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DHN 311 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Main steps of RNA synthesis?

A
  1. Initiation
  2. Elongation
  3. Termination

RNA polymerase travels along DNA until the promotor site is found. The promotor region is the starting point of transcription. RNA polymerase recognizes the promotor because of transcription factors on it. The process of adding nucleotides to form a new RNA stops when RNA polymerase reaches a termination signal.

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2
Q

What are transcription factors?

A

These proteins are involved in transcription in all eukaryotes. They bind to specific spots on DNA and control the rate of transcription. Transcription factors are the most common form of gene expression regulation.

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3
Q

What are the ways in which RNA can be transcriptionally regulated?

A
  1. Transcriptional regulation is mediated by regulatory signals binding directly to intracellular receptors. This process is when a ligand binds to an intracellular receptor which activates the receptor. This complex together is called a dimer. The dimer can bind directly to DNA to act as a transcription factor. Can increase or decrease gene expression.
  2. Transcriptional regulation is mediated indirectly by cell-surface receptors. This process is when a ligand binds to a cell surface receptor which causes a cell signalling cascade all the way to the nucleus.
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4
Q

What is a Single Nucleotide Polymorphism (SNP)?

A

This is the most common type of polymorphism. This is when only one nucleotide letter is changed. Accounts for 90% of human genetic variation.

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5
Q

What is RNA splicing?

A

RNA splicing is a form of gene regulation that occurs post-transcriptionally in RNA but before the protein is created. Splicing cuts out the introns that code for nothing and leaves the exons to form a mature mRNA molecule. Splicing creates isoforms of a single gene.

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6
Q

What is the role of tRNA?

A

Transfer RNA is the RNA that transfers amino acids to the ribosome to attach to a growing peptide chain to form a protein. tRNA does not become a protein.

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7
Q

What is the role of rRNA?

A

Ribosomal RNA is the RNA that serves as the location for protein synthesis. rRNA does not become a protein.

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8
Q

What is mRNA?

A

Messenger RNA is the RNA that is actually translated into sequences of amino acids. The final product of mRNA will be a new protein.

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9
Q

When does post-translational modification occur?

A

Polypeptide chain covalently modified after it is released from ribosome.

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10
Q

When does co-translational modification occur?

A

Polypeptide chain covalently modified while still attached the the ribosome.

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11
Q

What are the 2 products of gene expression?

A

RNA or Protein

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12
Q

What is the function of DNA polymerases?

A

DNA polymerases synthesize the new DNA strands in the 5’ to 3’ direction.

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13
Q

What is nutrigenomics?

A

The study of the effect of specific nutrients on the expression of genes. An example includes SFA increasing inflammation while PUFAs block that activity.

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14
Q

What is nutrigenetics?

A

The study of how variations in our genes may increase of decrease the body’s needs for a specific nutrient.

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15
Q

What is epigenetics?

A

Refers to the influence of the environment, lifestyle, age, and disease conditions to change gene expression without changing the actual DNA sequences.

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16
Q

What are the proteins called that bind to distinct sites on DNA that controls DNA transcription to RNA?

A

Transcription factors

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17
Q

Types of bonds associated with the primary structure of a protein?

A

Peptide bond

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18
Q

Types of bonds associated with the secondary structure of a protein?

A

Hydrogen bond

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19
Q

Types of bonds associated with the tertiary structure of a protein?

A

Hydrogen bonds, ionic interactions, hydrophobic interactions, and disulfide bonds

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20
Q

Types of bonds associated with the quaternary structure of a protein?

A

Hydrogen bonds, ionic interactions, hydrophobic interactions, and disulfide bonds

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21
Q

Which protein folding level do side chains/ R interact?

A

Tertiary structure is when R groups begin to interact.

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22
Q

What are some different functions of protein in the body?

A

Proteins can be enzymes, they are in muscle fiber, used in transport, make hormones, antibodies protect body, and overall regulation.

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23
Q

A dehydrogenase enzyme indicates what type of reaction is going to take place?

A

Reduction reaction

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24
Q

What is non-competitive enzyme inhibition? How is Vmax and Km affected in this situation?

A

Non-competitive inhibition occurs when the inhibitor and substrate bind at different sites on the enzyme. Inhibitors can bind just the enzyme or the enzyme-substrate complex. Non-competitive inhibitors decrease the Vmax and cause no change in the Km.

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25
Q

What is competitive inhibition? How is the Vmax and Km affected in this situation?

