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DENTFN 510 Fall 21 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

2 monosaccharides that make up sucrose?

A

Glucose and Fructose

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2
Q

2 monosaccharides that make up lactose?

A

Galactose and glucose

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3
Q

2 monosaccharides that make up maltose?

A

2 glucoses

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4
Q

Oligosaccharides?

A

3-10 monosaccharides

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5
Q

Polysaccharide?

A

More than 10 monosaccharides
Mostly storage
Linear and branched

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6
Q

What is starch made of and how is it linked?

A

Glucose

With alpha 1-4 glycosidic bonds

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7
Q

What catabolizes starch?

A

Amylase

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8
Q

What is glycogen made of and how is it linked?

A

Glucose
Linear links are alpha 1-4
Branches are alpha 1-6

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9
Q

Where is glycogen stored in humans and animals?

A

Liver and muscles

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10
Q

What is inulin?

A

Polymer of fructose
Found in onions and garlic
Water soluble
Not absorbed into blood and not secreted

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11
Q

Inulin is used for?

A

Determining glomerular filtration rate ie kidney function

Injected into bloodstream

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12
Q

What glycosaminoglycans ie GAGs?

A

Repeating disaccharide units with acidic sugar(COOH) and an amino Acetyl sugar.

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13
Q

GAGs are found where and one of their functions?

A

Cell surface or ECM
Long chains found in mucous and fluids around joints
Important structural components
Negatively charged and attract water to provide cushioning for structures

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14
Q

What bond can amylase not digest?

A

Alpha 1-6 glycosidic bonds

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15
Q

What is a source of glucose during hypoglycemia?

A

Liver glycogen

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16
Q

Major components of ECM?

A

Collagen and elastin

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17
Q

Another name for GAGs?

A

Mucopolysaccharides

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18
Q

List 6 major types of Mucopolysaccharides aka GAGs (glycosaminoglycans)?

A 
Chondroitin Sulfate
Hyaluronic Acid
Heparin Sulfate
Heparin
Dermatan sulfate
Keratan sulfate
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19
Q

Location of chondroitin sulfate?

A

Cartilage, bone, aorta, ligaments

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20
Q

Location of hyaluronic acid?

A

ECM, synovial fluid and vitreous humor

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21
Q

Location of heparan sulfate?

A

Basement membrane

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22
Q

Location of heparin?

A

Mast cell granules and anticoagulant

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23
Q

Location of dermatan sulfate?

A

Skin, blood vessels, and heart valves

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24
Q

Keratin sulfate location?

A

Cornea, cartilage, bone

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25
Q

2 GAGs involved with Hurler Syndrome?

A

Heparin and Dermatan sulfate

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26
Q

2 GAGs involved with Hunter Syndrome?

A

Heparan sulfate and Dermatan sulfate

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27
Q

What are proteoglycans?

A

Structural polysaccharides located in ECM
They are GAG tails attached to a protein core that is rich in serine and threonine

Each Proteoglycan then attaches to hyaluronan molecule via linker protein

Proteoglycan plus collagen = Cartilage

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28
Q

Cellulose?

A

Glucose monomers in long chains link by beta 1-4 glycosidic bonds
Found in plants and can’t be digested by humans although they do provide fiber which is useful in our digestion to keep things moving

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29
Q

What is chitin?

A

Structural poly saccharide found in exoskeletons of Arthropoda and fungal cell walls

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30
Q

4 steps in starch digestion?

Where and what?

A
  1. Mouth- Salivary amylase hydrolyzes alpha 1-4 bonds
  2. Stomach- high acid inactivates amylase and stops carb digestion temporarily
  3. Duodenum aka top of small intestine pancreatic alpha amylase continues breaking alpha 1-4 bonds
  4. Upper jenjunum mucosal lining processes the breaking of alpha 1-6 branch link
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31
Q

Lactose digestion?

