Chapter 11: Lipid Digestion and Absorption Flashcards

(97 cards)

1
Q

In addition to being a major source of energy in the body, lipid serve a variety of other functions in the body. What are they?

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2
Q

What do dietary fats consist of?

What is emulsification? What is the modification aided by?

Where is bile stored and secreted?

What are some pancreatic enzymes that hydrolize lipids?

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3
Q

Absorption of lipids into the blood from the small intestine.

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4
Q

What are micelles in the intestine formed by?

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5
Q

What is absorption of micelles?

What transports fat soluble vitamins, lipids, and certain apoproteins?

How do they leave the intestine?

Where do they re enter the bloodstream? Where is that thing located?

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6
Q

MCAT concept check lipid digestion and absorption 10.1 page 416 question 1

When lipids leave the stomach, what stages of digestion have been accomplished?

What enzymes are added to accomplish the next phase?

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Physical digestion is accomplished in the mouth in the stomach, reducing the particle size.

Beginning in the small intestine, pancreatic lipase, colipase, cholesterol esterase, and bile assist in the chemical digestion of lipids.

In the more distal portion of the small intestine, absorption occurs.

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7
Q

MCAT concept check lipid digestion and absorption 10.1 page 416 question 2

True or false: all lipids enter the circulation through the lymphatic system.

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False. Small free fatty acids enter the circulation directly.

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8
Q

MCAT concept check lipid digestion and absorption 10.1 page 416 question 3

Describe the structure of a micelle.

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Micelles are collections of lipids with their hydrophobic and oriented toward the center, and their charged ends oriented toward the aqueous environment.

Micelles collect lipids within their hydrophobic centers.

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9
Q

At night, the body is in a post absorptive state, utilizing energy stored instead of food for fuel.

What enzyme is activated by a fall in insulin levels? What do they yield?

What hormone activates hormone sensitive lipases?

A

In the postabsorptive state, fatty acids are released from adipose tissue and used for energy.

Human adipose tissue does not respond directly to glucagon.

A fall in insulin levels activates hormone, sensitive lipase (HSL) that hydrolysis tricylglycerols, yielding fatty acid and glycerol.

Epinephrine and cortisol activate HSL (as well as as a fall in insulin levels).

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10
Q

Where does released glycerol from fat go and for what?

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Released glycerol from fat may be transported to the liver for glycolysis or gluconeogenesis.

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11
Q

HSL is effective in hydrolyzing triglycerides and therefore yielding fatty acids and glycerol. However, the chylomicrons and VLDL (very low density lipoprotein transport molecules) need to be metabolized as well.

What enzyme metabolizes chylomicrons and VLDL?

A

Lipoprotein lipase is necessary for metabolism of chylomicrons and VLDL.

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12
Q

Mobilization of triacylglycerols and metabolism by the liver

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13
Q

MCAT concept check lipid mobilization 11.2 page 417 question 1

A patient who has diabetes begins insulin injections for management of blood glucose levels. What is the expected impact on the patient’s weight?

A

An increase in insulin levels will increase lipid storage and decrease lipid mobilization from adipocytes.

This will lead to weight gain in patients who have diabetes and begin insulin injections.

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14
Q

MCAT concept check lipid mobilization 11.2 page 417 question 2

What is the ratio of free fatty acids to glycerol produced through lipid mobilization?

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The ratio of free fatty acids to glycerol is 3:1.

A triacylglycerol molecule is composed of glycerol and three fatty acids.

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15
Q

What are lipoproteins? Apolipoproteins?

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16
Q

In terms of density and protein content, which are the least to most dense lipoproteins?

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Chylomicrons are the least dense (highest fat to protein ratio)

VLDL (very low density lipoproteins) is slightly more dense.

Intermediate density lipoproteins (IDL)

Low density lipoproteins (LDL)

HDL (high dentistry lipoproteins) lowest fat to protein ratio.

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17
Q

List the 5 lipoproteins in least to most dense.

What determines the density of a lipoprotein?