A

Competitive inhibition occurs when the inhibitors bind reversibly to the same site the substrate would normally bind to. Competitive inhibitors do not affect Vmax but increase the Km.

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26
Q

What is Vmax?

A

The maximal velocity of an enzyme-catalyzed reaction at saturating substrate concentration.

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27
Q

What is Km?

A

This is the Michaelis constant. It measures the affinity an enzyme has for its substrate. Basically, this is the substrate concentration when the reaction velocity is half Vmax.

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28
Q

What does having a high or low Km mean for an enzyme?

A

High Km values correspond to low enzyme affinity for a substrate. This means more substrate concentration is needed to reach 50% of Vmax.
Low Km values correspond to high enzyme affinity for a substrate. This means less substrate concentration is needed to reach 50% of Vmax.

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29
Q

What is the purpose of the two sites on an allosteric enzyme?

A

There is a catalytic site that fits the substrate and an allosteric site that fits the effector/ allosteric modulator.

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30
Q

What is the difference between a homotropic and a heterotropic enzyme?

A

An allosteric enzyme is homotropic if the substrate itself is also the modulator. It is heterotrophic when the modulator and substrate are two different molecules.

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31
Q

What type of curve do allosteric regulators generate?

A

Sigmoidal curve

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32
Q

What is cooperativity?

A

Cooperativity refers to the observation that the binding of a substance to one binding site increases or decreases the binding to another site.

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33
Q

Where is most NADH/FADH2 generated that goes to the electron transport chain?

A

The Krebs cycle/ citric acid cycle

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34
Q

Which pathways/ reactions generate CO2?

A

PDH complex and Krebs Cycle

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35
Q

What are the end products of oxidative phosphorylation? (Includes redox rxns and complex V)

A

NADH is broken down to release NAD+, 2 Hydrogens, and 2 electrons. FADH2 is broken down into FAD, 2 electrons, and 2 hydrogen atoms. We also form water and ATP.

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36
Q

Where does the electron transport chain take place?

A

The inner layer of the mitochondrial membrane. Both ETC and oxidative phosphorylation continue consistently in all tissues that contain mitochondria.

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37
Q

Where does the kreb’s cycle take place?

A

TCA/ Kreb’s/ Citric acid cycle occurs in the mitochondrial matrix, so it can be close to the ETC.

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38
Q

Where does gluconeogenesis take place?

A

90% in the liver and 10% in the kidneys

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39
Q

Where does glycolysis take place?

A

Carried out by all tissues and occurs in the cytosol.

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40
Q

What is the end product of gluconeogenesis, and what is the energy investment?

A

The end product is glucose. The energy investment for making 1 glucose molecule is 6 high-energy phosphate bonds (ATP/GTP), 2 NADH, and 6 carbons (coming from pyruvate, lactate, glycerol, or glucogenic amino acids).

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41
Q

What is the end product of glycogen breakdown?

A

90% of the product is glucose-1-phosphate and 10% of product is free glucose

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42
Q

Which macronutrient is used to generate glycogen?

A

Carbohydrates broken down into glucose.

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43
Q

In which tissues is glycogen stored and released?

A

100 grams stored in liver and 300-400 grams stored in skeletal muscle

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44
Q

Liver glycogen is broken down to provide energy for which tissues?

A

Tissues that can use glucose as an energy source to make ATP. The whole body basically

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45
Q

Muscle glycogen is broken down to provide energy for which tissues?

A

Muscle is selfish, the glycogen broken down here is used by the muscle to make energy.

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46
Q

Are glucagon and epinephrine receptors located on the liver and muscle tissue? What is the significance of the location of these receptors?

A

The liver has both glucagon and epinephrine receptors, while the muscle just has epinephrine receptors.

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47
Q

What are the end products of aerobic glycolysis?

A

2 Pyruvate, 2 ATP (made 4 but invested 2), and 2 NADH

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48
Q

What are the end products of anaerobic glycolysis?

A

2 lactate, 2 ATP, 0 NADH

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49
Q

Which enzymes are irreversible steps in glycolysis?

A
  1. Glucose to Glucose-6-phosphate by enzyme hexokinase/glucokinase.
  2. Fructose-6-phosphate to fructose-1,6-bisphosphate via phosphofructo kinase-1 (PFK1).
  3. Phosphoenol pyruvate to pyruvate via enzyme pyruvate kinase
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50
Q

Which enzymes are irreversible steps in gluconeogenesis?