Remember beta 1-4 linkage of galactose and glucose

A

Lactase in small intestine

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32
Q

If a person is lactase deficient what happens? Or what happens if any disaccharide reaches large intestine and colon?

A

They draw water in to intestine colon.
Bacteria break lactose down/ferment it in large intestine producing H2, lactic acid, CO2 and two carbon metabolites like acetic acid.
Gas and diarrhea

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33
Q

What are glucans and fructans?

A

Polysaccharides made by bacteria using glusosyltransferase or fructosyltransferase

Glucan makes up 10-20% of plaque

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34
Q

What is dextran?

A

Branched glucan that modulates bacterial adhesion

Aka
Glucans glue other bacteria’s like s mutans to teeth!!!!

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35
Q

What is an important bacterial made polysaccharide other that glucans or dextrans?

A

Levan

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36
Q

How is levan catalyze/made?

And what does it do?

A

Made by reaction with levansucrase.

Makes plaque by contributing to ecpm aka extracellular polysaccharide matrix

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37
Q

3 examples of complex carbs and what are complex carbs?

A

Sugars with proteins, lipids, enzymes with diverse functions

  1. Glycoproteins
  2. Saliva
  3. Glycolipids
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38
Q

Alternate name for glycolysis?

A

Embden-Meyerhof Pathway

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39
Q

Alternate names for citric acid cycle?

A

Krebs Cycle

TCA (tricarboxylic acid) cycle

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40
Q

Alternate name for Pentose Phosphate Pathway?

A

Hexose monophosphate shunt

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41
Q

Alternate name for Cori Cycle?

A

Lactic Acid Cycle

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42
Q

Alternate name for electron transport chain ie ETC?

A

Respiratory Chain

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43
Q

Livers role in glycogen storage?

A

Maintains steady blood glucose levels
Glucose is stored in liver during fed state and released from liver between meals

High insulin stimulates storage as glycogen and suppresses glucagon
Insulin also stimulate glucose uptake into muscles, fat cell and kidney etc
Glucagon stimulates breakdown of liver glycogen

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44
Q

Low blood sugar stimulates what to be released from pancreas?

A

Glucagon which stimulates glycogenolysis in liver

Breakdown of glycogen to glucose to be released in blood

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45
Q

What happens when liver runs out of glycogen to use for glycogenolysis and blood sugar is still low?

A

Body’s saves sugars for brain and RBCs and makes ketones from lipids via ketogenesis

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46
Q

What stimulates ketogenesis to begin?

A

Low levels of insulin and glucose

Starving state

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47
Q

What are ketones?

A

Alternative fuel made from lipids used by muscles and body organs

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48
Q

What is the pancreas’s roll in maintaining blood sugar?

A

Releases either insulin or glucagon depending on level of glucose in blood

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49
Q 
Type one diabetes 5 major characteristics-
Age onset
Nourishment state at onset
Genetic predisposition 
Defect or deficiency 
Treatment
A
  1. Rapid childhood or puberty
  2. Often undernourished
  3. Moderate
  4. Beta cells destroyed no insulin production
  5. Always treated with insulin
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50
Q

Type two diabetes 5 major characteristics-

  1. Age onset
  2. Nourishment state at onset
  3. Genetic predisposition
  4. Defect or deficiency
  5. Treatment
A
  1. After 35, gradually develops
  2. Usually obese
  3. Strong genetic link
  4. Resistant to insulin and beta cells can’t produce enough insulin
  5. Lifestyle, potentially insulin and other hypoglycemic drugs and blood pressure control
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51
Q

What are beta cells?

A

Cells in pancreas islets of Langerhans that produce and release insulin

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52
Q

What is GLUT1 function, Km and location?

A

Basal uptake of glucose
1mM Km aka high affinity
Found in plasma membrane of most cells
Maintains basal or continuous base rate of glucose uptake for cells

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53
Q

GLUT2 transporters function, Km and location?

