Metabolism (Exam 1) Flashcards

Carb absorption, metabolism, hormonal regulation, Glycogen production, sugar and alcohol

1
Q

Insulin binds to what type of receptors?

A

Tyrosine kinase

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2
Q

Intertissue integration is required for metabolic homeostasis. How is metabolic homeostasis achieved?

A
  1. The concentration of nutrients in the blood affect the rate at which they are stored and utilized
  2. Hormones carry messages to tissues
  3. CNS sends neuronal signals to control tissue metabolism
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3
Q

What is the goal of glucagon?

A

Glucagon is the major fuel mobilization hormone.

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4
Q

What is the goal of insulin?

A

Insulin is the major anabolic hormone for the body.

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5
Q

What happens to insulin levels when you eat a meal? What does insulin do to cell processes after you eat a meal?

A

Insulin levels rise and glucose enters cells. Fuel stores and growth in cells are increased.

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6
Q

What happens to glucagon a few hours after eating a meal?

A

Glucagon levels rise. The goal is to maintain fuel levels in the blood. Stored fueled is now utilized to produce ATP.

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7
Q

Where is insulin secreted from?

A

Insulin is secreted from the beta-cells of the islets within the pancreas.

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8
Q

Where is glucagon secreted from?

A

Glucagon is secreted from the alpha-cells of the islets in the pancreas.

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9
Q

Islets of the pancreas are very close to the vasculature. Why is this important?

A

Islets being close to the vasculature allows the cells to monitor the blood glucose levels and secrete insulin or glucagon accordingly.

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10
Q

What are the main functions of insulin?

A
  1. Promotes fuel storage after a meal
  2. Promotes growth
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11
Q

What are the 3 major metabolic pathways affected by insulin secretion?

A
  1. Stimulates glucose storage as glycogen in liver and muscle
  2. Stimulates fatty acid synthesis and storage in adipose tissue
  3. Stimulates amino acid uptake and protein synthesis
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12
Q

What are the main functions of glucagon?

A
  1. Mobilizes fuels
  2. Maintain blood glucose levels during fasting
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13
Q

What are the 2 major metabolic pathways affected by glucagon secretion?

A
  1. Activates gluconeogenesis and glycogenolysis in the liver during fasting
  2. Activates fatty acid release from adipose tissue
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14
Q

What is another hormone discussed that mobilizes fuels during acute stress?

A

Epinephrine

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15
Q

What are the two counterregulatory hormones of insulin?

A

Epinephrine and cortisol. As hypoglycemia is a stress signal, it stimulates the release of EPI and cortisol from the hypothalamic regulatory center (central HPA axis).

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16
Q

Where are the 3 locations where insulin acts?

A

Liver
Skeletal Muscle
Adipose tissue

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17
Q

What are the 2 locations where glucagon acts?

A

Liver
Adipose tissue
(NOT MUSCLE)

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18
Q

What is the process of the hormone insulin being made?

A
  1. Synthesized as a pre-hormone in the nucleus
  2. Moves to ER and is converted to preproinsulin
  3. Moves to golgi and the C peptide is cleaved
  4. Leaves golgi as active insulin and stored in vesicles with zinc.
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19
Q

What is the characteristics of the bonds within biologically active insulin?

A

The A and B chains are linked together by two interchain disulfide bonds.

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20
Q

What is the initiating step for insulin release from beta-cells?

A

Glucose levels have increased and enter the beta cells through GLUT2 where insulin is made and stored. This activates the release of insulin to the rest of the body.

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21
Q

What is the step-by-step breakdown of insulin release from beta-cells in the pancreas?

A
  1. Beta-cells detect glucose in the blood
  2. Glucose is taken up via GLUT2 transporters in beta cells
  3. Beta cells increase glycolysis, TCA cycle, oxidative phosphorylation, and then ATP
  4. Rise in ATP levels inhibits ATP-dependent K+ channels. This depolarizes the membrane
  5. Depolarization activates voltage-gated Ca2+ channels
  6. Increased intracellular calcium leads to vesicle fusion with membrane releasing insulin into the blood
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22
Q

Why would epinephrine reduce insulin secretion?

A

Epinephrine is the fight-or-flight hormone while insulin is the storage hormone. With EPI release, you want release and utilization of energy and not storage.

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23
Q

Explain the steps of insulin receptor cell signalling in terms of the tyrosine kinase receptor and GLUT4.

A
  1. Insulin binds to alpha subunits of tyrosine kinase receptors
  2. Insulin receptors dimerize
  3. Beta subunits of the tyrosine kinase receptor extend through the membrane and autophosphorylate each other
  4. Downstream signalling activates P13K which activates AKT
  5. This leads to the translocation of GLUT4 into the plasma membrane
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24
Q

What is the tissue response to insulin binding?

A
  1. Stimulates glucose and amino acid uptake into the cells
  2. Reverses glucagon-stimulated phosphorylation
  3. Initiates phosphorylation of enzymes
  4. Induces and suppresses enzyme synthesis
  5. Acts as a growth factor
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25
Q

What is the process of the hormone glucagon being made?

A
  1. Glucagon is synthesized in the alpha-cells of the pancreas. Initially produced in the rough ER
  2. Converted to proglucagon in the ER lumen
  3. Cleavage at certain sites produces the biologically active glucagon
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26
Q

What is the half-life of glucagon?

A

The half life is glucagon is 3-5 minutes as rapid regulation is needed.

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27
Q

What macronutrients stimulates the release of glucagon?

A

Amino acids

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28
Q

Does epinephrine increase or decrease glucagon secretion?

A

Epinephrine increases glucagon secretion in order to mobilize fuel stores.

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29
Q

Similar to another question asked, what are the 4 exact names of the metabolic pathways that insulin activates?

A

Glycogen synthesis
Fatty acid synthesis
Triglyceride synthesis
Liver glycolysis

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30
Q

Similar to another question asked, what are the exact names of the metabolic pathways that glucagon activates?

A

Glycogenolysis
Gluconeogenesis
Lipolysis
DECREASES LIVER GLYCOLYSIS

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31
Q

What happens when glucagon binds to its receptor, GPCR, in terms of cellular molecules?

A
  1. Glucagon binds to GPCR
  2. This activates cAMP signalling
  3. cAMP activates PKA
  4. PKA activates PPK
  5. Through several downstream signalling molecules, glycogen is broken down into glucose-1-phosphate to make glucose (liver)
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32
Q

What are the 5 major principles of molecule signalling regarding hormones?

A
  1. Specificity- action given by receptor expression
  2. Amplification- signalling cascade
  3. Termination- rapid stopping
  4. Integration- of cellular response
  5. Augmentation/ Antagonism of signal
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33
Q

Epinephrine is a potent stimulator of the _____________ receptors.

A

Adrenergic (alpha and beta)

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34
Q

What type of adrenergic receptor in present in the liver and skeletal muscle?

A

Beta2 Adrenergic receptors

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35
Q

When epinephrine binds to B2 on the liver and muscle, what does it do?

A

Epinephrine binding to beta2 on liver and muscle mobilizes the use of glucose as fuel.

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36
Q

How do adrenergic beta receptors signal?