A
  1. Pyruvate to oxaloacetate via enzyme pyruvate carboxylase
  2. Oxaloacetate to phosphoenol pyruvate via enzyme phosphoenol pyruvate carboxylase (PEPCK)
  3. Fructose-1,6-bisphosphate to fructose-6-phosphate via enzyme fructose-1,6-bisphosphatases (F16BP)
  4. Glucose-6-phosphate to glucose via the enzyme glucose-6-phosphatase
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51
Q

Does the Kreb’scycle occur in aerobic or anaerobic conditions?

A

Kreb’s cycle only occurs in aerobic conditions. This is because without oxygen, we will run out of NAD+ and FADH because the ETC is also not running.

52
Q

Does oxidative phosphorylation occur under aerobic or anaerobic conditions?

A

Oxidative phosphorylation occurs only in aerobic conditions.

53
Q

What is the difference between hexokinase and glucokinase?

A

Hexokinase is located in most tissues, including the brain and muscle. It has a low Km meaning it is activated by low glucose blood concentrations. Glucokinase is located in the liver and the pancreas and has a high Km. These high concentrations of glucose will activate fatty acid synthesis in the liver and release insulin from the pancreas. Only occurs when blood glucose concentrations are high.

54
Q

What is the significance of PFK-2 and fructose-2,6-bisphosphate?

A

PFK-2 allows the liver to continue making pyruvate even in the fed state. Insulin activates the enzyme PFK-2. This enzyme adds a phosphate to fructose-6-phosphate to form fructose-2,6-bisphosphate. That substrate is a potent activator of PFK-1, and it turns back on, which means glycolysis in the liver continues and eventually, we can convert acetyl CoA to fat.

55
Q

What tissues are involved with the Cori Cycle? What is the purpose of the Cori cycle?

A

The Cori cycle involves the liver and skeletal muscle. When lactate is generated in the muscles during anaerobic glycolysis, lactate will leave the muscle, enter the blood, and travel to the liver. Once in the liver, the lactate can enter into gluconeogenesis to generate glucose and then that glucose will leave the liver, go into the blood, and go fuel the muscle.

56
Q

What are the 4 gluconeogenic precursors?

A
  1. Lactate
  2. Glycerol
  3. Glucogenic Amino Acids
  4. pyruvate
57
Q

What are the specific hormones generated from cholesterol?

A

Steroid hormones are all generated from cholesterol.

58
Q

What tissue can regulate de novo cholesterol synthesis in response to dietary cholesterol levels?

A

Liver

59
Q

In which tissues and cell compartments does fatty acid synthesis take place?

A

Occurs in the liver, mammary glands, and adipose tissue. It takes place in the cytosol of the cell.

60
Q

In what tissues and cell compartments does beta oxidation take place?

A

Beta oxidation of fatty acids occurs in the mitochondrial matrix

61
Q

Which macronutrients are used in fatty acid synthesis to generate fat?

A

Carbohydrates and protein in excess. fat is just stored as fat.

62
Q

What is the end product of fatty acid synthesis?

A

16 carbon palmitic acid

63
Q

What is the complex that encompasses the enzymes involved in fatty acid synthesis?

A

Fatty acid synthase system

64
Q

What is elongation?

A

The palmitic acid end product of fatty acid synthesis can be elongated by elongases in the Smooth ER. Maloynl CoA is the carbon donor, and NADPH supplies the hydrogens.

65
Q

What is desaturation?

A

The palmitic acid end product of fatty acid synthesis can be desaturated in the Smooth ER via desaturases. It desaturates by adding a cis double bond.

66
Q

What is the function of hormone-sensitive lipase (HSL)?

A

Hydrolyzes stored triglycerides into free fatty acids and glycerol. Also known as the enzyme in lipolysis allowing free fatty acids and glycerol to enter circulation so it can be used for energy.

67
Q

How are free fatty acids transported through circulation?

A

Free fatty acids bind to plasma albumin.

68
Q

What is generated as free fatty acids go through beta-oxidation?

A

1 acetyl CoA for every 2 carbons cleaved off.

69
Q

What is the function of CPT I and II?

A

Fatty acid combined with CoA makes fatty acyl CoA. Carnitine then replaces the CoA group to form acyl carnitine. It can then enter into the mitochondrial matrix side. Once there, CPT 2 transfers the acyl from carnitine to CoA creating free carnitine and fatty acyl CoA inside the mitochondrial matrix, ready for oxidation.

70
Q

What tissues and cell compartments are ketones formed?

A

Only occurs in the mitochondria of liver cells.

71
Q

What are the three types of ketones, and which generate energy and which do not?