A

Found in the liver and pancreatic tissues
Liver they take up and release glucose
Pancreas they function as the beta cells glucose sensor
Km is 15 aka low affinity meaning glucose needs to be high for these to function

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54
Q

GLUT3 transporter location Km and function?

A

Found in most tissues
1Km = high affinity
Maintains basal rate of uptake and transports glucose in neuronal tissues including brain

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55
Q

GLUT4 transporter location, Km and function?

A

Skeletal muscles and adipose tissue
5 Km = medium affinity
Insulin stimulated glucose uptake in skeletal muscle and cardiac muscle to store glucose in muscles
Adipose tissues uptake and convert glucose to triglycerides for storage

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56
Q

What are pancreatic alpha cells?

A

They produce glucagon and are located in the islets of langerhans

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57
Q

How are glucagon and insulin balanced?

A

The release of insulin from pancreatic beta cells inhibits glucagon release from alpha cells and the pancreas regulates both of them which are released from islets to maintain balance of glucose in blood from either liver and or food intake and needs of the body for glucose

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58
Q

Describe the process of a Pancreatic beta cell exposed to blood glucose from carb rich foods?

A
  1. GLUT2 transporter (only active in high glucose aka high Km and low affinity) takes up glucose
  2. Glucose phosphorylated to glu-6-phosphate by Hexokinase IV aka glucokinase
  3. G6P goes into glycolysis and ETC to make ATP
  4. ATP used trigger signal pathway to make insulin which is secreted to blood
  5. Insulin in blood triggers uptake of glucose by muscles and adipose tissues to store it.
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59
Q

What happens when there is a mutation of Hexokinase IV/Glucokinase?

A

First step in glycolysis in pancreatic beta cells doesn’t happen and-
It doesn’t transfer the signal that glucose is high thus less insulin is made resulting in hypoglycemia…. Happens in Type II diabetes

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60
Q

2 things that normally happen when there is high sugar/carbs?

A

GLUT2 transporters in both liver and pancreas start to work to uptake glucose.

  1. Liver stores glucose as glycogen
  2. Pancreas releases insulin to signal muscles and fat to uptake and store glucose
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61
Q

What happens to monosaccharide sugars in the small intestine/jejunum?

A

Taken up by transporters
GLUT5- Fructose
SGLT1- Glactose and Glucose

All are the sent to circulation via GLUT2 transporter

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62
Q

What happens to disaccharide sugars in the small intestine/jejunum?

A

Alpha 1-6 bonds broken down to monosaccharides by brush border disaccharidases.

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63
Q

In what parts of the body is aerobic glucose metabolism important?

A

Heart, brain, skeletal muscle fibers

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64
Q

Where may glycolysis occur anaerobically?

A

Erythrocytes and exercising skeletal muscle

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65
Q

Where does glycolysis happen?

A

In cytosol

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66
Q

3 main fates of pyruvate after glycolysis and 2 minor ones?

A

Major-

  1. Most normal Aerobic- Acetyl CoA to Krebs/TCA
  2. Anaerobic aka exercise when O2 is low in muscles- to Lactate
  3. in low glucose/fasting state to Oxaloacetate to gluconeogenesis to make glucose for brain

Minor-

  1. To alanine by transamination to use up excess nitrogen
  2. To ethanol via fermentation In microorganisms koi
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67
Q

What happens to lactate when it is made in anaerobic exercise conditions?

A

When NADH is high in muscles, pyr to lac favored
Lactate builds up in muscle causing intercellular pH to drop
Lactate diffuses into blood and goes to liver to make pyruvate and into gluconeogensis

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68
Q

What does pyruvate dehydrogenase complex do and what is it?

A

Makes pyruvate into Acetyl CoA so it can enter the Citric Acid Cycle or used to make fatty acids, steroids or ketone bodies (lipid metabolism)
It is irreversible

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69
Q

What are cofactors needed for pyruvate dehydrogenase?

