Chapter 11: Lipid and Amino Acid Metabolism

Question 1

what are some lipoproteins?

Answer 1

chylomicrons, VLDL, IDL, LDL and HDL

Question 1

what is the rate limiting step in fatty acid sythesis?

Answer 1

acetyl-CoA carboxylase

Question 2

another name for fatyy acid synthase?

Answer 2

palmitate synthase

Question 3

what is the rate limitung step in fatty acid oxidation?

Answer 3

carniitne acyltranferase I

Question 4

what is the only fatty acid that humans can synthesize de novo

Answer 4

palmitate synthase

Question 5

glucogenic amino acids

Answer 5

all but leucine and lysine

Question 6

Where is the lipid digestion made?

Answer 6

It is minimum in the mouth and stomach, lipids are transported to the small intestine essentially intact.

Question 7

Digestion of lipids.

Answer 7

Upon entry into the duodenum, emulsification occurs, which is the mixing of two normally immiscible liquids.

Question 8

What helps with emulsification?

Answer 8

Is aided by bile, which contains bile salts, pigments and cholesterol, bile secreted by the liver and stored in the gallbladder. The pancreas secrets pancreatic lipase, colipase and cholesterol esterase into the small intestine. Together, these enzymes hydrolyze the lipid components to 2-monoacylglycerol, Free fatty acids and cholesterol.

Question 9

Micelle formation

Answer 9

Free fatty acids, cholesterol, and 2-monoacylglycerol and bile salts contribute to the formation of micelles. Those are vital in digestion, transport and absorption of lipid soluble substances starting from the duodenum all the way to the end of the ileum.

Question 10

What are my micelles?

Answer 10

Clusters of amphipathic lipids are soluble in the aqueous environment of the intestinal lumen.

Question 11

Absorption of lipids.

Answer 11

Absorbed into the mucosa and re-esterified to form triacylglycerols and cholesteryl esters and package into chylomicrons. These leave the cell via lacteals and re-enter the bloodstream via the thoracic duct.

Question 12

Lipid mobilization.

Answer 12

Fatty acids are released from adipose tissue and used for energy. A falling insulin levels activates a hormone sensitive lipase (HCL) that hydrolyzes triacylglycerols yielding fatty acids and glycerol. Release glycerol from fat may be transported to the liver for glycolysis or gluconeogenesis. HSL is effective within adipose cells, but lipoprotein lipase (LPL) is necessary for the metabolism of chylomicrons and very low density lipoproteins (VLDL).

Question 13

Lipid Transport.

Answer 13

Triacylglycerol and cholesterol are transported into blood as lipoprotein, aggregates of apolipoproteins and lipids. chylomicrons are the least dance with the highest fat to protein ratio. VLDL (very low density lipoproteins) is slightly more dense, followed by IDL (intermediate density), LDL (low density) and HDL (high density). LDL and HDL are primarily cholesterol transport molecules.

Question 14

Chylomicrons

Answer 14

Function in the transport of dietary triacylglycerol, cholesterol and cholesteryl esters to other tissues. Assembly of chylomicrons occurs in the intestinal lining and result in a nascent chylomicrons that contains lipids and apolipoproteins.

Question 15

VLDL, (very low density lipoprotein)

Answer 15

It’s produced in assembled in liver cells. The main function is the transport of triacylglycerols to the other tissues. It also contains fatty acids, though are synthesized from Maxis glucose or retrieved from chylomicrons remnants.

Question 16

IDL (Intermediate density lipoproteins)

Answer 16

Once triacylglycerol is removed from VLDL, the resulting particle is referred to as either a VLDL remmant or IDL. IDL exists as a transition particle between triacylglycerol transport and cholesterol transport.

Question 17

LDL (low density lipoprotein)

Answer 17

majority of the cholesterol measured in the blood is associated with LDL. The normal role is to deliver cholesterol to tissues for biosynthesis.

Question 18

HDL (high density lipoprotein)

Answer 18

released as dense protein rich particles into the blood. Contains apolipoproteins used for cholesterol recovery, that is the cleaning up of excess cholesterol from blood vessels for excretion. HDL also delivers necessary apolipoproteins to some of the other lipoproteins.