A
  1. Acetoacetate- generates energy
  2. Beta-hydroxybutyrate- generates energy
  3. Acetone- dead end.
72
Q

What are the fates of the carbon skeleton/ alpha-ketoacid derived from amino acids?

A

These alpha-keto acids will enter into the TCA cycle.

73
Q

What is the fate of the amino group taken off the amino acid?

A

The Urea Cycle. In most tissues, the enzyme glutamine synthetase combines free ammonia (NH3) with glutamate to form glutamine. Glutamine travels to the liver, and the enzyme glutaminase removes 1 one of the amino groups from glutamine, reforming glutamate. Glutamate can undergo a deamination reaction to excrete the final amino group still attached to it.
Glutamate generated can also be used in the glucose-alanine cycle between the liver and muscle.

74
Q

What tissues are involved in the glucose-alanine cycle (Cahill Cycle)?

A

The liver and muscle

75
Q

What is the purpose of the glucose-alanine cycle (Cahill Cycle)?

A

It is a mechanism used to get free ammonia out of the muscle while transferring glucose from gluconeogenesis in the liver back to the muscle.

76
Q

How does ammonia get to the liver from most tissues other than the muscle?

A

Glutamine Synthesis

77
Q

What is the purpose of lipoproteins?

A

Lipoproteins are composed of lipids and proteins. Their function is to transport lipids in plasma by providing an efficient mechanism for transporting their lipid contents to and from tissues.

78
Q

What are the 5 types of lipoproteins?

A
  1. Chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
79
Q

What is the apolipoprotein associated with chylomicrons?

A

Apo B48 is unique to chylomicrons. Nascent chylomicron also has Apo C and Apo C2. Apo E is received from circulating HDL which is needed to activate lipoprotein lipase (LPL)

80
Q

What is the purpose of Apo B48 on chylomicrons?

A

Apo B48 helps chylomicron carry the needs triglycerides, cholesterol, and vitamins to target tissues.

81
Q

What is the apolipoprotein associated with VLDL?

A

Apo B100 is unique to VLDL. They obtain Apo C2 and Apo E from circulating HDL.

82
Q

What is the function of Apo B100 in VLDL?

A

It helps it to be endocytosed as LDL into the liver and other tissues.

83
Q

What is the apolipoprotein associated with HDL?

A

Apo A1 is the apolipoprotein on HDL. HDL is circulated with Apo E and Apo C2 to give to other things. HDL takes up cholesterol.

84
Q

What is the function of Apo A1?

A

When cholesterol is taken up by HDL from tissues, it is esterified by the plasma enzyme LCAT. LCAT will bind to the nascent HDL and is activated by Apo A1. CHolesterol ester can then be transported to the liver.

85
Q

What is the primary component of chylomicrons?

A

Lipids

86
Q

What is the primary component of VLDL?

A

Higher ratio of protein to lipid than chylomicron.

Largely lipids

87
Q

What is the primary component of LDL?

A

cholesterol and cholesterol esters

88
Q

What is the primary component of HDL?

A

Protein

89
Q

Dietary-wise, what does a person have to eat to form chylomicrons and VLDLs?

A

Need to eat dietary fats.

90
Q

Where do LDLs come from?

A

LDLs and IDLs are transient molecules that are formed from the metabolism of VLDLs in circulation.

91
Q

What is the role of lipoprotein lipase (LPL), and which lipoproteins are recognized by this enzyme? What is the role of hepatic lipase?

A

Lipoprotein Lipase (LPL) degrades the triglycerides inside the chylomicron. LPL is located mainly in adipose tissue, cardiac muscle, and skeletal muscle. LPL is activated by circulating Apo C2.
One unique aspect of this is hepatic lipase in the liver is it degrades some TAGS in CM and VLDL and is important in HDL metabolism.

92
Q

Chylomicron lifecycle?

A

Assembled in intestinal mucosal cells rough ER and Golgi apparatus. NAscent CM with Apo B48 is released, where it picks up Apo C2 and Apo E from circulating HDL. CM enters the capillary, where LPL breaks down TAGS into free glycerol and free fatty acids. Now, Apo C2 is returned to HDL in circulation and chylomicron remnants are endocytosed into the liver with the help of Apo E.

93
Q

VLDL lifecycle?