A 
Thiamine pyrophosphate
Coenzyme A
Lipoate (form of Lipoic Acid)
FAD
NAD+
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70
Q

What happens in arsenic poisoning?

A

Arsenite binds to lipoic acid and inhibits PDH from making Acetyl CoA

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71
Q

What is another name for thiamine?

A

Vitamin B1

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72
Q

What is a disease caused by low thiamine?

A

Beriberi
Which leads Wernicke-Korsakoff syndrome in severe cases

Thiamine needed by PDH complex to convert pyruvate to Acetyl CoA not made

73
Q

Symptoms of Beriberi

A

Abnormalities in peripheral nervous system like numbness or reflexes
Painful weak muscles
Enlarged heart

74
Q

Wernicke-Korsakoff syndrome symptoms?

A

Apathy
Loss of memory
Rhythmical back and forth with eyes
Confusion->coma-> death

75
Q

Where do carbs, amino acids and fatty acids converge?

A

Citric Acid Cycle

76
Q

What is the main function of the citric acid cycle?

A

To provide intermediates (GTP, FADH2, NADH)needed for ETC and ATP production

77
Q

What is a secondary function or the citric acid cycle/krebs?

A

Provide intermediates for for other reactions such as making amino acids

78
Q

Krebs cycle score card?

A

1 glucose = 2 pyruvate = 2 turns of the cycle = 2 GTP, 2 FADH2, 6 NADH

Those are fed into ETC to make a total of 24 ATP

79
Q

Where does the Citric Acid Cycle take place?

A

In the mitochondrial matrix
Remember small molecule diffuse across pore in the outer membrane
Inner membrane is tight and has transporters

80
Q

4 intermediates in TCA cycle page she pointed out and what the do?

A

Citrate- shuttles Acetyl CoA to cytoplasm for fatty acid synthesis

Succinyl-CoA - used for heme synthesis and activating ketone bodies

Malate- Malate shuttle used to transfer oxaloacetate out of mitochondria during gluconeogenensis

Alpha-ketoglutarate- used for AA synth

81
Q

What is final product of TCA?

A

Oxaloacetate

82
Q

What is the pentose phosphate pathway and it’s purpose?

A 
Uses glucose and run parallel.
Makes NADPH (irreversible) and a 5 carbon sugar ribose for nucleotide synthesis (irreversible)
83
Q

Where does the pentose phosphate pathway take place?

A

Cytosol

84
Q

The irreversible pentose phosphate pathway?

A

Oxidative

Uses glucose-6-phosphate to make NADPH for use in fatty acid synth, glutathione reduction and detoxification reactions

85
Q

The reversible pentose phosphate pathway?

A

Non-oxidative

Uses fructose 6 phosphate or glyceraldehyde 3 phosphate to make ribose for nucleotides

86
Q

Tissues where the pentose phosphate pathway is active?

A

Liver, adipose, adrenal cortex, thyroid, mammary glands and erythrocytes

87
Q

Tissues where the ppp is not very active?

A

Muscle and brain where almost all glucose is used in glycolysis

88
Q

What is the only source of glutathione in red blood cells and what does it do?

A

G6PD via the irreversible oxidative PPP pathway

Glutathione eliminates free radicals in RBCs

89
Q

What is G6PD deficiency and what are the symptoms?

A 
Genetic disorder occurring mostly in males
RBCs break down prematurely leading to:
Hemolysis 
Hemolytic anemia
Jaundice
90
Q

What is the Entner-Doudorof Pathway?

A

Alternative to glycolysis used by bacteria

91
Q

Gluconeogenesis?

A

Uses lactate/lactate dehydrogenase or Alanine/ALT (alanine aminotransferase) to make pyruvate to make oxaloacetate to do reverse glycolysis and make glucose for brain in times of low glucose and starvation/fasting state

Also uses glycerol

92
Q

Where does gluconeogenesis happen?