A

Beta adrenergic receptors signal using stimulatory GPCR to activate adenylate cyclase and PKA.

(PKA stimulation leads to the breakdown of glycogen called glycogenolysis)

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37
Q

What is blood glucose for someone is who prediabetic?

A

Fasting glucose levels between 100 and 125 mg/dL

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38
Q

What are the two forms of plant starches in the diet?

A

Amylose and Amylopectin

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39
Q

What is the bond type that holds amylose together?

A

Glucose residues linked by alpha-1,4-glycosidic bonds

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40
Q

What is the bind type that holds amylopectin together?

A

Branched glucose residues are linked by alpha-1,4-glycosidic bonds connected by alpha-1,6-glycosidic bonds

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41
Q

What bond type holds together the disaccharide, lactose (galactose and glucose)?

A

beta-1,4-glycosidic bonds

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42
Q

What bond type holds together the disaccharide, sucrose (glucose and fructose)?

A

alpha-1,2-glycosidic bonds

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43
Q

What is the group name for the enzymes that hydrolyze glycosidic bonds?

A

Glycosidases

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44
Q

What is the first glycosidase encountered during digestion?

A

salivary alpha-amylase

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45
Q

What is pancreatic alpha-amylase?

A

This is the second glycosidase encountered. It is released from the pancreas along with bicarbonate into the stomach. It hydrolyzes alpha-1,4 bonds into random length polysaccharides.

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46
Q

Does pancreatic alpha-amylase have any action on alpha-1,6-glycosidic bonds?

A

No! It only has action on the alpha-1,4-glycosidic bonds.

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47
Q

What are the two enzymes in the small intestine that continue to break down carbohydrates?

A

Small intestinal disaccharidases and glucoamylase.

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48
Q

What is the function of small intestinal disaccharidases?

A

These cleave disaccharides in the small intestine.

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49
Q

What is the function of glucoamylase in the small intestine?

A

Glucoamylase is an alpha-1,4-exoglycosidase meaning that is cleaves the end of the sugar.

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50
Q

What is the function of the sucrase-isomaltase enzyme?

A

Sucrase-Isomaltase hydrolyzes 100% of the remaining alpha-1,6-glycosidic bonds.

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51
Q

_______________ accounts for 100% of the ability to hydrolyze sucrose.

A

Sucrase-isomaltase

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52
Q

What is the enzyme trehalase?

A

This enzyme hydrolyzes glycosidic bonds found in trehalose which is found in mushrooms, fungi, and insects.

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53
Q

What brush-border enzyme hydrolyzes the bond between glucose and galactose in lactose?

A

Lactase. Lactase is a beta-glycosidase complex. It cleaves the beta-1,4 bond.

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54
Q

What are the two transport mechanisms in which glucose crosses the intestinal epithelial cells?

A
  1. Facilitated diffusion
  2. Na+ Dependent facilitated transport
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55
Q

Explain the process of Na+ dependent transport and the Na+, K+-ATPase in the transport of glucose across the intestinal epithelial cells.

A

The high Na+ gradient in the lumen of the GIT drives glucose and galactose into the epithelial cells. The Na+, K+-ATPase kicks out 3 Na+, and brings in 2 K+ to maintain concentration gradient for the extracellular Na+. The ATPase hydrolyzes ATP to ADP and Pi to do this.

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56
Q

What are the characteristics of facilitated glucose transport?

A

They do not bind Na+. They move glucose from a high to low concentration. Includes GLUT1-5.

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57
Q

Where are GLUT2 transporters located?

A

GLUT2 transporters are located in the liver, kidney, pancreatic B-cells, and serosal surface of intestinal mucosa.

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58
Q

Where are GLUT3 transporters located?

A

Neurons of the brain

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59
Q

Where are GLUT4 transporters located?

A

Adipose tissue, skeletal muscle, and heart muscle.

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60
Q

What type of GLUT transporters transports fructose in the intestinal epithelium?

A

GLUT5

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61
Q

Once glucose has made it way through the intestinal epithelium, what is happening?

A

The glucose is now in the blood and signals insulin release in the pancreas

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62
Q

What type of receptors are insulin receptors?

A

Tyrosine kinase

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63
Q

How is glucose transported into the brain?

A
  1. Glucose passes through GLUT1 transporters in the endothelial cell membrane in the brain (rate-limiting)
  2. Once inside brain, neurons use GLUT3 to transport glucose from CSF to interior of the cell (fast)
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64
Q

Why does the difference in transporter between the PNS and CNS matter?

A

It matters because in the brain, the maximal rate of transport is similar to glucose utilization.

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65
Q

What is the name of the enzyme that is the primary mechanism by which starch is metabolized?

A

Amylase

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66
Q

Glycogen is composed of _____________ linked by glycosidic bonds.

A

Glucosyl units

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67
Q

__________ is the intermediate in glycogen formation.

A

UDP-glucose

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68
Q

Why is glycogen branched?

A

Glycogen is branched so that the body can store as much as possible. The branched structure also allows for rapid formation and degradation

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69
Q

What is the only non-glucosyl unit within glycogen?

A

Glycogenin. It is the initial residue in glycogen formation.

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70
Q

How is glycogen utilized in the skeletal muscle?

A

Glycogen is broken down to G1P which is converted to G6P via phosphoglucomutase. G6P enters glycolysis to provide energy via aerobic and anaerobic processes because it does not contain glucose-6-phosphate like the liver. It can generate ATP and lactate. Lactate is shuttled to the liver.

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71
Q

Glycogenolysis and gluconeogenesis are activated ___________ in the liver due to the hormone _________.

A

Together
Glucagon

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72
Q

Glycogen synthesis and breakdown are very similar. However, the synthesis pathway uses __________ phosphate bond for energy.

A

UTP

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73
Q

What is the regulated enzyme of glycogen synthesis?

A

Glycogen synthase

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74
Q

What molecules donates glycosyl residues to the reducing end of glycogen in glycogen synthesis?

A

UDP-glucose

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75
Q

What enzyme in glycogen synthesis links alpha-1,4-glycosidic bonds?

A

Glycogen synthase

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76
Q

What enzyme in glycogen synthesis creates branches on glycogen by forming alpha-1,6-glycosidic bonds?

A

Branching enzyme

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77
Q

What converts G1P to UDP-glucose in glycogen synthesis?

A

UDP-glucose pyrophosphorylase uses UTP to convert G1P to UDP-Glucose.

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78
Q

What two enzymes convert UDP-Glucose to glycogen through a long process?

A

Glycogen synthase and branching enzyme

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79
Q

What are the two enzymes that degrade glycogen?

A

Glycogen phosphorylase and debrancher enzyme.

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80
Q

What is the function of alpha-1,6-glucosidase enzyme in the breakdown of glycogen?

A

It cleaves the glucose residue linked at the alpha-1,6-bond which is released as one free glucose.

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81
Q

Every branch point on glycogen yields at least ______ glucose and _________ to _______ G1P residues.

A

1
7-9

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82
Q

Explain glucagon binding and downstream molecules it activates to breakdown glycogen?