What are their functions?

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18
Q

What is albumin?

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Albumin is a protein produced by the liver, making up the majority of plasma proteins, and plays a crucial role in maintaining fluid balance, transporting various substances, and supporting overall metabolic function.

One of the substances it transports are lipids. Linked to this study.

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19
Q

What are chylomicrons?

Where are they found?

Where are they assembled?

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20
Q

What are VLDL?

Where are are they produced and assembled?

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21
Q

What are IDL?

Why are they unique?

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22
Q

What do chylomicrons and VLDL primarily carry?

What do LDL and HDL primarily carry?

What does IDL primarily carry?

A

Chylomicrons and VLDL primarily carry triacylglycerols.

LDL and HDL primarily carry cholesterol.

IDL is intermediate, it is a transition state between VLDL and LDL, and changes between transporting triacylglycerol and cholesterol.

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23
Q

What is LDL?

What do they primarily carry?

What is the role of LDL?

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24
Q

What are HDL?

Where is it synthesized?

Do they have a lot of apolipoproteins?

Why is HDL considered “good cholesterol”?

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What are apolipoproteins?
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MCAT concept check lipid transport 11.3 page 421 question 1 What is the primary method of transporting fatty acids in the blood?
Free fatty acids remain in the blood, bonded to albumin and other carrier proteins. A much smaller amount will be unbonded.
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MCAT concept check lipid transport 11.3 page 421 question 2 Order the Lipo proteins from greatest percentage of protein to least percentage of protein. Circle the molecules that are primarily involved in triacylglycerol transport.
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MCAT concept check lipid transport 11.3 page 421 question 3 Lipoproteins are synthesized primarily by which two organs?
Lipoproteins are synthesized primarily by the intestine and liver.
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MCAT concept check lipid transport 11.3 page 421 question 4 When physicians order a lipid panel to evaluate a patient, which value do they prefer to see over a minimum threshold value than below a maximum?
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What is cholesterol?
Cholesterol is a ubiquitous component of all cells in the human body and plays a major role in the synthesis of cell membranes, steroid hormones, bile acids, and vitamin D.
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What are the sources of cholesterol?
Most cells derive their cholesterol from LDL and HDL. Cholesterol can be synthesized in the liver and is driven by acetyl CoA and ATP.
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What specific enzymes are involved in the transport of cholesterol?
Lecithin cholesterol-acyltransferase (LCAT) Cholesterol ester transfer protein (CETP) The citrate-malate shuttle is a biochemical pathway that transports acetyl-CoA from the mitochondrial matrix to the cytosol for fatty acid synthesis, using citrate and malate as intermediates.
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MCAT concept check cholesterol metabolism 11.4 page 422 question 1
HMG-CoA reductase (HMGCR) CHOLESTEROL BIOSYNTHESIS is a key enzyme in the mevalonate pathway, catalyzing the conversion of HMG-CoA to mevalonic acid, a crucial step in cholesterol and other isoprenoid biosynthesis, and is the target of statin drugs used to lower cholesterol.
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MCAT concept check cholesterol metabolism 11.4 page 422 question 2
Cholesteryl esters (CEs) are a type of dietary lipid that transport cholesterol through blood and store it in cells. They are formed by linking long-chain fatty acids to cholesterol's hydroxyl group. CEs play a key role in cholesterol homeostasis and metabolic pathways.
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What are fatty acids? Which is carbon 1 and which is carbon 2? What do fatty acids found in the body occur as?
Fatty acids are long chain carboxylic acids. The carboxyl carbon is carbon one. Carbon two is referred to as the alpha carbon. Fatty acids found in the body occur as salts that are capable of forming micelles or are esterified two other compounds such as membrane lipids.
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What are two important essential fatty acids?
Alpha linolenic acid and linoleic acid. They are important for maintaining cell membrane fluidity, which is critical for proper functioning of the cell. Humans can synthesize only a few of the unsaturated fatty acid; the rest come from essential fatty acids found in the diet that are transported in chylomicrons as triacylglycerols from the intestine.
