7. Synthesis of complex lipids

Last updated on November 19, 2018 at 17:16


  • Fuck this topic
  • Know the MRTs related to this
  • Complex lipids are glycerol molecules with fatty acids on carbon 1 and 2 or just 1, and with special groups on the third carbon.

Let’s tackle it

Glycerol 3-phosphate is an important precursor in complex lipid synthesis. It can be synthesized by attaching a phosphate group to a glycerol (glycerol kinase, only in liver), or by reduction of dihydroxyacetonephosphate (glycerol-3-phosphate dehydrogenase).

Acyl groups (fatty acids) can be attached to the first and second carbon of glycerol 3-phosphate, to give a phosphatidic acid.

Consider the glycerophospholipid below. Pretend that the head group is an inositol with 2 phosphate groups. There are 4 enzymes that can split complex lipids in 4 different places. They are phospholipase A1, A2, C and phospholipase D. A1 cleaves the molecule at the red line, A2 at the blue line, C at the green line and D at the yellow. In our case if we apply phospholipase C, we create a diacylglycerol, a molecule that can be recycled as energy or for lipid synthesis, while the inositol bisphosphate is released. Inositol bisphosphate (kinda) is a second messenger. This means that complex lipids can be used to “store” second messengers, to be ready to be excreted when the signal arrives.

The path phosphatidic acids can take.

Complex lipids are also used to build up membranes.

Otherwise, you should know that steroids inhibit production of arachidonate, while NSAIDs (non-steroidal inflammatory drugs) like aspirin inhibits cyclooxygenase. There are two kinds of cyclooxygenase. Type 1 creates prostaglandins that are needed for production of gastric mucin. Type 2 creates prostaglandins that mediate inflammation, pain and fever.

Phosphoenolpyruvate carboxykinase is an enzyme needed for gluconeogenesis, but also for the synthesis of glycerol (glyceroneogenesis). As glycerol is needed to create lipids, we need PEPCK in adipose tissue, even though adipose tissue doesn’t do gluconeogenesis. Only the liver does.

Glucocorticoids are a type of steroid hormones that activate transcription of PEPCK in the liver, and inhibits it in adipose tissue. That’s because glucocorticoids signal that the body should increase gluconeogenesis, but not lipid synthesis.

Thiazolidinedione is a medication used to treat diabetes type 2. It increases transcription of PEPCK in adipose tissue, to increase glycerol production, which increases production of triacylglycerol.

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6. Fatty acid synthesis (with elongation and desaturation)

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8. Structure and biological activities of steroids

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