A

In the liver

Starts in mitochondria where pyruvate is converted to oxaloacetate

93
Q

Cori Cycle composition and purposes?

A

Lactic Acid cycle
Uses lactic acid to connect glycolysis and gluconeogenesis

Rapid source of ATP in muscles during high activity

Prevent lactic acidosis by moving lactate out of muscle into liver

94
Q

Summarize Cori Cycle reactions?

A

In muscles:
Glucose-> glycolysis makes 2 ATP
Ends up with 2 pyruvate
Low O2 = no terminal receptor for ETC so makes 2 Lactate
Which diffuse into blood and go to liver
2 Lactate-> 2 pyruvate-> uses 6 ATP to make glucose release back into blood to go back to muscles
Not very efficient!

95
Q

Glycogenesis and glycogenolysis?

A

Stores glucose as glycogen and breaks the glycogen down
All happens in liver and muscle
Storage enzyme Glycogen Synthase activated by insulin
Breakdown enzyme phosphorylase inhibit by insulin

96
Q

Glycogenolysis helps with what?

A

Immediate energy in muscles during exercise when not enough Glucose and O2 can be delivered by blood

Liver glycogen provides energy during hypoglycemia

97
Q

Sources of glucose?

A

Food to blood stream
Glycogen storage in liver and muscles
Gluconeogenesis in liver

98
Q

Another names for ETC and purpose of it?

A

Oxidative phosphorylation
Make ATP
Creates a proton gradient uses O2 as final electron acceptor to make ATP

99
Q

Name 3 inhibitor/uncouplers of ETC/oxidative phosphorylation?

A

Cyanide- binds irreversibly to cytochrome
CO- binds to cytochrome and hemoglobin and myoglobin less O2 for ETC
Aspirin/ 2-4 dinitrophenol- decreases proton gradient

100
Q

What happens in ETC oxidative phosphorylation uncoupling?

A

ATP synth disrupted,

In hypoxia glycolysis increase to meet ATP needs, since no O2 glycolysis makes lactate leading to lactic acidosis

Nerves and cardiac muscles can’t meet ATP needs this way
Disaster! Membrane potential collapses, enzymes leak, lactic acidosis, protein precipitation and coagulation necrosis = myocardial infarction

101
Q

Von Gierke disease GSD type?

A

GSD 1

102
Q

Von Gierke enzymes affected?

A

1a is glucose 6 phosphatase

1b is glucose 6 phosphate translocase

Both affect glycogen breakdown and lead to low blood sugar

Affects liver and kidneys

103
Q

Pompe disease GSD type?

A

Type II

104
Q

Pompe Disease enzymes affected?

A

Alpha-glucosidase
Breaks alpha 1-4 glycogen bonds
Leads to build up of glycogen in tissues
Liver heart skeletal muscle lysosomes

105
Q

Cori disease GSD type?

A

GSD Type III

106
Q

Cori Disease enzyme affected?

A

Mutation in AGL gene which codes for Glycogen Debranching Enzyme for the 1-6 bonds

Causes buildup of glycogen in liver and muscles

107
Q

Andersen GSD type?

A

GSD Type IV

108
Q

Andersen affected enzyme?

A

Deficiency in glycogen debranching enzyme

Causes glycogen to build up and impairs function of some organs especially the liver and muscles

109
Q

McArdle disorder GSD type?

A

Type V

110
Q

McArdle disease affected enzyme?

A

Muscle glycogen phosphorylase ie myophosphorylase

Affects breakdown of glycogen in muscles

111
Q

Hers disease GSD type?

A

GSD type VI

112
Q

Hers disease enzyme affected?

A

Hepatic glycogen phosphorylase

Can’t break down liver glycogen

113
Q

Name 2 mucopolysaccharide diseases?

A

Hunter and Hurler syndromes

114
Q

Hunter versus Hurler severity?