A

Glucagon binds to GPCR
GTP stimulates adenylate cyclase
Adenylate cyclase converts ATP to Cyclic AMP
Cyclic AMP activates Protein Kinase A
Protein Kinase A activates Phosphorylase Kinase and deactivates glycogen synthase alpha to glycogen synthase beta.
Phosphorylase Kinase activates glycogen phosphorylase B to glycogen phosphorylase A. Phosphorylase A activates glycogen breakdown

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83
Q

What two molecules regulate glycogen breakdown in the muscle?

A

AMP and Ca2+

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84
Q

Why is glycogenolysis much more rapid than gluconeogenesis in the liver when activated?

A

Glycogen is sitting in the liver and can be broken down rapidly while non-carbohydrate precursors need to be recruited for gluconeogenesis.

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85
Q

Are glycogen synthesis and degradation regulated simulataneously?

A

Yes

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86
Q

Does PKA activation make glycogen phosphorylase kinase active or inactive?

A

PKA activation makes glycogen phosphorylase kinase active. Active phosphorylase kinase activates glycogen phosphorylase A therefore increasing glycogen breakdown.

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87
Q

Does PKA activation activate or inhibit glycogen synthase?

A

PKA activation inactivates glycogen synthase. Inactive glycogen synthase has a phosphate group attached to it and prevents glycogen storage.

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88
Q

Does protein phosphatase-1 activate or inactivate glycogen synthase?

A

Protein phosphatase-1 activates glycogen synthase by removing a phosphate group. This makes sense at PP1 is inhibited during fasting so it would be activated during the fed state allowing glucose to be stored as glycogen.

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89
Q

Does protein phosphatase-1 activate or inactivate phosphorylase kinase?

A

PP1 inactivates phosphorylase kinase by removing a phosphate group from it. This makes sense because PP1 is inhibited during fasting allowing phosphorylase kinase to stay active and activate glycogen phosphorylase A inducing glycogen breakdown to glucose.

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90
Q

Muscle lack the enzyme ___________ so it cannot restore blood glucose levels like the liver can.

A

Glucose-6-phosphatase

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91
Q

What two molecules regulate glyconeolysis in the muscle?

A

AMP and Ca2+. These are low energy indicators. AMP is produced from the degradation of ATP during muscle contraction. Ca2+ is released from sarcoplasmic reticulum due to neuronal impulses and it binds to calmodulin which activates phosphorylase kinase which activates glycogen phosphorylase B to A.

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92
Q

AMP is an activator of glycogen phosphorylase in the __________ but not in the liver.

A

muscle

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93
Q

Glycogen is made up of what types of glycosidic bonds?

A

Alpha-1,4 and alpha-1,6

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94
Q

The initial residue required for glycogen formation is ________.

A

Glycogenin

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95
Q

The biochemical breakdown of glycogen is called _________.

A

Glycogenolysis

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96
Q

Two enzymes required for glycogen breakdown are ___________ and ____________.

A

Glycogen phosphorylase and debrancher enzyme

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97
Q

Through what transporter does fructose enter intestinal epithelial cells?

A

GLUT5

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98
Q

What is the first step of fructose metabolism?

A

Fructose is converted to Fructose-1-phosphate via fructokinase. This step uses an ATP.

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99
Q

What is the 2nd step of fructose metabolism?

A

Fructose-1-phosphate is converted to glyceraldehyde via Aldolase B. Dihydroxyacetone-phosphate (DHAP) is cleaved off and enters glycolysis.

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100
Q

What is the 3rd step of fructose metabolism?

A

Glyceraldehyde is converted to glyceraldehyde-3-phosphate via triose kinase. G3P then enters glycolysis.

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101
Q

Where does fructose metabolism occur?

A

Primarily the liver

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102
Q

What is Polyol Pathways?

A

This is the conversion of glucose to fructose.

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103
Q

What are the steps in the polyol pathway?

A

Glucose ——> sorbitol via aldose reductase (step uses an NADPH)
Sorbitol ———> fructose via sorbitol dehydrogenase (produces an NADH)

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104
Q

What is a pathophysiology that occurs due to increased blood glucose levels due to the generation of sorbitol (alcohol sugar)?

A

Ocular glaucoma

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105
Q

What are the steps of galactose metabolism in the liver?

A
  1. Galactose + ATP —–> Galactose-1-phosphate + ADP via Galactokinase
  2. Galactose-1-phosphate + UDP-glucose —-> UDP-galactose + glucose-1-phosphate (G1P enter glycolysis)
  3. UDP-galactose —-> UDP-glucose via UDP-glucose epimerase
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106
Q

Galactose metabolism is _______ when we are younger and ________ when we are older.

A

HIGHER
SLOWER

This is due to galactose being the monosaccharide of lactose which is consumed in diary products like milk.

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107
Q

What is generated in the Pentose Phosphate Pathway?

A

The PPP generate NADPH and ribose-5-phosphate

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108
Q

What are the two phases of the pentose phosphate pathway?

A

Oxidative phase and nonoxidative phase

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109
Q

What is the 1st step of the pentose phosphate pathway?

A

Glucose-6-phosphate ——> 6-phosphogluconolactone via glucose-6-phosphate dehydrogenase

Makes an NaDPH

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110
Q

What is the 2nd step of the pentose phosphate pathway?

A

6-phosphogluconolactone ——> 6-phosphogluconate via gluconolactonase

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111
Q

What is the 3rd step of the pentose phosphate pathway?

A

6-phosphogluconate ——-> Ribulose-5-phosphate via 6-phosphogluconate dehydrogenase

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112
Q

What are the two fates of ribulose-5-phosphate once it is made in the oxidative phase of the pentose phosphate pathway?

A

It can become Ribose-5-phosphate and make nucleotides or it can become Xylulose-5-phosphate

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113
Q

What determines the directionality of the pentose phosphate pathway?

A

Energy needs of the cell.

If the cells is dividing, it needs nucleotides or is undergoing transcription and translation, ribose-5-phopshate will be made. It the cell is not doing those things, it will go towards converting to glucose.

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114
Q

How is NADPH used to combat reactive oxygen species?

A

NADPH is used in glutathione conjugation to convert hydrogen peroxide (H202) to 2 molecules of water.

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115
Q

Entry of Glucose-6-phopshate into the pentose phosphate pathways in regulated by _______ levels.

A

NADPH

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116
Q

If the need of the cell is only NADPH, what is the direction of the pentose phosphate pathway?

A

Oxidative rxns produce NADPH. Non-Oxidative rxns convert ribulose-5-phosphate to glucose-6-phopshate to make more NADPH.

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117
Q

If the energy needs of the cell are NADPH and Ribose-5-phosphate, what is the direction of the pentose phosphate pathway?

A

Oxidative rxns produce NADPH and ribuluse-5-phosphate. The isomerase rxn will convert ribulose-5-phosphate to ribose-5-phosphate.

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118
Q

If the energy needs of the cell are only ribose-5-phosphate, what is the direction of the phosphate pentose pathway?

A

Only the nonoxidative reactions. High NADPH levels inhibit glucose-6-phosphate dehydrogenase, so transketolase and transaldolase will be used to convert fructose-6-phosphate to glyceraldehyde-3-phosphate and ribose-5-phosphate.

