Lipid metabolism

Question 1

What are lipids?

Answer 1

Lipids are a chemically diverse group of compounds that are insoluble in water. They have diverse biological functions and are a principal source of stored energy.

Question 2

What are the major structural elements of biological membranes?

Answer 2

Phospholipids, glycolipids, and cholesterol are the major structural elements of biological membranes.

Question 3

What are the roles of lipids in metabolism?

Answer 3

Lipids play important roles in metabolism as enzyme cofactors, electron carriers, and emulsifying agents in the digestive tract.

Question 4

What are the roles of lipids in inter- and intra-signaling events?

Answer 4

Lipids are precursors of steroid hormones and can play important roles in inter- and intra-signaling events.

Question 5

What is the role of cholesterol in normal cellular function?

Answer 5

Cholesterol is a type of lipid that is a major structural component of cell membranes and is involved in cell signaling and the synthesis of steroid hormones.

Question 6

What are the two main categories of lipids?

Answer 6

The two main categories of lipids are storage lipids and membrane lipids.

Question 7

What are the structures of storage lipids?

Answer 7

Storage lipids, also known as neutral lipids, include triglycerides, which are made up of one glycerol and three fatty acids.

Question 8

What is the function of triglycerides?

Answer 8

Triglycerides constitute about 90% of dietary lipids and are the major form of metabolic energy storage in humans.

Question 9

What are the characteristics of fatty acids?

Answer 9

Fatty acids can be saturated, meaning they have no double bonds between carbon atoms, or unsaturated, meaning they have at least one double bond. Polyunsaturated fatty acids have more than one double bond. The melting points of fatty acids decrease with degree of unsaturation, making more unsaturated fatty acids more fluid.

Question 10

What are the structures of membrane lipids?

Answer 10

Membrane lipids are polar and include phospholipids, glycolipids, and cholesterol.
- phospholipids
- glycerophospholipid
- 1 glycerol, 2 fatty acids, alcohol and PO4
- Sphingolipids
- sphingosine, fatty acid, PO4 and choline
- glycolipids
- sphingolipids
- sphingosine, fatty acid, mono or oligosaccharide
- galactolipids/ sulfolipids
- glycerol, 2 fatty acids. mono or disaccharide and SO4

Question 11

What is the function of cholesterol?

Answer 11

Cholesterol is a type of lipid that is involved in membrane structure and fluidity, and is also a precursor to steroid hormones. It is not a major source of metabolic energy.

Question 12

What are the two major metabolic pathways for triglyceride metabolism?

Answer 12

Depending on metabolic requirements, there are two major metabolic pathways for triglyceride metabolism: oxidation in the mitochondria to release energy in the form of ATP, and synthesis of triglycerides from malonyl-CoA for storage.

Question 13

What is β-oxidation?

Answer 13

β-Oxidation is the oxidative process that releases free energy and occurs in the mitochondria. It involves the successive removal of 2-carbon fragments as acetyl-CoA from fatty acids.

Question 14

What are the stages of the complete oxidation of fatty acids to CO2 and H2O?

Answer 14

There are three stages of complete oxidation of fatty acids to CO2 and H2O: oxidation of long chain fatty acids to 2-carbon fragments in the form of acetyl-CoA (which is β-oxidation), oxidation of acetyl-CoA to CO2 in the citric acid cycle, and transfer of electrons from reduced electron carriers to mitochondrial respiratory chain.

Question 15

What is Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)?

Answer 15

Medium-chain acyl-CoA dehydrogenase deficiency (MCADD) is a syndrome that results from mutations in the enzyme complex that inhibits the first stage of β-oxidation. It is an autosomal recessive disorder of the ACADM gene and can cause clinical symptoms such as lethargy, hypoglycemia, seizures, and vomiting.

Question 16

What is the process of fatty acid synthesis?

Answer 16

Fatty acid synthesis occurs mainly in the liver and adipocytes and involves building long carbon chain molecules from 2-carbon units derived from acetyl-CoA and a 3C malonyl-CoA intermediate. This occurs in the cytosol, but acetyl-CoA is in the mitochondria.

Question 17

What is the citrate malate cycle?

Answer 17

The citrate malate cycle is how acetyl-CoA gets out of the mitochondria. Acetyl-CoA is converted to citrate for transport out of the mitochondria, then back to acetyl-CoA in the cytosol for use in fatty acid synthesis. The oxaloacetate produced is then converted back to pyruvate for transport back into the mitochondria for use in ATP synthesis.

Question 18

What are the rate-limiting steps in fatty acid oxidation and synthesis?

Answer 18

The rate-limiting steps in fatty acid oxidation and synthesis are the transfer of acetyl-CoA into the mitochondria for β-oxidation and the formation of malonyl-CoA from acetyl-CoA, which is catalyzed by acetyl-CoA carboxylase for fatty acid synthesis. Acetyl-CoA carboxylase is subject to phosphorylation under the control of glucagon.

Question 19

What is cholesterol and what is its role in the body?

Answer 19

Cholesterol is an amphipathic lipid that is synthesized from acetyl-CoA and can be eliminated as bile acids. It is an essential molecule in many animals, including humans, and is not required in the diet because all cells can synthesize it. It is a major component of cell membranes and can also be stored as cholesterol esters.

Question 20

What are bile acids, and what is their function in the body?

Answer 20

Bile acids are relatively hydrophilic cholesterol derivatives that are produced from cholesterol by the liver and excreted into the gall bladder for release into the small intestine. They act as emulsifiers, breaking up fats to form a suspension of tiny fat droplets in an aqueous medium, which increases the surface area of the fats available for enzymatic digestion.

Question 21

What is HMG-CoA reductase, and what is its role in cholesterol biosynthesis?