A

Hunter less severe but more aggressive

115
Q

Hunter type and affected GAGs?

A

Mucopolysacchardosis Type II

Affects heparan sulfate and Dermatan sulfate

116
Q

Hunter clinical features?

A 
Affects young males 
Macrocephaly 
Thick lips and gingiva
Broad nose and flared nostrils
Protruding tongue
Abnormal bone skin size
No corneal clouding
117
Q

Hunter inheritance pattern?

A

X-linked recessive

118
Q

Hurler inheritance pattern?

A

Autosomal recessive

119
Q

Hurler type and affected GAGs?

A

Mucopolysaccharidosis type I

Affected GAGs heparin sulfate and Dermatan sulfate

120
Q

Hurler clinical features?

A

Development delay, cognitive impairment, enlarge tissues and organs from GAGs accumulation in lysosomes, macrocephaly, macroglossia, enlarge liver and spleen, corneal clouding, thicken gingival and flat nasal bridge, flared and upturned nose
Large mouth and lips
Pitted hypoplastic primary teach
Narrow dentinal tubules
Micro gaps in enamel dentin junction
Cyst like lesions that destroy bone of unerrupted permanent teeth

121
Q

4 Lipid functions?

A

Cellular structure
Metabolism
Transport of nutrients
Energy storage

123
Q

3 types of lipids?

A

Triglycerides aka fat
Phospholipids
Steroids

124
Q

Components of triglyceride?

A

Glycerol backbone with 3 fatty acid tails

125
Q

3 types of lipids in membranes?

A

Phospholipids, glycolipids, sterols

126
Q

4 Types of phospholipids and where they are found?

A

Phosphatidycholine- membrane
Spingomyelin- membrane and nerve tissue
Lecithin-membrane
Cephalins- nerve tissue

127
Q

Glycolipid function?

A

Membrane stability

128
Q

Sterol functions?

A

Precursor for steroids bile salts sex hormones and vit D

Also membrane fluidity/stability regulation

129
Q

Differences between trans and cis unsaturated fats and saturated?

A

Saturated is solid at room temperature
Cis unsaturated has more double bonds and bent tails, liquid at room temp lower LDL and increase HDL

Trans not natural and solid at room temp

135
Q

Name two essential fatty acids?

A

Linolenic acid

Linoleic acid

136
Q

Essential fatty acid function and what a deficit can lead to?

A

Structural component of cell membrane

Deficiency leads to scaly dermatitis- inability to provide water barrier in skin and loss of water

137
Q

Linolenic Acid?

A

Precursor to omega 3
FroM salmon
Reduces TAGs aka triglycerides, prevents blood clots by lowering thromboxane

138
Q

Linoleic Acid?

A

Precursor to Omega 6
Found in nuts and seeds
Lowers HDL and LDL

139
Q

2 conditionally essential fatty acids?

A

Oleic acid

Arachidonic Acids

140
Q

Oleic Acid?

A

Body makes a small amount so must get from food

141
Q

Arachidonic Acid?

A

Precursors to prostaglandin synthesis and eicosanoids

Only needed if there is deficiency in linoleic acid or lack of conversion from linoleic to arachidonic

142
Q

What starts fatty acid synthesis and why?

A

Citrate transported from mitochondria to cytoplasm via citrate shuttle

In high energy/ATP state step TCA cycle not needed to make products for ETC and Isocitrate dehydrogenase inhibited. This is rate limiting step and slows/stops TCA causing citrate to leave for FA synthesis

143
Q

2 step in fatty acid synthesis?

A

Citrate is turned into Acetyl CoA and Oxaloacetate by ATP Citrate Lyase

144
Q

3rd step in Fatty Acid synthesis?

A

Acetyl group plus Malonyl group make Palmitate the most common FA

This is what happens to excess carbs in fed state, they get stored as fat

145
Q

Triglyceride functions?