Question 19

Cholesterol Metabolism Source

Answer 19

Synthesis of cholesterol occurs in the liver and is driven by Acetyl-Coa and ATP. This side trace shadow carries mitochondrial acetyl COA into the cytoplasm. Synthesis of mevalonic acid in the smooth endoplasmic reticulum is the rate limiting step in cholesterol biosynthesis and is catalyzed by HMG CoA reductase.

Question 20

How is cholesterol synthesis regulated?

Answer 20

Increased levels of cholesterol can inhibit further synthesis by feedback inhibition mechanism. Insulin promotes cholesterol synthesis.

Question 21

What are the specific enzymes involved in cholesterol synthesis?

Answer 21

LCAT, which means lecithin-cholesterol acetyl transferase. Is an enzyme found in bloodstream that is activated by HDL apoproteins. It adds a fatty acid to cholesterol which produces soluble cholesteryl ester, such as those in HDL. HDL cholesteryl ester can be distributed to other lipoproteins like IDL which becomes LDL by acquiring these cholesteryl ester. The cholesteryl ester transfer proteins (CETP) facilitates this transfer process.

Question 22

Fatty acids.

Answer 22

Are long chain of carboxylic acids. The carboxyl carbon is carbon one, and the carbon 2 is referred to as the alpha carbon.

Question 23

Nomenclature of fatty acids.

Answer 23

Total number of carbons is given along with the number of double bonds written as carbons:double bonds.

Question 24

What are two important fatty acids?

Answer 24

Alpha linolenic acid and linoleic acid.

Question 25

Why is lipid and carbohydrate synthesis often called nontemplate synthesis?

Answer 25

Because they do not rely directly on the coating of nucleic acid, unlike proteins and nucleic acid synthesis.

Question 25

Fatty acid biosynthesis.

Answer 25

It occurs in the liver, and its products are subsequently transported to adipose tissue for storage. Both of the major enzymes of fatty acid synthesis are Acetyl-CoA carboxylase and fatty acid synthase.

Question 25

Acetyl-CoA Shuttling

Answer 25

Acetyl-CoA Is the product of pyruvate dehydrogenase complex and it coupled with oxaloacetate to form citrate. As cell becomes more energetically satisfied, it slows the citric acid cycle, which causes citrate accumulation. Citrate and then diffuse across the mitochondrial membrane. In the cytosol citrate lipase split citrate back into acetylcholine and oxaloacetate.

Question 26

Acetyl-CoA Carboxylase.

Answer 26

It is the rate limiting enzyme of fatty acid biosynthesis. It requires biotin and ATP to function and add CO2 to Acetyl-CoA to form Malonyl-CoA. The enzyme is activated by insulin and citrate.

Question 27

Fatty acids Synthase

Answer 27

It can also be called palmitate synthesis because palmitate is the only fatty acid that humans can synthesize. It happens in the cytosol, where rapidly induced in the liver following a meal high in carbohydrates because of elevated insulin levels. There are five steps involved in fatty acid biosynthesis:

1) Attachment to an Acyl carrier protein (ACP)

2) Bond formation between activated manonyl-CoA and the growing chain.

3) Reduction of a carbonyl group.

4) Dehydration.

5) Reduction of a double bond.

Question 27

Triacylglycerol synthesis.

Answer 27

Attaching 3 fatty acids to glycerol. Its formation from fatty acids and glycerol 3 phosphate occurs primarily in the liver and somewhat in adipose tissue.

Question 28

Beta oxidation.

Answer 28

Occurs in the mitochondria. Insulin indirectly inhibits beta oxidation, while Glucagon stimulates this process. The first step is activation. When fatty acids are metabolized, they first become activated by attachment to CoA. Which is catalyzed by fatty-acyl-Coa synthetase.

Question 29

Fatty acid entry into mitochondria.