A

Made in smoother ER and Golgi apparatus of the liver. They contain cholesterol and cholesterol esters. Nascent VLDL is secreted by the liver into the blood, where it picks up Apo C2 and Apo E from circulating HDL. It enters the capillary, where extracellular lipoprotein lipase breaks down the TAGS in VLDL. Once TAGS are broken down, we are left with the intermediate IDL, which returns Apo C2 and Apo E to circulating HDL. Once those apoproteins are gone, we are left with LDL that is taken up by the liver with the help of Apo B100 by the LDL receptor.

94
Q

HDL Lifecycle?

A

Made by the liver and intestines. HDL functions as a circulating reservoir for Apo C2 and Apo E. Also functions in taking up cholesterol from tissues and returning then to the liver as cholesterol esters.

95
Q

What can down-regulate LDL receptors?

A
  1. Decreasing expression of the LDL receptor gene. Less receptor means less cholesterol uptake.
96
Q

What is the role of the ACAT enzyme?

A

Cholesterol that is not required immediately will be esterified by ACAT. This allows the body to store cholesterol as cholesterol esters which decreases the cell supply of cholesterol. ACAT also increases its activity when cholesterol levels increase.

97
Q

What is the role of the enzyme LCAT?

A

LCAT is the enzyme that immediately esterifies cholesterol taken up from tissues by HDL. LCAT is made by the liver. It is activated by Apo A1.

98
Q

What are the eight steps in the formation of atherosclerotic plaque?

A
  1. In response to injury, endothelial cells try to repair themselves by attracting immune cells.
  2. More and more helps come and tries to repair this blood vessel, but it isn’t working. Lymphocytes and monocytes start to migrate deep into the extracellular matrix, where more recruitment takes place.
  3. Cytokines and macrophages begin to attach to the vascular wall.
  4. Cytokines call for even more recruitment. Monocytes are directed into the inner layer of the wall.
  5. Monocytes differentiate into macrophages and take up lipid-rich LDL by endocytosis. They continue to engulf all this cholesterol until they are called foam cells. They are called foam cells because they are macrophages full of LDL cholesterol. Heavy contributor to fatty streaks and plaque formation.
  6. Cytokines attract more monocytes into the intima and media layers of the vessel. The process continues as a fibrous cap is formed from smooth muscle cells. These cells migrate past the intima and go into the lumen and begin to proliferate to contain the original inflammation.
  7. These smooth muscle cells produce extracellular proteins, collagen and elastin, which all contribute to the formation of the fibrous cap that covers the plaque. Monocytes and macrophages begin to die in the center leaving a necrotic core.
  8. Eventually, the vessel wall can no longer expand. The fibrous cap begins to crack, and multiple of these cracks contribute to a plaque rupture. When the rate of cracking surpasses the rate of repair, plaques rupture and clots form.
99
Q

What are the three layers of a blood vessel?

A
  1. Tunica intima- innermost layer composed of endothelial cells
  2. Tunca media- middle layer where the largest percentage of smooth muscle is located
  3. Tunica adventiti- most outer layer
100
Q

Where are macrophages and foam cells derived from?

A

Monocytes differentiate into macrophages. Foam cells are macrophages that have ingested LDL cholesterol.

101
Q

What is the significance of the scavenger receptors on macrophages?

A

Scavenger activity mediates the endocytosis of chemically modified LDL in which lipid components or Apo B have been oxidized. Scavenger receptor is not down regulated, and because of this, they turn into foam cells.

102
Q

What comprises a fibrous cap?

A

Smooth muscle cells producing extracellular proteins, collagen, and elastin.

103
Q

How does the necrotic core form?

A

Macrophages and monocytes involved in the original reaction die and result in necrotic tissue.

104
Q

What are three examples of factors that can cause endothelial damage?

A

Hypertension, dyslipidemia, oxidized LDL

105
Q

What role does HDL have in modifying plaque formation and development?

A

HDL opposes atherosclerosis directly by removing cholesterol from foam cells, inhibiting the oxidation of LDLs, and limiting the inflammatory processes that underlie atherosclerosis.

106
Q

How do saturated fats, trans fat, and cholesterol contribute to the risk of atherosclerosis?

A

Saturated fat intake increases LDL cholesterol when compared to other nutrients except for trans fat. Saturated fats increase LDL cholesterol by inhibiting LDL receptor activity and enhancing Apo B100 which continues lipoprotein production.

107
Q

What is insulin resistance?

A

Insulin resistance is the decreased ability of target tissue to respond properly to normal/elevated glucose levels. Characterized by uncontrolled hepatic glucose production and decreased glucose uptake by tissues.

108
Q

How are serum insulin and glucose levels reflected in an insulin-resistant state?