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119
Q

If the energy needs of the cell are NADPH and pyruvate, what direction does the pentose phosphate pathway go?

A

Both oxidative and nonoxidative rxns are used. Oxidative rxns will generate NADPH and ribulose-5-phopshate. Non-oxidative will convert ribulose-5-phosphate to fructose-6-phosphate and glyceraldehyde-3-phopshate and glycolysis will convert them to pyruvate.

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120
Q

What are the 3 major enzymes of ethanol metabolism?

A

Alcohol dehydrogenase
Acetaldehyde dehydrogenase
Microsomal ethanol oxidizing system (MEOS)

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121
Q

What is the metabolite of alcohol that causes nausea and vomiting?

A

Acetaldehyde

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122
Q

What are the steps of ethanol metabolism?

A

Ethanol ———> acetaldehyde via alcohol dehydrogenase. NADH produced

Acetaldehyde ——–> acetate via acetaldehyde dehydrogenase. NADH produced

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123
Q

What is the drug disulfiram (antabuse)?

A

Disulfiram is an acetaldehyde dehydrogenase inhibitor.

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124
Q

What is acetate converted to?

A

Acetate is converted to Acetyl CoA in the liver, muscle and other tissues to enter the TCA cycle.

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125
Q

When is the MEOS or CYP2E1 system activated for alcohol metabolism?

A

This system is activated during to chronic drinking.

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126
Q

How much energy is produced from one mole of ethanol?

A

With alcohol and acetaldehyde dehydrogenase, 13 ATP/ mole of ethanol is made.
With the CYP2E1 system, 8 ATP/ mole of ethanol is made.

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127
Q

What is the main enzyme in the MEOS?

A

CYP2E1

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128
Q

What are the acute effects of ethanol metabolism?

A

Increased NADH/NAD+ ratio leading to inhibition of FA oxidation therefore they are reesterified into triacylglycerols and incorporated into VLDL.

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129
Q

What are the chronic effects of ethanol metabolism?

A

Long-term, there is so much NADH that other metabolism processes begin to backup. Acetyl CoA becomes ketone bodies which leads to ketoacidosis due to OAA being pushed towards malate and therefore no citrate synthesis. Hypoglycemia can also occur due to the use of non-carb precursors to convert pyruvate to lactate. Lactate can produce ethanol-induced lactic acidosis.

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130
Q

In a general sense, what are the results of chronic ethanol use?

A

Lactic acidosis, ketoacidosis, and hypoglycemia due to very high NADH/NAD+ ratio.

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131
Q
A
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132
Q

What is the only enzyme that can cleave fructose-1-phosphate?

A

Aldolase B

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133
Q

T or F: Galactose metabolism requires an initial energy investment.

A

True

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134
Q

What phase of the pentose phosphate pathway is responsible for the majority of cellular NADPH?

A

Oxidative phase

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135
Q

What are the 3 major dietary carbohydrates?

A

Starch, lactose, and sucrose

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136
Q

________ enzyme digests starch.

A

Amylase

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137
Q

Sucrose is a disaccharide of _______ and ________.

A

Glucose and fructose

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138
Q

____________ are enzymes that hydrolyze glycosidic bonds.

A

Glycosidases

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139
Q

Which of the following enzymes has activity at alpha-1,6-glycosidic bonds?

A. Amylose
B. Glucoamylase
C. Sucrase-isomaltase complex
D. All of the above

A

C. Sucrase-isomaltase complex

Amylase breaks a-1,4 bonds and glucoamylase is an alpha-1,4-exoglucoaside and cleaves the end sugar molecules

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140
Q

What type of bond is present in amylose?

A

Alpha-1,4

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141
Q

What type of bond is present in Lactose?

A

Beta-1,4

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142
Q

What type of bond is present in sucrose?

A

Alpha-1,2

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143
Q

What type of bond is present in amylopectin?

A

alpha-1,6 bonds
alpha-1,4 also present

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144
Q

B-glycosidase complex catalyzes which enzyme?

A. Lactase
B. Amylase
C. Sucrase
D. Glucoamylase

A

A. Lactase

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145
Q

T or F: Glucose can be symported with Na+.

A

True. Glucose and Galactose are transported by Na+-glucose cotransporters on the luminal side of absorptive cells.

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146
Q

T or F: GLUT1 is the glucose transported found in the liver and pancreas.

A

False. GLUT2 in found in the liver and pancreas

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147
Q

T or F: GLUT4 is the insulin sensitive transporter present in skeletal muscle, adipose tissue, and heart muscle.

A

True

148
Q

T or F: Neurons use GLUT3, which is a slow process.

A

False. It is true that neurons use GLUT3 but that is a fast process.

149
Q

Glycogen is broken down into ________ then converted to ________ to enter glycolysis.

A

G1P and G6P

150
Q

T or F: Formation of UDP-glucose requires energy.

A

True. It requires UTP.

151
Q

T or F: UDP-glucose is formed in glycogen degradation

A

False. UDP-glucose is formed in glycogen synthesis

152
Q

T or F: Glycogen metabolism is regulated by AMP, Ca2+, and epinephrine.

A

True

153
Q

T or F: Glycogen phosphorylase primarily works near alpha-1,6-branches.

A

False. Glycogen phosphorylase cleaves alpha-1,4 bonds.

154
Q

T or F: Glycogenolysis responds to glucose needs more rapidly than gluconeogenesis.

A

True

155
Q

What is the most important hormonal regulator of blood glucose levels and activates hepatic phosphatase-1 (PP1) for signalling?

A. Glucagon
B. Glycogen
C. Insulin
D. Cortisol

A

C. Insulin. Insulin activates hepatic PP1

156
Q

Skeletal muscle cannot restore blood glucose levels because it lacks what enzyme?

A

Glucose-6-phosphate

157
Q

What chains are present in the active form of insulin?

A

A and B chains

158
Q

T or F: Insulin allows glucose and amino acids to be transferred out of the cell.

A

False

159
Q

T or F: Epinephrine increases the release of glucagon.

A

True

160
Q

Which of the following are involved in the cellular signalling of glucagon (choose multiple)?

A. Calcium
B. GPCR
C. GLUT2
D. cAMP
E. PKA

A

B, D, and E

161
Q

Fructose metabolism primarily occurs in the _________.

A

Liver

162
Q

Fructose is converted to __________ and __________.

A

DHAP and glyceraldehyde-3-phosphate

163
Q

___________ is the enzyme that cleaves fructose-1-phopshate

A

Aldolase B

164
Q

Fructose enters epithelial cells through the ___________ transporter.

A

GLUT5

165
Q

What is one reason the body needs a pathway to convert glucose to fructose?

A

Increased blood glucose levels cause elevated ocular osmotic pressure.

166
Q

Which patient population has the highest ability to metabolize galactose?

A

Infants

167
Q

T or F: The reactions in the nonoxidative phase of the pentose phosphate pathways are irreversible and unidirectional.

A

False.

168
Q

Which of the following are true regarding ethanol metabolism?

