Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Module Exam > GI Metabolism > Flashcards

GI Metabolism Flashcards

1
Q

What are the substrates of gluconeogenesis? What is the end product?

A

Lactate, alanine and glycerol are the substrates. Glucose is the end product.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the main substrate of glycogen synthesis? What is its end product?

A

G-1-P is substrate. And glycogen is the end product, duh.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main substrates for lipogenesis? What is the end product?

A

Acetyl CoA and glycerol are substrates. End products are FA’s and TGs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Main substrates of glycolysis? End products?

A

Main substrate: glucose. End products: pyruvate, ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Main substrates of TCA cycle? End products?

A

NADPH, FADH2, CO2, ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Main substrate of pentose phosphate pathway? End products?

A

G-6-P is substrate. End products are NADPH, pentose and Co2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why can’t muscle share its glycogen stores with other tissues?

A

It lacks Glucose-6-phosphatase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which tissues can store creatine?

A

Muscle and the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What role does the kidney play in metabolism?

A

It receives AA’s from skeletal muscle; it converts them into glucose, which it can send to the brain. The released ammonium ion as well as urea from the liver is then exerted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which tissues are capable of TG consumption? What enzyme is necessary for this uptake?

A

The only tissues that can receive TG’s are skeletal muscle, adipose tissue and the heart. LpL is required to break TGs into FA’s for tissue consumption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the skeletal muscle and heart do with FAs? What does adipose tissue do with FAs?

A

It breaks them down to acetyl CoA and extracts ATP. CO2 and H2O are released. Adipose tissue turns the FA’s back into TG’s for storage with the help of glycerol-3P (which is made from glucose).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Amino acids and glucose stimulate what hormone? Hint: epinephrine inhibits the hormone.

A

Insulin. Insulin is made from Prepro-insulin in the pancreas’s B-cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

True or False: Insulin has no effect on glucose transport in the brain or in RBCs.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Insulin affects lipid metabolism by (increasing/decreasing) hormone-sensitive lipase adipose tissue.

A

Decreases. We want to decrease breaking apart lipids!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Insulin (increases/decreases) lipoprotein lipase in the arteries.

A

Increase! We want to start breaking down these TGs for storage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Insulin (increases/decreases) FA synthesis in adipose and liver tissues.

A

Increases! We just ate all the materials we need to make FAs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In what tissues does insulin increase glucose uptake? How does it do this?

A

Muscle and adipose. Increase GLUT4 to membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Glucagon acts on just one tissue. What is it?

A

The liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What increases glucagon synthesis and release? What inhibits it?

A

Amino acids and epinephrine stimulate glucagon. Glucose inhibits it obviously.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Glucagon (increases/decreases) ketone body formation in the liver. What are these ketone bodies made from?

A

Increases because we are need of energy. Made from lipids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

True or False: SKM has glucagon receptors.

A

False! Skeletal muscle lacks glucagon receptors. It must always get the energy it needs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Epinephrine is antagonistic to insulin because it (increases/decreases) glycogen breakdown, gluconeogenesis, lipolysis and FA ox.

A

Increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which enzyme is responsible for relaying glucagon’s message?

A

PKA. Which turns on with help from adenyl cyclase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What signaling molecules are responsible for relaying effects of catecholamines?

A

cAMP/ Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the main difference between epinephrine and glucocorticoids?

A

Glucocorticoids are important in long-term management; epinephrine is effective within seconds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

A class of ligand-activated transcription factors that use nuclear hormone receptors. These transcription factors also control lipid metabolism and regulate gene expression.

A

Peroxisome Proliferator-Activated Receptor (PPAR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some insulin-inducible enzymes of the liver? What is an insulin-inhibited enzyme?

A

Carbohydrates: Gluckokinase and PFK-1/2 are upregulated because glycolysis and glycogen synthase are upregulated. HMP is also upregulated.

Lipids: Pyruvate dehydrogenase, citrate lyase, magic enzyme, G6P dehydrogenase. Acetyl CoA carboxylase. FA synthase complete.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What enzyme necessary for lipid metabolism is induced by insulin? What enzyme necessary for lipid metabolism is inhibited by insulin?

A

Lipoprotein lipase. It is induced in adipose tissue.

Hormone-sensitive lipase on the other hand is inhibited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

During exercise, most glucose is converted into _______ and shunted to the liber for the Cori Cycle.

Bonus: What is the Cori Cycle?

A

Lactate!

Cori Cycle is the process by which lactate from glycolysis moves from the muscles to the liver to be converted into glucose. The glucose then goes back to the muscles where it becomes lactate once again.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Two truths and a lie:

1) Brain contains no significant glycogen stores.
2) Brain contains significant stores of TGs.
3) FFAs cannot cross the blood-brain barrier.

A

Brain does NOT contain significant stores of TGs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

The liver uses carbon skeletons to break glycogen down into glucose. What are the three main sources of these skeletons?