Answer 29

Short chain fatty acids and medium chain fatty acids diffuse freely into the mitochondria where they are oxidized. In contrast, while long chains fatty acids are also oxidizing the mitochondria, they require transport via carnitine shuttle. Carnitine acetyltransferase one is the rate limiting enzyme of fatty acid oxidation.

Question 29

Beta oxidation in mitochondria.

Answer 29

oxidizing and releasing molecules of Acetyl-CoA. The pathways repetition of four steps; Each four step cycle releases one Acetyl-CoA And reduces NAD Plus and FAD Two NADH and FADH2. The four steps in beta oxidation are:
1) Oxidation of fatty acid to form a double bond.

2) Hydration of the double bond to form a hydroxyl group.

3) Oxidation of hydroxyl group to form a carbonyl

4) Splitting of the beta-ketoacid into a shorter Acyl-CoA and Acetyl-CoA

Question 30

What happens if there’s an odd number fatty acid ?

Answer 30

They yield 1 acetyl-CoA way and one propionyl-CoA. Odd carbon fatty acids represent an exception to the rule that fatty acids cannot be converted to glucose in humans.

Question 30

What happens if we have an unsaturated fatty acid?

Answer 30

Two additional exams are necessary because double bonds can disturb the stereochemistry needed for oxidative enzymes to act on the fatty acid. To function, these enzymes can have a most 1 double bond in their active site. This bond must be located between carbons 2 and 3. Enoyl-CoA isomerase rearrange is cis double bonds at the 3,4 position to trans double bonds at the 2,3 position once enough Acityl-CoA has been liberated to isolate the double bond within the first three carbons. In polyunsaturated fatty acids, a further reduction is required using 2,4-dienoyl-CoA reductase To convert 2 conjugated double bonds to just one double bond at the 3,4 position.

Question 30

Ketone bodies.

Answer 30

In fasting states, the liver converts excess acetyl-COA from beta oxidation to fatty acids into the ketone bodies acetoacetate and 3-hydroxybutyrate to Acetyl-CoA. Ketone bodies are essentially transportable forms of Acetyl-CoA. They are produced by the liver and used by other tissues during prolonged starvation.

Question 30

Ketogenesis

Answer 30

Occurs in the mitochondria of liver cells when excess Acetyl-CoA accumulating the fasting state. HMG-CoA synthase forms, HMG-CoA and HMG-CoA lyase breaks down HMG-CoA into acetoacetate, which can subsequently be reduced to 3-hydroxybutyrate.

Question 31

Ketolysis

Answer 31

Acetoacetate picked up from the blood is activated in the mitochondria by succinyl-CoA acetylacetyl-CoA transferase, commonly called thiophorase, An enzyme present only in tissues outside the liver. During this reaction, acetoacetate is oxidized to acetylacetyl-CoA.

Question 32

Ketolysis in the brain.

Answer 32

In the brain, when ketones are metabolized to Acetyl-CoA, Pyruvate dehydrogenase is inhibited. Glycolysis and glucose uptake in the brain decreases. It allows the brain to indirectly metabolize fatty acid as ketone bodies.

Question 32

What is proteolysis?

Answer 32

Breakdown of proteins. It begins in the stomach with pepsin and continues with the pancreatic proteases trypsin, chymotrypsin and carboxypeptidase A and B. Protein digestion is completed by a small intestinal brush border enzyme dipeptidase and aminopeptidase. The main products of protein digestions are amino acid dipeptides and tripeptides.

Question 33

Glucogenic amino acids.

Answer 33

Can be converted into glucose through gluconeogenesis. They include all but leucine and lysine.

Question 34

Ketogenic amino acids.

Answer 34

Can be converted to Acetyl-CoA And ketone bodies.

Question 35

The amino group removed by transamination or deamination constitute a potential toxin to the body. What does it do?

Answer 35

Because it forms ammonia, it must be extruded safely. They urea cycle occurs in the liver and is the body’s primary way of removing excess nitrogen from the body.

Question 36

What does LCAT catalyzes?

Answer 36

Formation of cholesteryl esters for transport with HDL.

Question 37

What does CETP Catalyzes?

Answer 37

Transition of IDL to LDL by transferring cholesteryl esters from HDL.