A. Decreased NADH/NAD+ ratio in the liver
B. Decreased activity of the TCA cycle
C. Decreased beta-oxidation
D. Decreased Acetyl CoA levels
E. Decreased lipid levels

A

B and C

169
Q

Ethanol induced lactic acidosis can result due to :

A

Increased NADH leading to increased lactate

170
Q

Which process occurs first when insulin levels decrease and glucagon increases?

A

Glycogenolysis

171
Q

Using fuel from ketone bodies prevents excess breakdown of which energy source?

A

Proteins

172
Q

When lactate is used to form pyruvate via lactate dehydrogenase, which product is formed?

A

NADH

173
Q

What are the 3 precursors for gluconeogenesis?

A

Lactate, glycerol, and amino acids

174
Q

Alanine is converted to pyruvate by _______________________.

A

Alanine aminotransferase

175
Q

Oxaloacetate is converted to _____________ and then to glyceraldehyde-3-phosphate.

A

Phosphenolpyruvate

176
Q

Oxaloacetate is _________ so it must be shuttled out of the mitochondria

A

polar

177
Q

PEPCK expression levels are altered by ___________________.

A

Hormonal changes

178
Q

PEPCK is an ____________ enzyme.

A

Inducible

179
Q

Acetyl CoA activates pyruvate carboxylase which is an example of a ___________ feedback loop.

A

Negative

180
Q

Gluconeogenesis occurs primarily in what organ?

A

Liver

181
Q

The rate of gluconeogenesis actually _______ in long-term starvation in order to preserve protein.

A

Decreases

182
Q

What the two enzymes in gluconeogenesis that differ from glycolysis?

A

Glucose-6-phosphate and Fructose-1,6-bisphosphate

183
Q

What are the 3 major gluconeogenic percursors?

A

The amino acid Alanine
Lactate
Glycerol

184
Q

What are the two precursors of gluconeogenesis that must be converted to pyruvate before entering?

A

Alanine and lactate

185
Q

What reversible reaction and enzyme interconverts alanine to pyruvate?

A

Alanine Aminotransferase. Alanine to pyruvate generates a glutamate while the reverse generates an a-ketoglutarate.

186
Q

What is glycerol converted to before it can enter gluconeogenesis?

A

Dihydroxyacetone Phosphate (DHAP)

187
Q

What is the reaction of converting glycerol to DHAP to enter gluconeogenesis?

A

Glycerol ——–> glycerol-3-phosphate via glycerol kinase (uses an ATP)

glycerol-3-phosphate ——-> DHAP via glycerol-3-phosphate dehydrogenase (makes an NADH)

188
Q

Once alanine and lactate are converted to pyruvate, what is the major molecule pyruvate must be converted to in order to activate gluconeogenesis?

A

Phosphoenolpyruvate

189
Q

What is the reaction and catalyzing enzyme for the making of phosphoenolpyruvate?

A

Pyruvate ——-> oxaloacetate via pyruvate carboxylase

Oxaloacetate —–> phosphoenolpyruvate (PEP) via phosphoenolpyruvate carboxykinase (PEPCK)

190
Q

In what cellular location is pyruvate converted to OAA?

A

Mitochondria

191
Q

In what cellular location is OAA converted to PEP?

A

Cytosol

192
Q

How does OAA get out of the cell?

A

Malate-aspartate shuttle

193
Q

Why must OAA be converted to PEP in the cytosol?

A

PEPCK is only in the cytosol

194
Q

What are the two enzymes that are different in gluconeogenesis compared to glycolysis?

A

Fructose-1,6-bisphosphate ——> fructose-6- phosphate via fructose-1,6-bisphosphatase

Glucose-6-phosphate ——> glucose via glucose-6-phosphatase

195
Q

Where in the cell is glucose-6-phosphatase located?

A

ER

196
Q

What are the 3 activities that activate gluconeogenesis?

A

Prolonged exercise, a high protein diet, and stress.

197
Q

Pyruvate kinase is the enzyme in glycolysis that converts phosphoenolpyruvate to pyruvate. However, what happens to that enzyme when glucagon is released?

A

Increase glucagon inhibits pyruvate kinase in glycolysis there increasing concentrations of phosphoenolpyruvate (PEP).

198
Q

How does glucagon inactivate pyruvate kinase?

A

Glucagon phosphorylates pyruvate kinase via cAMP.

199
Q

During times of fasting, the concentration of ADP initially decreases. This results in the inactivation of the PDC. Therefore pyruvate is converted to _______ instead of _______.

A

OAA
Acetyl CoA

200
Q

What is the other molecule besides initial decreases in AMP that inactivate the PDC complex allowing pyruvate to be converted to OAA?

A

NADH

201
Q

Pyruvate carboxylase is the enzyme that converts pyruvate to OAA in the mitochondria. What is the molecule that activates pyruvate carboxylase?

A

Acetyl CoA

202
Q

How is the feedback of Acetyl CoA on pyruvate carboxylase an example of a negative feedback loop?

A

Increased Acetyl CoA concentrations makes the path from pyruvate to Acetyl CoA less used.

203
Q

PEPCK (enzymes that converts OAA to PEP to enter gluconeogenesis) is an __________ enzyme.

A

Inducible

204
Q

PEPCK expression levels are altered by __________ changes.

A

Hormonal

205
Q

How does glucagon increase the expression of PEPCK?

A

Glucagon increases cAMP which increase CREB which is the transcription factor that increases the expression of PEPCK.

206
Q

What is the main activator for glucose-6-phosphatase (enzyme that converts glucose-6-phosphate to glucose)?

A

Decreased blood glucose levels

207
Q

What is the enzyme involved in gluconeogenesis that is an example of negative feedback?

A

Pyruvate carboxylase

208
Q

The main route of digestion of triacylglycerols is hydrolysis to _________ and _____________ in the intestine.

A

Fatty acids and 2-monoacylglycerol

209
Q

What enzyme initiates the breakdown of triacylglyercols?

A

Lipases

210
Q

What is the function of lipases?

A

Lipases are pancreatic enzymes that cleave off the R groups (long carbon chains) via hydrolysis.

211
Q

What are bile salts?

A

Bile salts emulsify dietary fats. They are secreted from the gallbladder.

212
Q

What are the 3 important types of bile salts discussed in class?

A

Cholic acid, glycocholic acid, and deoxycholic acid

213
Q

Release of bile is mediated by stomach content entering the _______________. Intestinal cells release _______ which stimulates gallbladder to release bile salts.

A

Small intestine
Cholecystokinin (CCK)

214
Q

___________ also stimulates the release of ___________ enzymes involved in fat digestion.

A

CCK
Pancreatic

215
Q

What is the function of colipase?

A

Colipase binds to dietary fat and lipase to relieve bile salt inhibition of enzymatic breakdown. Basically, pancreatic lipase cannot digest TAGs without pulling off bile salts with the help of colipase.

216
Q

Once TAGs are broken down into FFAs and 2-monoacylglycerol, they are packaged into _________ with bile salts.

A

Micelles

217
Q

What is a micelle?

A

Micelles are microdroplets containing FAs, 2-monoacylglycerol, cholesterol, and bile salts.

218
Q

Micelles transfer their content to the __________ cells.