A

Amino acids, lactate and glycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name some gluconeogenesis- related enzymes that are upregulated when glucagon is high.

A

PEP, F16BP and G6P.

F16BP is increased because F26BP is low.

33
Q

Name some lipid- related enzymes that are upregulated when glucagon is high.

A

Using PKA, lipase are activated to breakdown TGs into FAs to make glycerol. Synthesis of ketone bodies starts to happen as well: mitochondrial HMG-CoA lyase.

34
Q

In adipose tissue, decreased insulin and increased catecholamines (especially norepinephrine) lead to activation of what two lipases?

A

Adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL).

35
Q

Where does the released FAs and glycerol go after TGs are broken down?

A

FAs bind albumin and are transported to other tissues. Glycerol goes to the liver to be used for gluconeogenesis.

36
Q

Two most important amino acids for gluconeogenesis?

A

Alanine and glutamine.

37
Q

During the first 24 hours of starvation, your skeletal muscle relies upon _______. During the first two day of starvation, your skeletal muscle uses _______ from adipose tissue. and ________ from liver as fuel.

A

First 24 hours: glycogen
First 48 hours: FAs from adipose tissue and ketone bodies from liver
First several days: Rapid breakdown of muscle protein.

38
Q

What is the benefit of using ketone bodies when starving?

A

Once gluconeogenesis can no longer take place, brain uses ketone bodies. Ketone bodies do not require a carbon skeleton like gluconeogenesis does. Thus, ketone bodies decrease protein catabolism.

39
Q

Sprinters use ______ while endurance athletes rely on complete oxidation of glucose into C02. Why does this explain fatigue of sprinters?

A

Glycolysis is used by sprinters. Glycolysis quickly leads to lactate accumulation, which reduces PFK activity. When PFK activity is reduced, glycolysis cannot be maintained.

Endurance runners use oxidative phosphorylation which is 100x slower than glycolysis.

40
Q

Endurance runs have increased glycogen stores compared to sprinters. Why is it important that endurance runners consume equal parts FAs and glycogen during a run?

A

FAs will ensure that runner can keep running even after “hitting the wall” (when muscle and liver glycogen are used up).

41
Q

Under what circumstances can a person store the most amount of glycogen?

A

Perform intense glycogen-depleting exercise before carb loading. This will stimulate expression of glycogen synthesizing enzymes.

42
Q

Which enzyme controls whole body homeostasis during prolonged physical activity?

A

AMPK. This enzyme inactivates acetyl coA carboxylase which reduces synthesis of malonyl co A. Because of AMPK, carnitine palmitoyltransferase- I (CPT-1) stimulates great FA ox in the mitochondria so muscles can make glucose.

43
Q

Which enzyme does metformin use?

A

AMPK.

44
Q

Ketone bodies are made for the brain using which enzyme?

A

HMG- CoA lyase

45
Q

Cholesterol is produced in the liver cytosol using which enzyme?

A

HMG-CoA reductase

46
Q

What does the drug disulfiram do? Hint: It is also called antabuse.

A

This drug blocks acetaldehyde dehydrogenase, stopping acetaldehyde from turning into acetate. Acetaldehyde is associated with negative effects, so by keeping it in the body longer, it should act as a deterrent by drinking.

47
Q

What does the drug fomepizole do? Hint: It is also called Antizole.

A

This drug blocks alcohol dehydrogenase. This stops ethanol from turning into acetaldehyde. It is also used for ethylene glycol (antifreeze poisoning) and methanol ingestion.

48
Q

Why does alcohol cause a buildup of TGs?

A

Because ADH and ALDH deplete NAD+ which is also needed in FA oxidation –> decreased catabolism shifts process towards FA biosynthesis.

Alcohol also impairs secretion and assembly of lipoproteins so fat cannot be exported.

49
Q

Macrovesicular steatosis indicates what process in the liver? Which zone does this start in?

A

Steatosis= accumulation of lipid droplets in hepatocytes. As this process occurs, larger lipid droplets distend the nucleus and push it aside. Zone 3.

50
Q

Cytochrome P450 (CYP2E1) is important for alcohol metabolism. What is one way alcohol can injure hepatocytes?

A

Cytochrome produces reactive oxygen species.

51
Q

What are fatty acid ethyl esters (FAEEs)?

A

FAs that directly interact with alcohol and can damage liver.

52
Q

In what zone of the hepatocyte does most glycogen and plasma protein synthesis take place?

A

Zone 1. It is the first to receive O2, hormones and nutrients from blood stream. Most susceptible to viral infection.

53
Q

An acetaminophen overdose would lead to death of what zone in the hepatocyte?

A

Zone 3. It is the last to receive blood and is subject to ischemia. Also the site of drug detox.

54
Q

Heme oxygenate is responsible for conversion of _______ into ______ and Fe2+.

A

Heme; biliverdin.

55
Q

What is biliverdin reductase?

A

Enzyme that takes biliverdin and NADPH and turns it into bilirubin (the important bile pigment).

