride synthesis. Fatty acid synthesis begins with acetyl-CoA. Acetyl-CoA can be derived from carbohydrates, in which the final product of glycolysis, pyruvate, reacts with coenzyme A to form acetyl-CoA. It can also be derived from beta-oxidation, in which a fatty acid is broken down into acetyl-CoA subunits.
The first step of fatty acid synthesis involves transporting acetyl-CoA from the mitochondrion to the cytosol. First, citrate synthase catalyzes the condensation of acetyl-CoA and oxaloacetate to form citrate and coenzyme A. Then, citrate transport protein (CTP) transports citrate from the mitochondrion to the cytosol. ATP-citrate lyase catalyzes the conversion of citrate and coenzyme A to oxaloacetate and acetyl-CoA in the cytosol. In the cytosol, acetyl-CoA carboxylase catalyzes the carboxylation of acetyl-CoA to malonyl-CoA by consuming ATP. This is the rate-limiting step of fatty acid synthesis.
The next seven reactions involve the enzyme fatty acid synthase catalyzing the synthesis of palmitate from malonyl-CoA and an acyl group (which starts off as acetyl-CoA). Fatty acid synthase is a dimer of two identical polypeptides, and each polypeptide has six active sites that catalyze the seven reactions.
In the endoplasmic reticulum or mitochondrion, elongase catalyzes the synthesis of fatty acids longer than sixteen carbons from palmitate. In the endoplasmic reticulum, desaturatase catalyzes the desaturation of saturated fatty acids to form unsaturated fatty acids.
Once fatty acid synthesis is complete, triglycerides can then be synthesized. Triglycerides can be synthesized with different starting materials. In the enterocytes of the small intestine, triglyceride synthesis mainly uses monoglycerides from digestion as the starting material. In other cells, fatty acids are bonded to glycerol-3-phosphate, which is synthesized from various precursor molecules. In adipocytes, which lack the enzyme glycerol kinase that converts glycerol to glycerol-3-phosphate, DHAP is mainly used as the starting material. The liver mainly uses glycerol as the starting material but will also use DHAP. Glycerol and DHAP are first converted to glycerol-3-phosphate before triglyceride synthesis begins. Glycerol-3-phosphate can also be synthesized via glyceroneogenesis, in which other molecules such as pyruvate, alanine, or glutamine are used as starting materials.
Triglyceride synthesis starts with fatty acid activation. Long-chain fatty acyl-CoA ligase catalyzes the formation of a fatty acyl-CoA using a fatty acid, coenzyme A, and ATP. Next, acyltransferase catalyzes the esterification of a saturated fatty acyl-CoA to carbon 1 of glycerol-3-phosphate and an unsaturated fatty acyl-CoA to carbon 2 to form phosphatidic acid. Phosphatidate phosphatase catalyzes the dephosphorylation of phosphatidic acid to a diglyceride. Finally, acyltransferase catalyzes the esterification of a third fatty acyl-CoA to carbon 3 of the diglyceride to form a triglyceride.
Lipogenesis is regulated by different hormones and pathway intermediates. As previously stated, the reaction catalyzed by acetyl-CoA carboxylase is the rate-limiting step of fatty acid synthesis. This step is inhibited by palmitoyl-CoA, the product of fatty acid synthesis. Fatty acid synthesis is allosterically activated by citrate.
Insulin is a hormone secreted by the pancreas mainly in response to increased blood glucose levels. Insulin stimulates lipogenesis by increasing the uptake of glucose into adipocytes. Growth hormone inhibits lipogenesis by decreasing insulin sensitivity, thus decreasing fatty acid synthase expression in adipocytes, and by phosphorylating transcription factors needed for lipolysis. Leptin is a hormone secreted mainly by adipocytes that inhibits lipogenesis by stimulating the release of glycerol from adipocytes.
Lipogenesis is the synthesis of triglycerides from acetyl-CoA via fatty acid synthesis followed by triglyceride synthesis. Fatty acid synthesis forms fatty acids from several molecules of acetyl-CoA using the enzyme fatty acid synthase. Acetyl-CoA is a molecule that consists of the nucleotide coenzyme A bonded to an acetyl group. Fatty acids are long hydrocarbon chains bonded to a carboxylic acid at one end. Triglyceride synthesis involves bonding three fatty acids to glycerol-3-phosphate to form a triglyceride.
Lipogenesis occurs mainly in the cytoplasm and endoplasmic reticulum of liver cells and adipose cells. The degradation of carbohydrates provides the starting materials acetyl-CoA and glycerol-3-phosphate for lipogenesis to occur. The triglycerides produced by lipogenesis are stored in adipose tissue to be used as an energy reserve. Lipogenesis is regulated by different metabolic pathway intermediates and hormones. Insulin increases the rate of lipogenesis, while growth hormone and leptin decrease lipogenesis.
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Lipogenesis is the synthesis of triglycerides from acetyl-CoA into fatty acids which are then converted to triglycerides. Lipolysis is the degradation of triglycerides into glycerol and free fatty acids.
The purpose of lipogenesis is to produce triglycerides from acetyl-CoA subunits. These triglycerides are then used as an energy reserve stored in adipose tissue.
Lipogenesis consists of fatty acid synthesis and triglyceride synthesis. First, fatty acids are synthesized from acetyl-CoA subunits. Then, three fatty acids are esterified to glycerol-3-phosphate to form a triglyceride.
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