A

Intestinal epithelial

219
Q

Once the content of micelles are dumped into the intestinal epithelial cells, what happens to FAs and 2-MG?

A

FAs and 2-MGs are converted back to TAGs in the smooth ER of the intestinal epithelial cells and packaged into nascent chylomicrons with phospholipids and ApoB48

220
Q

Bile salts are reabsorbed via enterohepatic circulation at _______%

A

95

221
Q

What protein on the surface of chylomicrons denotes where is came from?

A

Apo

222
Q

What Apo protein is on chylomicrons from the intestinal epithelial cells?

A

B-48 (C-II is also present on these)

223
Q

What Apo protein is on chylomicrons from liver hepatocytes?

A

B-100 (present in VLDL)

224
Q

Nascent chylomicrons that leave the intestinal epithelial cells are considered immature. What do they need to receive to become mature?

A

ApoCII and ApoE proteins from HDL

225
Q

ApoCII is also the activator of _____________.

A

Lipoprotein lipase

226
Q

What is lipoprotein lipase?

A

This is a protein located on endothelial cells of muscle and adipose tissue. It interacts with the chylomicrons and converts the TAGs inside it to FAs and glycerol.

227
Q

Once a chylomicron interacts with Lipoprotein lipase and releases is content, they are now called ______________.

A

Chylomicron remnants. They go to the liver and are taken up via recepter-mediated endocytosis and are digested into fatty acids, cholesterol, amino acids, and glycerol.

228
Q

What is the drug Alli (Orlistat)?

A

This is a pancreatic lipase inhibitor. It works by forming covalent bonds with pancreatic lipase. It decreases the absorption of fat by not allowing the body to break it down.

229
Q

Chylomicrons contains what percentage of fatty acids?

A

85%

230
Q

Fatty acid synthesis requires the generation of _______, produced by the enzyme ________.

A

Malonyl CoA
Acetyl CoA Carboxylase

231
Q

The release of insulin for beta-cells of the pancreas requires an increase in intracellular ________ and ________.

A

ATP and CA2+

232
Q

What is enzyme responsible for the cleavage of alpha-1,4-glycosidic bonds present within glycogen during glycogenolysis?

A

Glycogen phosphorylase

233
Q

Where does the pentose phosphate pathway occur in the cell?

A

Cytosol

234
Q

Fatty acid synthesis occurs in the _________ from Acetyl CoA.

A

Cytosol

235
Q

Fatty acid are produced in the _____ from excess glucose.

A

Liver

236
Q

Generation of fatty acids requires cytosolic ____________.

A

Acetyl CoA

237
Q

How is cytosolic Acetyl CoA generated? (PDC occurs in the mitochondrial matrix)

A

Citrate from TCA cycle is shuttled out of mitochondria into cytosol. There, citrate lyase converts citrate to OAA and Acetyl CoA.

238
Q

Why do we need to convert Acetyl CoA to citrate in the mitochondria and not just kick Acetyl CoA out?

A

Acetyl CoA cannot cross the mitochondrial membrane but citrate can.

239
Q

Cytosolic Acetyl CoA from pyruvate is regulated by _____________ ratio.

A

Insulin/glucagon

240
Q

Increased insulin= increased PDC activity= Increased Acetyl CoA levels= increases ______________ export from mitochondria to cytosol to make _______________.

A

Citrate
Cytosolic Acetyl CoA

241
Q

What molecule is the donor of 2 carbons added to the growing fatty acid chain?

A

Malonyl CoA

242
Q

Acetyl CoA is converted to Malonyl CoA via what enzyme?

A

Acetyl CoA Carboxylase. This reaction requires biotin, CO2, and ATP.

243
Q

What is the rate-limiting enzyme of fatty acid synthesis?

A

Acetyl CoA Carboxylase

244
Q

How does insulin activate Acetyl CoA carboxylase?

A

Insulin activates phosphatase which removes a phosphate group from inactive Acetyl CoA carboxylase to make it active.

245
Q

What is fatty acid synthase?

A

Fatty acid synthase is a very large enzyme complex that contains an acyl carrier protein segment (ACP).

246
Q

What is the key portion of the acyl carrier protein segment on the fatty acid synthase enzyme?

A

Sulfhydryl group (SH)

247
Q

What is the 16 carbon fatty acid discussed in class that is the general fatty acid used in teaching?

A

Palmitate

248
Q

How many carbons are added to the growing fatty acid via fatty acid synthase?

A

2 carbons

249
Q

Through what reaction are oxygen removed from the long fatty acid chain?

A

Reduction

250
Q

Reduction of fatty acids on fatty acid synthase uses _________as the reducing agent.

A

NADPH

251
Q

What two compounds activate Acetyl CoA Carboxylase?

A

Insulin and citrate

252
Q

What compounds inhibits Acetyl CoA Carboxylase?

A

Palmityl CoA

253
Q

Why does Malonyl CoA inhibit CPT1, an enzyme involved in getting fatty acids into the mitochondria for beta-oxidation?

A

Malonyl CoA inhibits CPT1 so that new synthesized fatty acids do not undergo immediate oxidation.

254
Q

What is desaturation of fatty acids and where does it occur?

A

Desaturation of fatty acids is the oxidation of fatty acids and NADH. It occurs in the endoplasmic reticulum and requires oxygen and cytochrome B5.

255
Q

What are the 3 molecules involved in the desaturation of fatty acids?

A

O2, NADH, and cytochrome B5

256
Q

What are eicosanoids?

A

Eicosanoids are biologically active lipids derived from 20 carbon fatty acids. They act as local hormones and are crucial mediators of the inflammatory responses.

257
Q

What are the 3 main types of eicosanoids?

A

Prostaglandins, thromboxanes, and leukotrienes

258
Q

________________ is the most common precursor for eicosanoids.

A

Arachidonic acid

259
Q

_______________, an essential fatty acid, produces arachidonic acid.

A

Linoleic acid

260
Q

Arachidonic acid is converted to prostaglandins and thromboxanes via what enzyme?

A

Cyclooxygenase (COX)

261
Q

Prostaglandin G2 (PGG2) is converted to Prostaglandin H2 (PH2) by ______________. PH2 can then be converted into different types of prostaglandins and thromboxane.

A

Peroxidase

262
Q

NSAIDS target ___________ enzyme.

A

COX

263
Q

What are the two types of cyclooxygenase?

A

COX1- constitutive and found in platelets
COX2- inducible form regulated by cytokines and growth factors

264
Q

When fatty acids are being stored as triacylglycerides, what is the typical intermediate?

A

Glycerol-3-phosphate

265
Q

Aspirin is an irreversible inhibitor of ____________.

A

COX-1

266
Q

The liver exports newly made triacylglycerides to ___________.

A

Blood as VLDL

267
Q

In the fasted state, triacylglycerides are broken down into fatty acids in adipose tissue. This is stimulated by _____________.

A

Low insulin and high glucagon

268
Q

What is the enzyme responsible for the breakdown of triacylglycerides to fatty acids to be released into the blood?

A

Hormone-sensitive lipase

269
Q

When glucagon binds it stimulates increased levels of ____________ which activates PKA. PKA then ___________ hormone-sensitive lipase.