A

Energy source
Stores in adipose tissues
Transported in plasma by lipoproteins
Increase in them is linked to atherosclerosis, heart disease and stroke

146
Q

How are eicosanoids derived?

A

In response to hormones or cell damage- Phospholipase A2 releases arachidonic acid from plasma membrane phospholipids

147
Q

What is a major eicosanoid production pathway and what does is make?

A

COX (cyclooxygenase) pathway

Makes prostaglandins prostacyclin and thrombaxanes

148
Q

Prostaglandins are involved in what and what inhibits the pathway to make them?

A

Vasodilation, inflammatory pain

NSAIDs (aspirin, Advil, naproxen) inhibit Cox pathways blocking their formation

149
Q

Where are bile salts formed?

A

From cholesterol in liver

150
Q

What do bile salts do?

A

Aid in lipid absorption by emulsifying fats

151
Q

What happens to bile salts?

A

Reabsorbed in ileum and returned to liver

Extra is stored in gall bladder

152
Q

What happens to bile salts in CF patients?

A

Thickening of mucous barrier in intestine blocks bile salt reassorbtion and causes bile salt loss in feces

153
Q

What else go wrong in CF patients other than bile salts being excreted regarding Lipid metabolism?

A

Pancreatic ducts get clogged and enzymes can’t reach intestine.
Only digest fats with lingual and gastric lipases

154
Q

5 classifications of Lipoproteins?

A 
Chylomicron 
Bad ones-
VLDL-Very low density lipoprotein 
IDL- intermediate density lipoprotein
LDL- low density lipoprotein 
Good one
HDL- high density lipoprotein
155
Q

Steps in fat digestion?

A
  1. Triglycerides and cholesterol broken down to free cholesterol and free FAs and monoglycerides
  2. All those are solubilized by bile salts and transported to microvilli and absorbed
  3. Reassembled into triglycerides and cholesterol which then are made into chylomicrons
156
Q

What happens to chylomicron after it is made by intestine mucosa?

A
  1. Chylomicrons are secreted to lymph and blood systems
    They have apo CII on their surface

2 When they reach tissues like adipose and muscles the Apo CII activates Lipoprotein lipase to break them down

3 Chylomicron remnants get sent to the liver and Te ie Ed by the remnant receptor

157
Q

What happens in case of Lipoprotein Lipase or Apo CII deficiency?

A

Chylomicrons accumulate in plasma triglycerides not degraded and increase risk of acute pancreatitis aka inflammation of the pancreas and abdominal pain

158
Q

How are VLDLs made and what do they do?

A

Made in liver from chylomicrons remnants or synthesized

Carry endogenous triglycerides to peripheral tissues

159
Q

Do VLDLs have Apo CII on surface?

A

Yes when they mature from nascent VLDL into mature one they pick up Apo CII, Apo E and cholesteryl

160
Q

What happens to VLDLs when they reach tissues?

A

Apo CII activates LPL (lipoprotein lipase) which releases fatty acids, Apos and phospholipids which can make HDL

Remnant is IDL

Some IDL get picked up by ApoE receptor in liver
Some IDL stays in blood and get broken down to LDL

161
Q

What happens when there is and imbalance in liver triglycerides synthesis and VLDL synthesis?

A

Non alcoholic fatty liver

162
Q

Nonalcoholic fatty liver often happens in what two diseases?

A

Obesity and type II diabetes

163
Q

How are LDLs made and what do they do?

A

Made from remnants of VLDLs and IDLs

They are cholesterol rich and deliver cholesterol to tissues

164
Q

What happens to LDLs?

A

1/2 cleared by liver picked up by hepatic LDL receptors and the rest are picked up by scavenger LDL receptors in blood and plasma systems

165
Q

What happens when cholesterol is high?

A

Scavenger receptors are NOT down regulated and they pick up cholesterol esters and lead to plaque formation in arteries

166
Q

2 things HDL does?