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What is the nomenclature and numbering system for fatty acids?
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Are trans double bonds found in natural fatty acids? What quality do they posses that make them contribute to arterial disease?
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How are fatty acids used by the body for fuel typically supplied?
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What is nontemplate synthesis?
Nontemplate synthesis is a term for lipid and carbohydrate synthesis. Carbohydrate and protein acquired from the diet can be converted to fatty acids and stored as energy reserves in the form of triglycerides. Lipid and carbohydrate synthesis are often called nontemplate synthesis process because they do not rely directly on the coding of a nuclear acid, unlike protein and nucleic acid synthesis.
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Where does fatty acid biosynthesis occur? Where are the products of fatty acid biosynthesis transported? What are the major enzymes of fatty acid synthesis? What are they stimulated by?
Fatty acid biosynthesis primarily occurs in the liver and its products are subsequently transported to adipose tissue for storage. Adipose tissue can also synthesize smaller quantities of fatty acids. Acetyl CoA carboxylase and Fatty acid synthase are enzymes involved in fatty acid biosynthesis. They are stimulated by insulin.
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What is the primary end product of fatty acid biosynthesis?
Palmitic acid (palmitate) is the primary in product of fatty acid biosynthesis.
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Following a large meal, acetyl CoA accumulates in the mitochondrial matrix it needs to be moved to the cytosol for fatty acid biosynthesis. What is acetyl CoA a product of? What does it couple with to form at the beginning of the citric acid cycle? What is the rate limiting step of the citric acid cycle? What does that important?
Acetyl CoA is the product of pyruvate dehydrogenase complex. Acetyl CoA couples with oxaloacetate to form citrate at the beginning of the citric acid cycle. Isocitrate dehydrogenase is the rate limiting enzyme of citric acid cycle. The cell slows the citric acid cycle when the cell becomes energetically satisfied, which causes citrate accumulation. Citrate can then diffuse across the mitochondrial membrane and be split back into acetyl CoA and oxaloacetate by citrate lyase. The OAA can return to the mitochondria to continue moving acetyl CoA.
44
What is acetyl CoA carboxylase? What does it require to function?
Acetyl CoA is activated in the cytoplasm for incorporation into fatty acids by acetyl CoA carboxylase. Acetyl CoA carboxylase needs biotin and ATP to function. It adds CO2 to acetyl CoA, making malonyl-CoA.
45
What enzyme is responsible for fatty acid biosynthesis? What is the only fatty acid that humans can biosynthesize de novo? Where is it found?
Fatty acid synthase, also called PALMITATE SYNTHASE because palmitate is the only fatty acid that humans can synthesize de novo. Rapidly induced in the liver following a meal high in carbohydrates because of elevated insulin levels.
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What is the opposite of fatty acid synthesis?
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What is beta oxidation?
Most fatty acid catabolism proceeds via beta oxidation that occur occurs in the mitochondria.
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How are triglycerides synthesized?
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How are fatty acids activated for metabolism?
Fatty acids become activated by attachment to CoA, which is catalyzed by fatty-acyl-CoA-synthetase. The product is called fatty acyl-CoA or acyl-CoA.
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How do fatty acids enter the mitochondria? What happens when they get there?
Short chain fatty acids (2-4 C) and medium chain fatty acids (6-12 C) diffuse freely into the mitochondria where they are oxidized. Long chain fatty acids (14-20 C) are also oxidized in the mitochondria, but they require transport via a carnitine shuttle.
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What is the rate limiting enzyme of fatty acid oxidation in the mitochondria.
Carnitine acyltransferase I is the rate limiting enzyme of fatty acid oxidation. Very long chain fatty acids (over 20C) are oxidized elsewhere in the cell.
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Draw acetyl CoA
It has an acetyl group on coenzyme A.
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What are the four steps involved in beta oxidation in the mitochondria?
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Describe beta oxidation in the mitochondria. What does each four step cycle produce?