A

cAMP
Activates

270
Q

_______ break down dietary proteins into amino acids.

A

Proteases

271
Q

___________ initiates protein breakdown in the stomach.

A

Pepsin

272
Q

Proteins are targeted for degradation by ______________.

A

Ubiquitination

273
Q

Protein degradation occurs in the _____________ and is dependent on ATP.

A

Proteasomes

274
Q

Enzymes that digest proteins begin as ___________.

A

Zymogens

275
Q

What are zymogens?

A

Zymogens are enzymes that are activated by being cleaved.

276
Q

Pepsinogen activates it own cleavage to ________ as the pH of the stomach drops.

A

Pepsin

277
Q

Trypsinogen is converted to trypsin via what enzyme?

A

Enteropeptidase

278
Q

What is trypsin important?

A

Trypsin catalyzes the cleavage and activation of several other pancreatic zymogens.

279
Q

How are amino acid brought in from the lumen to the intestinal epithelial cells?

A

Amino acid are brought in by the Na+ dependent carriers. Na+ concentration gradient is maintained by the Na+K+ ATPase. Very similar to carbohydrate transport.

280
Q

What are the two main functions that newly broken down amino acids can be used for?

A

Energy or new proteins

281
Q

The catabolism of amino acids produces __________.

A

Urea

282
Q

What is urea?

A

Urea is the not toxic carrier of nitrogen

283
Q

Urea synthesis occurs in the ____________.

A

Liver

284
Q

____________ and ____________ carry amino acid nitrogen to the liver.

A

Alanine and glutamine

285
Q

What is transamination?

A

Transamination is the major process of removing nitrogen from amino acids.

286
Q

What are the two amino acids that do not undergo transamination?

A

Threonine and lysine

287
Q

What is the required cofactor for transamination?

A

Pyridoxal Phosphate (PLP)

288
Q

What enzyme catalyzes transamination reactions?

A

Aminotransferases

289
Q

Nitrogen from amino acids is released as __________ or ______________.

A

Ammonia or Ammonium ions (NH4+)

290
Q

What is the physiological ratio of NH4+ (ammonium ions) to NH3 (ammonia)?

A

100:1. The ammonium ions are not as toxic as ammonia.

291
Q

Can ammonia (NH3) cross cell membranes?

A

Yes

292
Q

What are the two types of reactions that can convert alpha-ketoglutarate to glutamate and back?

A
  1. Transamination reaction (malate-aspartate shuttle)
  2. Glutamate dehydrogenase enzyme (GDH)
293
Q

What is the reaction that is catalyzed by glutamate dehydrogenase?

A

Glutamate ———-> a-ketoglutarate via GDH
Creates NADPH or NADH and released an ammonium ion

294
Q

Glutamate plays a central role in ____________ synthesis?

A

Amino acid

295
Q

How do glutamate play a key role in amino acid synthesis?

A

Glutamate collects nitrogen from other amino acids by transamination reactions. Nitrogen can be released as NH4+ via glutamate dehydrogenase.

296
Q

What are the two major carriers of nitrogen to the liver for the urea cycle?

A

Alanine and glutamine

297
Q

What is the glucose-alanine cycle?

A

In the muscle, pyruvate can be transaminated by glutamate to form alanine. Alanine is shuttled to the liver where it can enter to urea cycle or be used as a gluconeogenic precursor to make glucose. If glucose is made, it is shuttled back to muscle.

298
Q

How is glutamine formed?

A

Glutamate ———–> glutamine via glutamine synthetase
Uses NH4+ and ATP

299
Q

What is nitrogen balance?

A

This means the amount of nitrogen excreted as urea equals the amount of nitrogen ingested. Nitrogen balance is maintained by the urea cycle.

300
Q

What is the first step of the urea cycle and where does it occur?

A

NH4+ + HCO3- ————> Carbamoyl Phosphate via CPS1
Uses 2 ATP

Occurs in mitochondria

301
Q

What is the 2nd step of the urea cycle?

A

Carbamoyl phosphate using ornithine ———> citrulline via Ornithine transcarbamoylase

Citrulline is transported out of the mitochondria into the cytosol

302
Q

What is the 3rd step of the Urea cycle?

A

Citrulline using aspartate ———> argininosuccinate via argininosuccinate synthetase

Uses and ATP and occurs in the cytosol

303
Q

What is the 4th step of the Urea cycle?

A

Argininosuccinate ——–> fumarate and Arginine via Argininosuccinate lyase

304
Q

Once fumarate is made in the urea cycle, what can it be converted into?

A

Fumarate can be converted into malate or regenerated as cytosolic OAA (used in that malate-aspartate shuttle that keeps coming up everywhere!)

305
Q

What is the 5th step of the urea cycle?

A

Arginine ———-> ornithine via arginase

Here the NH2 and NH group are pulled from arginine and combined with H2O to form urea.

306
Q

What happens to ornithine once it is regenerated at the end of the urea cycle?

A

It goes back into the mitochondria to participate in the 1st step of the urea cycle again.

307
Q

What two molecules activate the enzyme CPSI in the urea cycle?

A

Arginine and N-Acetyl-glutamate

308
Q

What is the enzyme the catalyzes the deamination reaction of glutamate?

A

Glutamate dehydrogenase

309
Q

What is the enzyme that catalyzes the formation of carbamoyl phosphate?

A

Carbamoyl phosphate synthetase I (CPSI)

310
Q

Does amino acid metabolism require cofactors?

A

Yes! AA metabolism requires pyridoxal phosphate, tetrahydrobiopterin (BH4), and tetrahydrofolate (FH4)

311
Q

Degradation of amino acids result in ___________ being converted to _____________.

A

Nitrogen
Urea

312
Q

When amino acids are metabolized, they are split into carbon and nitrogen. What happens with the carbons?

A

The carbon backbone of amino acids go into gluconeogenesis to make glucose then ATP.

313
Q

When amino acids are metabolized, they are split into carbon and nitrogen. What happens with the nitrogen?

A

The nitrogen get converted to urea and peed out.

314
Q

What are the 3 things that amino acids are used for discussed in class?

A

NTs, Purine and Pyrimidines, and Heme

315
Q

Which amino acid is essential for growth in children, but nonessential in adults?

A

Arginine

316
Q

What enzyme converts serine to glycine?

A

Serine Hydroxymethyl transferase with PLP. Requires the cofactor FH4

317
Q

Are there two ways in which glycine can be made?

A

Yes! Converting serine to glycine via Serine Hydroxymethyl transferase or converting threonine to glycine via a transamination reaction.

318
Q

What are the two big reasons that glutamate is so important?

A
  1. Glutamate can be used to make other amino acids including glutamine, proline, ornithine (required in urea cycle), and arginine.
  2. It can be converted to glucose in the liver (enter gluconeogenesis)
319
Q

How is glutamate converted to arginine?

A

Glutamate semialdehyde ——-> ornithine via TA rxn by ornithine aminotransferase.
Ornithine enters to Urea cycle where after a few steps in that cycle, arginine is produced.

320
Q

What essential amino acid produces the non-essential amino acid tyrosine?

A

Phenylalanine

321
Q

What enzyme converts phenylalanine to tyrosine?