A

Glucose levels in the blood tend to be similar to a normal person. Higher insulin levels are required to control the blood glucose levels in an IR-obese individual.

109
Q

What effect does insulin have on adipose, liver, and muscle tissues under normal and abnormal conditions? Be specific about HSL, LPL, and glut 4 receptors.

A

Under normal conditions, insulin secreted in response to glucose levels will decrease lipolysis and glucose production by inhibiting HSL, glycogen synthase, glycogen phosphorylase, PFk-2, and F26BP. It will also increase glucose uptake from the blood into tissue via GLUT 4 receptors.

Under abnormal conditions, the pancreas loses its ability to compensate and begins to fail. Cells will also begin to ignore the insulin signal to take up glucose. There is now less insulin signalling causing an increase in lipolysis, glucose output, and a decrease in glucose uptake. The blood is now filled with free fatty acids and glucose. This is called lipotoxicity and glucotoxicity. These are the two factors that lead to beta cell dysfunction.

110
Q

Why is insulin binding to its receptor and the resulting phosphorylation cascade critical to lowering blood glucose levels to normal?

A

When insulin binds to its cell surface receptor, there is a stimulation of cascade of cell signalling that includes the phosphorylation of insulin receptor residues (IRS). Insulin promotes the recruitment of insulin-sensitive glucose transporter called GLUT4 to the cell surface.

111
Q

What are the metabolic changes that occur that lead to lipotoxicity and glucotoxicity?

A

These are the major contributors that drive beta cell dysfunction.
Enlarged adipocytes become less sensitive to insulin which leads to increased blood glucose levels because GLUT4 receptors are not coming to the cell surface. The action of HSL increases, which increases plasma-free fatty acids because HSL keeps breaking down stored fat. In the liver, FFA and decreased glucose utilization trigger fasted state processes like gluconeogenesis in the liver. This increases blood glucose levels even more. This leads to increased chylomicrons and VLDL. In muscles, FFA is taken up and stored as TAGs.

112
Q

What pathways are catabolic?

A

Catabolism is the breakdown of larger molecules into smaller molecules. These processes create energy. They oxidize nutrients and create reducing agents.

Glycolysis, Kreb’s Cycle (Both), Oxidative phosphorylation, beta-oxidation of fatty acids, urea cycle, glycogenolysis and lipolysis

113
Q

What pathways are anabolic?

A

Anabolism is the buildup of smaller molecules to form a larger molecule. They require reducing agents and invests energy.

Kreb’s cycle (Both), Pentose Phosphate Pathway, Gluconeogenesis, fatty acid synthesis, glycogenesis

114
Q

Which pathways are on in the FED state?

A

Glycolysis in extrahepatic tissues (always on basically though), glycolysis in the liver, Glycogen synthesis, Fattu acid synthesis, Cholesterol synthesis, and protein synthesis.

115
Q

Which pathways are on in the FASTED state?

A

Gluconeogenesis, glycogen breakdown, beta-oxidation, and ketogenesis (carb starved)

116
Q

What is oxidized LDL?

A

This occurs when LDL is abundant in circulation and begins to interact with free radicals becoming pro inflammatory molecules.

117
Q

Start and end products of glycolysis? (aerobic)

A

Invest 1 glucose and 2 ATP
End with 2 pyruvates, 2 NADH, and 2 ATTP

118
Q

Start and end products of glycolysis? (anaerobic)

A

Invest 1 glucose
End with 2 lactate, 2 ATP, and 0 NADH

119
Q

Start and end products of gluconeogenesis?

A

Start with glucogenic amino acids, pyruvate, lactate, or glycerol
End with glucose

120
Q

Start and end products of glycogenesis?

A

Start with glucose-6-phosphate
End with glycogen

121
Q

Start and end products of glycogenolysis?

A

Start with glycogen
End with free glucose and glucose-1-phosphate

122
Q

Start and end products of fatty acid synthesis?

A

Start with acetyl CoA turned to Malonyl CoA, 1 NaDPH, and 1 ATP
End with 16-C Palmitic acid

123
Q

Start and end products of beta-oxidation?

A

Start with fatty acid palmitic acid
End with 8 Acetyl CoA, 7 NADH, and 7 FADH2

124
Q

Start and end products of ketogenesis?

A

Start with acetyl CoA
End with Ketone bodies

125
Q

Start and end products of cholesterol synthesis?

A

Start with Acetyl CoA
End with cholesterol

DHN 311 (2 decks)

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