Each four step cycle produces one molecule of acetyl CoA and reduces NAD+ and FAD, producing NADH and FADH2, which are oxidized in the ETC, eventually producing ATP. In muscle and adipose tissue, acetyl CoA enters the citric acid cycle. In the liver, acetyl CoA, WHICH CANNOT BE CONVERTED TO GLUCOSE, stimulates gluconeogenesis by activating pyruvate carboxylase.
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Fatty acid, activation and transport, and beta oxidation in mitochondria image from textbook
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What is the propionic acid pathway?
Fatty acids with an odd number of carbons undergo beta oxidation in the same manner as even numbered carbon fatty acids for the most part. The only difference is observed during the final cycle, where even numbered fatty acids for the most part yield to acetyl CoA molecules (from the four carbon remaining fragment) and odd numbered fatty acids yield one acetyl CoA and one propionyl CoA (from the five carbon remaining fragment). Propionyl CoA carboxylase and methylmalonyl CoA mutase convert propionyl CoA to Succinyl CoA. Succinyl CoA is a citric acid cycle intermediate (step 5: succinate formation via succinyl CoA synthetase and succinyl CoA). Succinate may be oxidized to malate, which can enter the gluconeogenesic pathway. ODD CARBON FATTY ACIDS THUS REPRESENT AN EXCEPTION TO THE RULE THAT FATTY ACIDS CANNOT BE CONVERTED TO GLUCOSE IN HUMANS.
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Can fatty acids be converted to glucose in humans?
Fatty acids cannot be converted to glucose in humans EXCEPT FOR ODD CARBON FATTY ACIDS, which undergo the propionic acid pathway, which makes a citric acid intermediate (Succinyl CoA), which can be converted to mate to enter the glucogenic pathway in the cortisol.
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What does enoyl-CoA isomerase do (unsaturated fatty acids)?
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What is 2,4 dienyl CoA (unsaturated polyunsaturated fatty acid)?
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Eonyl CoA isomerase and 2,4 dienoyl CoA reductase
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How does acetyl CoA make it back into the mitochondria when the cell is energetically satisfied?
Acetyl CoA is product of pyruvate dehydrogenase complex. Couples with oxaloacetate to form citrate. Recall isocitrate dehydrogenase is rate limiting of citric acid cycle. As cell becomes energetically satisfied, citric acid slows, causing citrate accumulation. Citrate can diffuse across mitochondrial matrix. In cytosol, citrate lyase splits citrate back into oxaloacetate and acetyl coA. Oxaloacetate returns to mitochondria, acetyl CoA does the biosynthesis.
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MCAT concept check 11.5 fatty acids and triacylglycerols page 434 question 1
This is about understanding the nomenclature for fatty acids. (# of carbons, # of double bonds) Omega numbering system used for unsaturated fatty acids. Count from the end carbon (omega 1) and backward to the double bonds. (Example: omega 6 fatty acid will have a double bond at the 6th carbon from the end)
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MCAT concept check 11.5 fatty acids and triacylglycerols page 434 question 2 Five steps in addition of acetyl CoA to growing fatty acid chain? Draw this a couple times.
Attachment to acyl protein carrier Bond formation between molecules Reduction of carbonyl group Dehydration Reduction of double bonds
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MCAT concept check 11.5 fatty acids and triacylglycerols page 434 question 3 How does beta oxidation of unsaturated fatty acids differ from that of saturated fatty acids?
There is an additional isomerase and an additional reductase for the beta oxidation of unsaturated fatty acids, which provide the stereochemistry necessary for further oxidation.
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MCAT concept check 11.5 fatty acids and triacylglycerols page 434 question 4 True or false: fatty acids are synthesized inside the cytoplasm and modified by enzymes in the smooth endoplasmic reticulum.
True.
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How should we think about and understand ketone bodies?
Ketone bodies are essentially transportable forms of acetyl CoA. Produced by the liver and used by other tissues during prolonged starvation.
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In a fasting state, the liver converts excess acetyl CoA from beta oxidation of fatty acids. How by which do this does?
The liver conveys excess acetyl CoA from beta oxidation into KETONE BODIES: Acetoacetate 3-hydroxybutyrate (beta hydroxybutyrate) These can used for energy. Cardiac and skeletal muscle as well as the renal cortex can metabolize 3-hydroxybutyrate and acetoacetate into acetyl CoA, preventing accumulation of acetyl CoA into the bloodstream. After about a week, acetyl CoA concentration reaches a level high enough where the brain can metabolize acetoacetate and 3-hydroxybutyrate.
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Draw acetyl CoA, and the ketones it forms: 3-hydroxybutyrate and acetoacetate.