A

Phenylalanine hydroxylase

322
Q

What is the cofactor and reducing equivalent required for the conversion of phenylalanine to tyrosine via phenylalanine hydroxylase?

A

BH4 and NADH

323
Q

What are the 4 amino acids that can enter into the TCA cycle through several steps as succinyl CoA?

A

Valine
Threonine
Isoleucine
Methionone

324
Q

What are glucogenic amino acids?

A

These are amino acids that get enter into the TCA by being converted to intermediates. These are know as analperotic reactions.

325
Q

What are ketogenic amino acids?

A

These are amino acids that enter into ketone body production by being converted into different intermediates of ketone body production.

326
Q

What are the 3 steps of conversion of methionine to succinyl CoA to enter to TCA cycle?

A

Methionine to a-ketobutyrate
a-ketobutyrate to propionyl CoA
Propionyl CoA to Succinyl CoA

Succinyl CoA enters TCA cycle and make glucose via gluconeogenesis

327
Q

The initial reactions of branched chain amino acid metabolism like Valine , isoleucine, and Leucine all include transamination reactions where the AAs are converted to ____________ analogs.

A

a-keto

328
Q

Phenylalanine can be converted into tyrosine via phenylalanine hydroxylase. What other 2 molecules can phenylalanine be converted to?

A

Dopamine (the other catecholamines like NE and Epi too) and Melanin

329
Q

What is the first step of dopamine synthesis?

A

Phenylalanine ——-> L-Tyrosine via phenylalanine hydroxylase with BH4

330
Q

What is the 2nd step of dopamine synthesis?

A

L-tyrosine ——-> DOPA via tyrosine hydroxylase with BH4

331
Q

What is the 3rd step of dopamine synthesis?

A

DOPA ——-> dopamine via DOPA decarboxylase using PLP

332
Q

Where does the creation of dopamine and the other catecholamines like epinephrine and norepinephrine occur?

A

Brain

333
Q

What is the enzyme that converts phenylalanine to melanin and where does it occur?

A

Tyrosine hydroxylase with Cu2+
Melanocytes

334
Q

What is the required cofactor for catecholamine synthesis?

A

BH4

335
Q

What element is required for the conversion of phenylalanine to melanin via tyrosine hydroxylase?

A

Copper

336
Q

The synthesis of serotonin requires what essential amino acid?

A

Tryptophan

337
Q

What is the 1st step of serotonin synthesis?

A

Tryptophan ——–> 5-hydroxytryptophan via tryptophan hydroxylase with BH4

338
Q

What is the 2nd step of serotonin synthesis?

A

5-hydroxytryptophan ———> Serotonin (5-HT) via DOPA decarboxylase with PLP

339
Q

Serotonin can eventually be converted into ___________.

A

Melatonin

340
Q

What is the required cofactor for serotonin synthesis?

A

BH4

341
Q

What are the two precursors and the enzyme that creates acetycholine?

A

Acetyl CoA and Choline
Choline Acetyltransferase

342
Q

What is the enzyme that degrades acetylcholine back into acetyl coa and choline?

A

Acetylcholinesterase

343
Q

What precursor and enzyme creates the NT glutamate?

A

Glutamine
Glutaminase

344
Q

What is the precursor and enzyme that creates histamine in peripheral tissues?

A

Histidine
Histidine Decarboxylase

345
Q

What is the name of the enzyme that converts glycine to serine?

A

Serine Hydroxymethyl Transferase

346
Q

What is the enzyme that converts glutamate semialdehyde to ornithine for use in the urea cycle?

A

Ornithine Aminotransferase

347
Q

What is the enzyme responsible for the breakdown of acetylcholine?

A

Acetylcholinesterase

348
Q

What is the cofactor required for the production of dopamine and serotonin?

A

BH4

349
Q

Which is an example of an essential fatty acid?

A. Triacylglycerol
B. Palmitate
C. Fatty Acyl CoA
D. Alpha-linoleic acid

A

D

350
Q

The pyruvate dehydrogenase complex is regulated by which of the following?

A. Phosphatase
B. Succinate
C. Fatty Acyl CoA
D. None of the above

A

D. None of the above
PDC is regulated by Acetyl CoA, NADH, Pyruvate, ADP, and Ca2+

351
Q

What is the intracellular signalling mediator responsible for the activation of hormone sensitive lipase in adipocytes?

A. Ca2+
B. AMP
C. STAT3
D. PKA

A

D. PKA
Hormone sensitive lipase released FAs from triglycerides in adipose tissue which is stimulated by glucagon binding. Glucagon activates cAMP which activates PKA to turn lipase active.

352
Q

The conversion of pyruvate to Acetyl CoA by the PDC generates?

A. NADH
B. H20
C. ADP
D. All of the above

A

A. NADH
PDC generates an NADH and a CO2

353
Q

Glycolysis is the oxidation of glucose by what mechanism?

A. Dephosphorylation
B. Glycogenolysis
C. Substrate level phosphorylation
D. Oxidative dephosphorylation

A

C. Substrate level phosphorylation

354
Q

The enzyme Acetyl CoA Carboxylase is involved in lipid synthesis. It mediates what reaction?

A. OAA to pyruvate
B. Pyruvate to Acetyl CoA
B. Malonyl CoA to Palmitate
D. Acetyl CoA to Malonyl CoA

A

D.
Acetyl CoA Carboxylase is the rate-limiting enzyme of lipid synthesis.

355
Q

T or F: Catalase serves to protect cells from bursts in respiratory activity.

A

True.
Catalase reduced H202 to water and is present in peroxisomes

356
Q

What is the enzyme that relieves bile salt inhibition for enzymatic breakdown of dietary fats?

A. Lipase
B. Colipase
C. 2-Monoacylglycerol
D. Cholesterol Esterase

A

B. Colipase

357
Q

What is the apolipoprotein that is present in chylomicrons and is one of their identifying proteins?

A. B-100
B. ApoC-III
C. B-48

A

C. B-48

358
Q

What is the transcription factor that regulates increases in the expression of PEPCK?

A. TF-2
B. cAMP
C. PKA
D. CREB

A

CREB

359
Q

T or F: The F0 portion of ATP synthase is composed of 12 C subunits.

A

True

360
Q

Glutamate is used to make multiple other amino acids. List all amino acids that are made from glutamate.

A

Glutamine
Proline
Ornithine
Arginine

361
Q

Which two metabolic process can amino acids be integrated into?

A

TCA and ketone body production

362
Q

What are the 4 amino acids that can be converted to succinyl CoA?

A

Methionine
Isoleucine
Threonine
Valine

363
Q

What percentage of chylomicrons are made up of proteins?

A

5%

364
Q

Fatty acids are produced in the ________ from glucose.

A

Liver

365
Q

Increased pyruvate dehydrogenase activity is caused by _________________.

A

Increased insulin

366
Q

What reducing agent is used on fatty acids in fatty acid synthase?

A

NADPH

367
Q

Hormone sensitive lipase is activated to break down triacylglycerol by which conditions? Select all that apply.

A. High insulin
B. Low insulin
C. High glucagon
D. Low glucagon

A

B and C