A
  1. Transports cholesterol from peripheral tissues to other cell, other lipoproteins, or to liver to clear
  2. Is a circulating reservoir for apo lipoproteins
167
Q

How is cholesterol made?

A

Acetyl CoA from beta oxidation make HMG CoA

HMG CoA reductase which is activated by insulin and inhibited by glucagon and statins converts HMG CoA to Mevalonate which then goes through a few more steps to make cholesterol

168
Q

Where is cholesterol made?

A

All tissues but mainly liver, intestine and reproductive tissues

169
Q

What happens when sterol levels are low?

A

Transcript factor up-regulates HMG CoA reductase synthesis so more cholesterol can be made

170
Q

How are triglycerides broken down in adipose tissue?

A

By lipase into glycerol and FAs

Glycerol sent to liver

FAs transported out of adipose tissue to tissues where needed where beta oxidation happens to make Acetyl CoA

171
Q

What enzymes breaks down glycerol in liver and what does it turn into?

A

Glycerol kinase makes glycerol 3 phosphate which then is transformed to Glucose 6 Phosphate by plugging it into gluconeogenesis

172
Q

Another name for beta oxidation?

A

Fatty Acid Spiral

173
Q

What does beta oxidation do and when is it active?

A

Makes Acetyl CoA froM FAs to plug into the Citric Acid Cycle to make energy

It is active in low energy times

Insulin stimulates fatty acid synthesis and storage

174
Q

How does beta oxidation work?

A

Free FAs taken up by cells that need energy

They are transformed to Acyl CoA which is transported into mitochondria via the Carnitine shuttle as Acylcarnitine then separated and oxidized to Acetyl CoA

175
Q

What does the presence of Acetyl CoA from beta oxidation stimulate?

A

It activates pyruvate dehydrogenase which stimulates gluconeogenesis

176
Q

3 potential fates of Acetyl CoA?

A
  1. TCA cycle and ATP energy
  2. HMG CoA which can take two different pathways ketone bodies or cholesterol
  3. Fatty Acid Synthesis and storage via malonyl CoA
177
Q

2 fates of HMG CoA?

A

Cholesterol synthesis via HMG CoA lyase

Or Ketone body synthesis with HMG reductase

178
Q

What conditions trigger ketone body synthesis and what tissues can use them?

A

Fasting/starving state or diabetes mellitus
Liver makes them from Acetyl CoA
Skeletal and cardiac muscle use them first

After ~3 wks brain will metabolize them and muscles will stop using them as much (small molecules so they can cross blood brain barrier)

179
Q

3 types of ketone bodies?

A

Acetoacetate

Can make

Acetone (spontaneous and dead end)or

3-hydroxybutyrate

180
Q

Acetoacetate and 3-Hydroxybutyrate ketone body fates?

A

Transported by blood to tissues and converted back to Acetyl CoA and used inTCA cycle

181
Q

What is spared during ketogenesis and how?

A

Protein
Pyruvate dehydrogenase blocked

Also no glucose uptake in brain

182
Q

Ketoacidosis causes?

A

Low insulin high glucagon and epinephrine
FAs released from adipose tissues and excessive ketone synthesis

Also can be caused by infection or trauma from increased epi

183
Q

Signs and symptoms of ketoacidosis?

A

Osmotic dieresis leads to dehydration’s and electrolyte imbalances = excessive thirst and frequent urination

Plasma pH level less than 7.3

Fruity odor on breath due to acetone production

Death

184
Q

Why can’t liver use ketones for energy?

A

No thiophorase to convert ketone bodies to Acetyl CoA

Probably to prevent a useles cycle of liver making and using ketones

185
Q

Name 5 lipid metabolic diseases?

A 
Gauchers 
Niemann-pick
Tay-Sachs
Fabry’s
Krabbe’s

DENTFN 510 Fall 21 (5 decks)

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