Answer 21

MG-CoA reductase is the enzyme that catalyzes the rate-determining step in cholesterol biosynthesis, which is the conversion of HMG-CoA to mevalonate. It is regulated by feedback inhibition from both cholesterol and mevalonate, and is also a target site for statin drugs. Its activity is also regulated by insulin and glucagon.

Question 22

What are the four stages of cholesterol biosynthesis?

Answer 22

The four stages of cholesterol biosynthesis are the synthesis of mevalonate from acetate, the conversion of mevalonate to two activated isoprenes, the condensation of six isoprene units to form squalene, and the cyclization of squalene to the four-ring steroid nucleus.

Question 23

Why do we transport lipids around the body?

Answer 23

Lipids are transported around the body to bring dietary lipids to cells for energy production or storage, move lipids from storage in adipose tissue for use in energy production, provide lipids from the diet to cells for synthesizing cell membranes, and carry cholesterol from peripheral tissues to the liver for excretion.

Question 24

How are lipids transported in the blood?

Answer 24

Short-chain fatty acids are transported bound to blood proteins like albumin. The bulk transport of neutral lipids, which are insoluble in water, requires special carrier proteins called lipoproteins, which are composed of hydrophilic, hydrophobic, and amphipathic molecules.

Question 25

What are plasma lipoproteins, and what determines their specific function?

Answer 25

Plasma lipoproteins are specific carrier proteins that combine with lipids to form several classes of lipoproteins. Each lipoprotein has a specific function that is determined by the point of synthesis, lipid composition, and apolipoprotein content. The apolipoproteins act as signals targeting the lipoproteins to specific tissues or activating enzymes that act on lipoproteins.

Question 26

What are the major classes of plasma lipoprotein and their functions?

Answer 26

The major classes of plasma lipoproteins are chylomicron, VLDL, LDL, and HDL. Chylomicrons transport dietary fats, VLDL transports endogenous lipids to muscle and adipose tissue, LDL carries cholesterol to muscle, adrenal glands and adipose tissue, HDL originates in the liver and small intestine and is involved in returning cholesterol to the liver.

Question 27

What is atherogenesis and how are LDL and HDL involved?

Answer 27

Atherogenesis is the process of forming fatty plaques in the arteries that can lead to heart disease and stroke. LDL, especially small dense LDL, is involved in the deposition of cholesterol in the artery walls, while HDL is involved in the reverse transport of cholesterol from the peripheral tissues back to the liver.

Question 28

What is a lipid profile and what does it typically include?

Answer 28

A lipid profile is a blood test that measures the levels of various lipids and lipoproteins in the blood. It typically includes measurements of total cholesterol, LDL, HDL, and triglycerides.

Question 29

What is the relationship between lipid profiles and cardiovascular disease?

Answer 29

Elevated levels of LDL and triglycerides and low levels of HDL are associated with an increased risk of cardiovascular disease. Measuring lipid profiles can help identify individuals who may be at increased risk of developing heart disease or stroke.

Question 30

How are triacylglycerols digested and absorbed?

Answer 30

Dietary triacylglycerols are first emulsified by bile acids and then hydrolyzed by pancreatic triacylglycerol lipase. The products of lipid digestion are a mixture of fatty acids and mono- and diacylglycerols, which can be absorbed by the intestinal mucosa.

Question 30

What is the exogenous lipid transport pathway?

Answer 30

The exogenous transport pathway involves the transport of lipids from the intestine as dietary fat through the intestinal mucosa, where it is packaged as chylomicrons. These chylomicrons travel to tissues where the ApoC-II apolipoprotein stimulates tissue-bound lipoprotein lipase enzymes to release triacylglycerides. The remnants are then endocytosed by the liver, which recognizes them by their ApoE apolipoprotein.

Question 30

What is the endogenous lipid transport pathway?

Answer 30

The endogenous transport pathway involves the transport of lipids from the liver to adipose/muscle tissues as VLDL lipoproteins. ApoC-II activates tissue-bound lipoprotein lipases, which releases fatty acids. Triacylglyceride-depleted remnants of VLDLs form IDL, which on further loss of triacylglycerides become low-density lipoproteins. These cholesterol/cholesterol ester-rich lipoproteins are taken up by endocytosis within the extrahepatic tissues by binding of the ApoB-100 apolipoprotein to the LDL receptors on the cell surface of the liver and extrahepatic tissue.

Question 30

What is the reverse transport pathway?

Answer 30

The reverse transport pathway involves the transport of endogenous cholesterol and cholesterol esters from the extrahepatic tissues back to the liver via HDL (high-density lipoproteins). These do not enter the liver by endocytosis but instead bind to scavenger receptors (SR-B1) on the cell surface that mediate transfer of cholesterol into the cell.

Question 31

How is LDL (cholesterol) taken up by cells?

Answer 31

LDL (cholesterol) is taken up by cells through mediation by LDL receptors on the cell surface that bind to ApoB-100. The LDL receptors are then separated from LDL and recycled back to the cell surface. The endosome fuses with lysosome, and the lytic enzymes degrade ApoB-100, releasing amino acids, fatty acids, cholesterol, and cholesterol esters.

Question 32

How is intracellular cholesterol regulated in the short term?

Answer 32

Short-term regulation of cellular cholesterol levels is achieved by modifying HMG-CoA reductase activity, which controls the biosynthesis of cholesterol

Question 33

How is intracellular cholesterol regulated in the long term?

Answer 33

Long-term regulation is achieved by modifying the numbers of molecules involved in maintaining cellular cholesterol levels, such as HMG-CoA reductase and LDL receptors. Transcription and protein production are increased under low cholesterol levels and repressed under high levels. Protein degradation of HMG-CoA and LDL receptors reduces their numbers under high cholesterol levels.