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Image showing ketogenesis and ketolysis
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What is ketogenesis? Where does it occur? When does it occur?
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What is ketolysis? Where does it occur?
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What is ketoacidosis?
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Describe ketolysis in the brain. When does it happen?
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MCAT concept check ketone bodies 11.6 page 436 question 1 Why are fatty acids used to create ketone bodies instead of creating glucose?
Fatty acid degradation results in large amounts of acetyl CoA, which cannot enter the glucogenic pathway to produce glucose. Only odd number fatty acids can act as a source of carbon for gluconeogenesis. Even then, only the final malonyl CoA molecule can be used for gluconeogenesis. Energy is packed into ketone bodies for consumption by the brain and muscles.
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MCAT concept check ketone bodies 11.6 page 436 question 2 What conditions and tissues favor ketogenesis? Ketolysis?
Ketogenesis is favored by a prolonged fast and occurs in the liver. Ketogenesis is stimulated by increasing concentrations of acetyl CoA. Ketolysis is also favored during a prolonged fast, but is stimulated by a low energy state in muscle and brain tissues and does not occur in the liver. Liver does not contain succinyl CoA acetoacetyl CoA tranferase so that it cannot catabolized the ketone bodies that it produces.
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When does protein catabolism occur?
Protein is very rarely used as an energy source because it is so important for other functions. Routine routinely breaking down protein would result in serious ill illness. However, under conditions of extreme energy deprivation, proteins can be used for energy. In order to provide a reservoir of amino acids for protein building by the cell, proteins must be digested and absorbed.
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What is proteolysis? Where does it occur and how?
Proteolysis is the breakdown of protein. Pepsin in the stomach, continues with pancreatic proteases trypsin, chymotrypsin, carboxypeptidase an and b. All of which are released as zymogens. Protein digestion is completed by the small intestinal brush border enzymes: dipeptidase and aminopeptidase.
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Absorption of AA and peptides in the intestine is accomplished by what?
Secondary active transport linked to sodium, simple and facilitated diffusion transports.
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What must AA undergo before they are able to be used for energy? What does this cause? What are glucogenic and ketogenic AA?
Transanimation or deamination must occur first. This can be a potential toxin in the body in the form of ammonia and must be excrete safely.
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MCAT concept check protein catabolism 11.7 page 439 question 1 True or false: bodily proteins will commonly be broken down to provide acetyl CoA for lipid synthesis.
False. Proteins are more valuable to the cell than lipids, thus they will not commonly be broken down for lipid synthesis.
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MCAT concept check protein catabolism 11.7 page 439 question 2 Where does the bulk of protein digestion occur?
The bulk of protein digestion occurs in the small intestine.
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MCAT concept check protein catabolism 11.7 page 439 question 3 During protein processing, what is the eventual fate of each of the following components: carbon skeleton, amino group, and side chains?
The carbon skeleton is transported to the liver for processing into glucose or ketone bodies. The amino group of feed into the urea cycle for excretion. Side chains are processed, depending on their composition. Basic side chains will be processed like amino groups, while other functional groups will be treated like carbon skeletons.
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 1
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 2
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 3
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 4
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 5
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 6
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 7
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 8
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 9
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 10
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 11
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 12
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 14
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MCAT mastery chapter 11 lipid and amino acid metabolism page 410 question 15