56
Q

Bilirubin attached to albumin in the free (unconjugated form). What is the goal of conjugation and how does it become conjugated?

A

Goal of conjugation is to make bilirubin water soluble (it is normally not detected in healthy people). It is conjugated in the liver by UDP glucuronyl transferase.

57
Q

Conjugated bilirubin is also called urobilinogen. When released into the kidney oxidation happens, turning urobilinogen into?

A

Urobilin. Similarly, when urobilinogen is released into intestines it is converted into stercobilinogen and then stercobilin.

58
Q

In pathophysiological conditions, conjugated bilirubin is excreted in the kidney. What is a symptom of this?

A

Dark urine.

59
Q

Hemolytic jaundice results in accumulation of what form of bilirubin?

A

Bilirubin-albumin (unconjugated or free)

60
Q

Neonatal jaundice also results in bilirubin-albumin overload. What enzyme is responsible for the delay in converting the free bilirubin to conjugated?

A

UDP glucuronyl transferase

61
Q

How does one treat neonatal jaundice?

A

Phototherapy

62
Q

Obstructive jaundice is due to what? What is a symptom of this?

A

Gallstones obstructing conjugated bilirubin’s path to the intestines. The conjugated bilirubin then backs up in liver and is excreted into urine (dark urine).

63
Q

Primary bile acids are synthesized from what two acids? Hint: These two acids are derived from cholesterol.

A

Cholic acid and chenodeoxycholic acid.

64
Q

What synthesizes secondary bile acids?

A

Bacteria in the lumen of the intestine.

65
Q

After secondary bile acids return to the liver via ___________ circulation, what do they form?

A

Enterohepatic circulation.

Form conjugated bile acids, called bile salts!

66
Q

Through what mechanism is bile in the gallbladder concentrated?

A

Absorption of water and small electrolytes.

67
Q

Which zone does fibrosis begin in?

A

Zone 3 around central veins

68
Q

There are two phases of drug metabolism. Phase I is mediated by cytochrome p450 enzymes. What is their purpose?

A

To convert fat soluble pro-drugs/drugs into water soluble compounds (a.k.a polar metabolites).

69
Q

TRUE or FALSE: Phase I drug metabolism can lead to either activation or inactivation.

A

TRUE. A non-toxic drug can be converted into a toxic derivative.

70
Q

TRUE or FALSE: Phase II of drug metabolism makes the metabolites even more soluble. Why is this more soluble?

A

TRUE. More soluble means the drug is less toxic. It also makes the drug easier to urinate.

71
Q

Cytochromes require ______ as a cofactor.

A

Heme. When CO binds to Fe2+ in the heme group, CYPs show absorption maximum.

72
Q

CYPs are found in different location. Where is NADPH-CYP450 reductase found? What is NADPH-adrenodoxin reductase?

A

Smooth ER (think about how NADPH-CYP450 is an acronym as is ER).

Mitochondria (ends in an A and NADPH-adrenodoxin reductase starts with A..

73
Q

CYPs add one oxygen molecule so they are known as…

A

monooxygenases!

74
Q

Mechanisms for getting rid of epoxide?

A

Epoxide hydrolase-mediated hydrolysis of epoxides. Conjugation of epoxide to Glutathione by Glutathione- S-transferase (GST).

75
Q

How does Tylenol (APAP) metabolism work? Why can it skip Phase I?

A

APAP can skip Phase I because it is already hydroxylated. During Phase II, 90% of APAP is conjugated and excreted as non-toxic.

76
Q

What happens to the other 5-10% of Tylenol (APAP) that is not excreted after Phase II transformation?

A

APAP is converted into NAPQI which is a hepatoxin. To get rid of NAPQI, the GST enzymes convert it to a non-toxic glutathione conjugate. This can be then excreted/

77
Q

What is a prodrug?

A

A drug that is active until metabolized by CYP. After Phase I, the active drug is no longer active.

78
Q

Why is it dangerous for a chronic alcoholic to take APAP after a night of heavy drinking for a hangover?

A

Alcohol induces CYP2E1 in the liver, which means metabolism of APAP into NAPQI (hepatoxin) increases. This causes a decrease in the glutathione reserves —> leads to vomiting, nausea, liver tenderness, jaundice, death, etc.

79
Q

CYP450 may be induced by what metabolites? Inhibited by what metabolites?

A

Inducer: Chronic alcohol abuse, St. Johns Wort, Phenytoin, Phenobarbital, Nevirapine, Rifampin, Griseofulvin, Carbamazapine

“Chronic alcoholics steal phen-phen and never refuse greasy carbs.”

Inhibitor: Sodium valproate, isoniazid, cimetidine, ketoconazole, fluconazole, acute alcohol abuse, chloramphenicol, erythromycin, sulfonamides, ciprofloxacin, omeprazole, metranidazole

“SICKFACES.COM”

GI Module Exam (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions