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Metabolism/Nutrition > Block 2 > Flashcards

Block 2 Flashcards

1
Q

is gluconeogenesis fast or slow to maintain blood glucose

A

slow

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2
Q

what is a rapidly mobilizable source of glucose

A

glycogen

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3
Q

what enzyme decides if the organ is involved in releasing glucose into the blood

A

glucose 6 phosphatase

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4
Q

glucose is stored in the form of __

A

glycogen

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5
Q

what is the main type of bond in glycogen

A

alpha 1,4-glycosidic (straight line)
*also have alpha 1,6- at branch points

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6
Q

glucose is stored as glycogen mostly in what 2 cells

A

liver and muscle

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7
Q

muscle uses glycogen for what

A

energy for itself

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8
Q

liver uses glycogen for what

A

blood glucose

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9
Q

why does muscle glycogen not contribute to blood glucose

A

absence of glucose 6-phosphatase

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10
Q

where does glycogenesis occur

A

cytosol

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11
Q

what is glycogenesis

A

synthesis of glycogen

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12
Q

glycogenesis requires energy supplied by __ and __

A

ATP
UTP

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13
Q

when does glycogenesis occur

A

if there is an excess of glucose in the blood

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14
Q

GLUTs are what type of molecule

A

protein

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15
Q

what is the committed step of glycogen synthesis

A

glucose 6-phosphate—>glucose 1-phosphate

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16
Q

the energy for glycosidic bond for glycogen is coming from __

A

UDP

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17
Q

the glycogen form used for glycogenesis is ___

A

UDP- glucose

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18
Q

what supplies the energy for bond formation of UDP-glucose in glycogenesis

A

PPi released from UTP

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19
Q

what is the enzyme of glycogenesis that makes glycogen structure, release UDP to connect glucose, and make alpha 1,4 bonds

A

glycogen synthase

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20
Q

what enzyme of glycogenesis, due to increased amount of linear glycogen structure, cuts alpha 1,4 bond to paste it a 1,6 position

A

branching enzyme

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21
Q

what is the primer enzyme/protein used in glycogenesis

A

glycogenin

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22
Q

what remains as the core of glycogen

A

glycogenin

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23
Q

what enzyme is used to shorten glycogen (glycogenolysis)

A

glycogen phosphorylase

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24
Q

what does glycogen phosphorylase do in glycogenolysis

A

break alpha 1,4 glycosidic bonds`

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25
Q

what coenzyme is required with glycogen phosphorylase

A

B6 (pyridoxal phosphate)

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26
Q

what is limit dextrin

A

any partly broken down starch

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27
Q

what is the function of phosphorylase in glycogenolysis

A

breaks alpha 1,4 glycosidic bonds, release glucose 1-P

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28
Q

what is limit dextrin found in glycogenolysis

A

where phosphorylase has acted but waiting for debranching enzyme to arrive
*can be seen on liver biopsy

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29
Q

what is the function of debranching enzyme in glycogenolysis

A

break 1, 4
make 1, 4
*creates straight line structure
break 1, 6 to release a free glucose

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30
Q

glucose 6-phosphatase is an enzyme for what 2 pathways

A

glycogenolysis and gluconeogenesis

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31
Q

what is the main function of glycogenolysis and glycogenesis

A

maintain blood glucose

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32
Q

what organ functions to maintain blood glucose

A

liver

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33
Q

a small amount of glycogen is degraded by ___ in the lysosome

A

alpha 1, 4- glucosidase (acid maltase)

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34
Q

what is Pompe disease

A

deficiency in alpha 1,4-glucosidase (acid maltase) in the lysosome causing an accumulation of glycogen in lysosome

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35
Q

in the liver in a fed states, glycogenesis or glycogenolysis predominates

A

glycogenesis

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36
Q

in the liver in a fasting state, glycogenesis or glycogenolysis predominates

A

glycogenolysis

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37
Q

in skeletal muscle, does glycogenolysis or glycogenesis occur during exercise

A

glycogenolysis

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38
Q

glucagon is related to __ (anabolic or catabolic) reactions, and responds to __ (high or low) glucose

A

catabolic
low

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39
Q

liver responds to what 3 things to start glycogenolysis

A

insulin/glucagon ratio
epinephrine
*hypoglycemia

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40
Q

muscle responds to what 3 things to start glycogenolysis

A

epinephrine
*high AMP (low ATP)
*calcium ions from contracting muscle

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41
Q

glucagon and epinephrine cause breakdown of glycogen using what type of receptor signals

A

G-protein coupled receptors

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42
Q

what is the 2nd messenger for hypoglycemia (glucagon release)

A

cAMP

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43
Q

glucagon activates __ enzymes

A

glycogenolysis

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44
Q

what are the 3 sources of glucose for use in the body (from 1st source to 3rd/final source)

A

food
glycogen stores
gluconeogenesis

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45
Q

glycogen is synthesized from what form of glucose

A

alpha-D-glucose

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46
Q

where does glycogenesis occur

A

cytosol

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47
Q

what is the committed step of glycogenesis and what enzyme is involved

A

glucose 6-phosphate–> glucose 1-phosphate by phosphoglucomutase

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48
Q

in glycogenesis, what acts as both an enzyme and a primer, and also remains at the core of a glycogen molecule

A

glycogenin

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49
Q

how does glycogen synthase differ from branching enzyme in regards to making/breaking glycosidic bonds

A

glycogen synthase makes alpha 1,4 bonds
branching enzymes break alpha 1,4 bonds then make alpha 1,6 bonds

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50
Q

where does glycogenolysis occur

A

cytosol

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51
Q

what are the 2 enzymes used in glycogenolysis

A

phosphorylase
debranching enzyme

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52
Q

the action of phosphorylase vs debranching enzyme in glycogenolysis differs in the type of glucose released. Phosphorylase releases ___ while debranching enzyme releases ___

A

glucose 1-phosphate
free glucose

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53
Q

insulin is related to __ (anabolic or catabolic) reactions, and responds to __ (high or low) glucose

A

anabolic
high

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54
Q

does glucagon activate or inactivate glycogen phosphorylase, leading to glycogen degradation

A

activates

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55
Q

how does insulin decrease the breakdown of glycogen

A

insulin activates phosphatase= dephosphorylation
dephosphorylation inactivates phosphorylase kinase leading to inactivation of glycogen breakdown

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56
Q

why does insulin decrease glycogen breakdown

A

insulin is released in a fed state
in a fed state we have enough glucose so we don’t need to use our storage

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57
Q

what 2 specific AA residues are commonly phosphorylated, leading to activation or inactivation

A

serine
threonine

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58
Q

what is the effect of insulin on phosphodiesterase

A

activates
so cAMP is deactivated, decreasing glycogenolysis, saving glycogen stores

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59
Q

what is the function of phosphodiesterase in glycogen metabolism

A

degrades cAMP (2nd messenger) into 5’-AMP to decrease breakdown of glycogen

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60
Q

if there is excess glycogen storage in the liver that can’t be broken down, the main symptom is ___

A

hypoglycemia

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61
Q

if there is excess glycogen storage in muscle, the main symptoms are __ and __

A

weakness
difficulty with exercise

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62
Q

what is a glycogen storage disease

A

defective glycogen synthase so no synthesis of glycogen

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63
Q

glycogen storage disease type 1 is also called

A

von gierke disease

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64
Q

what enzyme is involved in Von Gierke disease

A

defective glucose 6-phosphatase (in liver)

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65
Q

what are the 5 main presentations of Von Gierke disease

A

can’t release free glucose= severe fasting hypoglycemia
buildup of glycogen in liver= hepatomegaly
hyperuricemia
hyperlipidemia
lactic acidemia

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66
Q

what are the reasons behind the presentation of Von Gierke disease

A

glucose 6-phosphate isn’t converted to glucose, leading to a decrease in glucose release (fasting hypoglycemia)
glucose 6-phosphate overwhelms glycolysis, leading to an increase in lactate (lactic acidemia) and fatty acids (hyperlipidemia)
glucose 6-phosphate also acts in the pentose phosphate pathway and leads to an increase in uric acid (hyperuricemia)

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67
Q

when does Von Gierke disease typically manifest

A

6 months when an infant’s feeding schedule begins to be more spaced out

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68
Q

why do symptoms of Von Gierke disease likely arise during the fasting state

A

glucose is prevented from leaving liver cells and entering the bloodstream due to deficiency in glucose 6-phosphate

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69
Q

why is Von Gierke disease only associated with the liver and not muscle

A

muscle does not have glucose 6-phosphate, the deficient enzyme in Von Gierke disease

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70
Q

what is the treatment to Von Gierke disease

A

frequent oral glucose (meals) throughout the day

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71
Q

what enzyme is deficient in Pompe’s disease

A

lysosomal alpha 1,4 glucosidase (acid maltase)

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72
Q

Pompe’s disease is classified as a __ storage and __ storage disease

A

glycogen storage and lysosomal storage disease

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73
Q

what is the effect of Pompe’s disease

A

glycogen can’t be degraded in lysosomes= buildup of glycogen in lysosomes

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74
Q

what is the presentation of Pompe’s disease in juvenile onset

A

muscle hypotonia
cardiomegaly (leads to death by heart failure by age 2)

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75
Q

why is hypoglycemia not present in Pompe’s disease

A

the enzyme involved, lysosomal alpha 1,4-glucosidase) only accounts for 1-3% of glycogen breakdown

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76
Q

how does juvenile differ from adult onset of Pompe disease

A

juvenile= lysosomal alpha 1,4-glucosidase completely absent
adult= lysosomal alpha 1,4-glucosidase enzyme not completely absent

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77
Q

what is the enzyme affected in Cori disease

A

glycogen debranching enzyme (usually alpha 1,6-glucosidase component)

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78
Q

what are 2 other names for Cori disease

A

Forbes disease
Limit Dextrinosis

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79
Q

what gene mutation leads to Cori disease

A

AGL

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80
Q

what is the presentation of Cori disease

A

buildup of single glucose residue at branch-points or limit dextran present (partial glycogen degradation)
abnormal glycogen buildup= hepatomegaly
mild hypoglycemia

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81
Q

what is the defective enzyme in McArdle disease

A

muscle phosphorylase (myophosphorylase)

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82
Q

what is the presentation of McArdle disease

A

onset of exercise experiencing muscle aches, cramping
myoglobinuria (dark urine after exercise due to myoglobin in muscle breaking down)

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83
Q

what are the laboratory findings in McArdle disease

A

normal fasting blood glucose
normal glycogen structure in muscle biopsy
no plasma lactate after exercise (no glycogen metabolism)

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84
Q

what is the disease with an abnormal glycogen structure

A

Cori

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85
Q

why is there an absence of lactate in McArdle disease

A

we don’t have glucose because there is no metabolism of glycogen–>glucose
(first enzyme of glycogenolysis is defective)

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86
Q

what process clears the buildup of lactate during exercise

A

gluconeogenesis

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87
Q

what enzymes are released as a result of McArdle disease

A

creatine kinase
aldolase

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88
Q

what enzyme is defective in Hers disease

A

liver phosphorylase

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89
Q

what enzyme is defective in Anderson disease

A

branching enzyme

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90
Q

what is the main source of fructose

A

sucrose

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91
Q

where is sucrase present

A

brush border of intestine

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92
Q

what are the main sources of fructose in the diet

A

fruit
honey
corn syrup
table sugar (sucrose)

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93
Q

fructose is rapidly absorbed by ___

A

GLUT 5

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94
Q

is fructose transport into the cell insulin dependent

A

no

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95
Q

for fructose metabolism, it must first be phosphorylated by ___

A

fructokinase

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96
Q

what is the function of aldolase B in fructose metabolism

A

splits fructose 1-phosphate

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97
Q

what aldose is the only one that has affinity for fructose 1-phosphate in fructose cleavage

A

B

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98
Q

why is the rate of fructose metabolism faster than glucose

A

fructose 1-phosphate bypasses PFK-1, the rate limiting enzyme in glycolysis

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99
Q

what enzyme is deficient in essential fructosuria

A

fructokinase

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100
Q

what enzyme is deficient in hereditary fructose intolerance

A

aldose B

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101
Q

why is essential fructosuria benign

A

because of hexokinase, it can be partially used up and participate in glycolysis and the rest is excreted in the urine
*it doesn’t build up

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102
Q

where does fructose 1-phosphate get trapped

A

in cytosol

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103
Q

with aldose B deficiency, there is a buildup of fructose 1-phosphate, leading to what being trapped

A

phosphate

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104
Q

if the body’s phosphate is decreased, what does the patient feel

A

lethargic due to decreased ATP and drop in Pi (no glycogenolysis- glycogen needs to be phosphorylated)
hypoglycemia (trapping of phosphate)
hyperuricemia (trapping of phosphate)

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105
Q

what is the presentation for hereditary fructose intolerance

A

vomiting and hypoglycemia 20-30 minutes after fructose intake

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106
Q

when is hereditary fructose intolerance evident

A

when baby is weaned from milk and begins consuming food containing sucrose and fructose (ex: fruit)

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107
Q

how does hereditary fructose intolerance lead to hyperuricemia

A

our body has a limited store of Pi
Pi gets trapped with fructose
when all the Pi is trapped in our body stores, the rest of the fructose is excreted in the urine

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108
Q

what are the 2 main determinants of hereditary fructose intolerance

A

fructose in urine
aldose B deficiency

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109
Q

what is the treatment for hereditary fructose intolerance

A

remove fructose and sucrose from diet

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110
Q

what are 2 ways of trapping a monosaccharide (sugar)

A

add phosphate
add an alcohol group (polyol- a sugar alcohol)

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111
Q

what is the function of aldose reductase

A

reduce glucose to sorbitol

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112
Q

where is aldose reductase present

A

all tissues

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113
Q

what are the 2 enzymes involved in glucose–>fructose

A

aldose reductase
sorbitol dehydrogenase

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114
Q

what is the function of sorbitol synthesis

A

glucose–>sorbitol–>fructose

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115
Q

in sorbitol synthesis, what does aldose reductase do

A

converts D-glucose to D-sorbitol

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116
Q

in sorbitol synthesis, what does sorbitol dehydrogenase do

A

converts D-sorbitol to D-fructose

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117
Q

what is the effect of high glucose (hyperglycemia) in the body on sorbitol production

A

sorbitol increases

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118
Q

what is one of the main cell types that benefits from sorbitol synthesis (polyol pathway)

A

sperm cells which use fructose as their main energy source

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119
Q

what is the effect of long term hyperglycemia on cataract formation

A

high glucose= oversaturation of polyol pathway= glucose–>sorbitol
since sorbitol can’t cross the cell membrane, it’s trapped= increase in osmosis and oxidative stress= buildup of water= cataract formation
*similar to in kidneys and nerves

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120
Q

sorbitol= alcohol of __

A

glucose

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121
Q

in what tissues is insulin required for glucose entry (through GLUT4)

A

adipose
muscle

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122
Q

sorbitol dehydrogenase effect is the result of __ or __

A

oversaturation
physiological absence in nerves, kidney, and lenses

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123
Q

with cataract formation what enzyme is increased

A

aldose reductase

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124
Q

the buildup of __ leads to cataracts

A

sorbitol

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125
Q

what cataract formation, what enzyme in decreased

A

sorbitol dehydrogenase

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126
Q

what is the major source of galactose

A

lactose

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127
Q

what is the enzyme for digestion of lactose

A

beta-galactosidase (lactase)
*brush border intestinal enzyme

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128
Q

in galactose metabolism, what is the function of galactokinase

A

galactose–>galactose 1-phosphate

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129
Q

galactose 1-phosphate must be converted to UDP-galactose to enter glycolysis. the enzyme involved is ___

A

galactose 1-phosphate uridylyl transferase (GALT)

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130
Q

galactose is first converted to ___ before being broken down to glucose to enter into glycolysis

A

glycogen

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131
Q

what is the relation between glucose and galactose

A

C4 epimers

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132
Q

galactosemia is the result of what enzyme deficiency

A

galactokinase

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133
Q

what is the presentation of galactokinase deficiency

A

cataracts
galactosuria

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134
Q

how does galactokinase cause cataracts

A

galactose (aldose sugar) builds up, some is excreted, some isn’t
aldose reductase is activated
galactose–>galactitol= cataracts in 3-5 months

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135
Q

when is galactokinase deficient evident

A

days after birth with consumption of milk

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136
Q

what enzyme is deficient in classic galactosemia

A

galactose 1-phosphate uridylyltransferase

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137
Q

what is the treatment for galactosemia

A

removal of galactose/lactose from diet
addition of soy milk (contains sucrose which is metabolized to glucose and fructose)

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138
Q

nursing mother has galactosemia and can’t eat galactose. She can make galactose through what reaction via glucose

A

epimerization of glucose

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139
Q

if someone doesn’t eat galactose/fructose, how can they still make it (through what reaction)

A

epimerization of glucose

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140
Q

what are the 2 end products of the pentose phosphate pathway

A

NADPH
ribose

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141
Q

where does the pentose phosphate pathway occur

A

cytosol

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142
Q

what are the 2 reactions involved in the pentose phosphate pathway

A

oxidative
non-oxidative

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143
Q

oxidative, irreversible, pathways make __ and __

A

NADPH
pentoses

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144
Q

non-oxidative, reversible, pathways converts ___ to ___

A

glycolysis components
pentoses

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145
Q

what is the rate limiting step of pentose phosphate pathway

A

glucose 6-phosphate dehydrogenase

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146
Q

what is the first product following the committed step of pentose phosphate pathway

A

6-phosphogluconate

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147
Q

what is the first reaction of the pentose phosphate pathway that produced NADPH

A

glucose-6-phosphate dehydrogenase

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148
Q

what is the function of transketolase and transaldolase

A

shuffle carbons between glycolysis and pentose phosphate pathway
*links pentose phosphate pathway to glycolysis

149
Q

transketolase in pentose phosphate contains a __ group as a cofactor

A

thiamine

150
Q

what are the 3 symptoms of Wernicke syndrome

A

opthalmoplegia
confusion
ataxia

151
Q

what causes Wernicke syndrome

A

thiamine deficiency especially in patients with alcoholism
*alcohol inhibits absorption of thiamine

152
Q

what 3 pathways is thiamine (B1) used as a cofactor

A

pyruvate dehydrogenase
alpha-ketoglutarate dehydrogenase
transketolase

153
Q

if a test is ordered to determine if a patient has thiamine deficiency, what enzyme is tested

A

transketolase
*it’s the only coenzyme used by the enzyme

154
Q

thiamine deficiency results in decrease in what utilization

A

glucose

155
Q

what is the treatment for Wernicke syndrome

A

IV thiamine followed by glucose infusion

156
Q

what is a diagnostic for thiamine deficiency

A

RBC transketolase levels after thiamine infusion increases

157
Q

transketolase is an enzyme of the oxidative or non-oxidative part of pentose phosphate pathway

A

non-oxidative

158
Q

what is the main control regulator of the pentose phosphate pathway

A

NADP+ level

159
Q

can the oxidative and non-oxidative pathway of pentose phosphate pathway function independently of each other

A

yes depending on the cellular requirement

160
Q

from glycolysis to pentose phosphate pathway is oxidative or non-oxidative

A

oxidative

161
Q

back to glycolysis is oxidative or non-oxidative

A

non-oxidative

162
Q

what is the function of pentose phosphate in RBC

A

saves RBC from oxidative damage

163
Q

what 3 AA make up glutathione

A

glutamate
cysteine
glycine

164
Q

what helps protect RBC against oxidative stress

A

glutathione

165
Q

is reduced or oxidized glutathione required for RBC protection against reactive oxidizing agents

A

reduced

166
Q

what from the pentose phosphate pathway is used to maintain the reduced form of glutothione

A

NADPH

167
Q

what are 2 effects of glucose 6-phosphate dehydrogenase deficiency

A

jaundice
hemolytic anemia
*due to oxidant stressors

168
Q

what are Heinz bodies

A

oxidized hemoglobin conglomerates

169
Q

when Heinz bodies are cleared by macrophages, leftover parts are called __

A

bite cells

170
Q

glucose 6-phosphate dehydrogenase deficiency is what type of inheritance

A

X linked recessive

171
Q

are glucose 6-phosphate dehydrogenase deficiencies usually 100% deficiency

A

no

172
Q

what enzyme catalyzes the reduction of oxidized glutathione

A

glutathione reductase

173
Q

why is glucose 6-phosphate dehydrogenase deficiencies most severe in RBC

A

it’s the only way for RBC to generate NADPH

174
Q

hemolytic anemia can be the result of what 3 enzyme deficiencies

A

G6PD
glutathione reductase
glutathione peroxidase

175
Q

G6PD deficiency is seen to provide protection against ___

A

malaria

176
Q

what is the cytochrome p450 enzyme system

A

enzymes that works on foreign things in the body by adding an -OH group form hydroxylation and detoxification to make the foreign substance soluble for excretion

177
Q

how is cytochrome 450 related to pentose phosphate pathway

A

it uses NADPH as it’s cofactor

178
Q

what is the cause of chronic granulotamous disease

A

NADPH oxidase deficiency

179
Q

what test is used to determine the presence of NADPH oxidase

A

nitroblue test

180
Q

what are glycosides

A

sugars linked to other molecules through glycosidic bonds

181
Q

what are glycosaminoglycans (GAGS)

A

linear glycans with >100 repeats of amino and acidic sugar dissacharides

182
Q

what is the charge of amino sugars

A

+

183
Q

what neutralizes the positive charge of amino sugars

A

acetylations

184
Q

what is the charge of acidic sugars

A

negative

185
Q

O linked sugars are linked to the OH of what 2 amino acids

A

serine
threonine

186
Q

N linked sugars are linked to the NH2 of what amino acid

A

asparagine

187
Q

what is glycosylation

A

enzymatic attachment of a sugar to another molecule

188
Q

what is glycation

A

pathogenic, non-enzymatic attachment of excessive glucose to another molecule

189
Q

in diabetes, persistently high glucose levels results in glycation of __, creating HbA1

A

hemoglobin

190
Q

what is the enzyme used for O linked glycoproteins

A

glycosyl transferase

191
Q

what is the trisaccharide core of O linked glycoproteins

A

GlcNAc/GalNAc-Gal-Neu5AC (NANA)

192
Q

what is the pentasaccharide core of N linked glycoproteins

A

2 GlcNAc and 3 mannoses

193
Q

in N linked glycoproteins, what is the terminal molecule in complex types

A

sialic acid

194
Q

what is the function of dolichol phosphate in N linked glycoprotein synthesis

A

it acts as a scaffold for oligosaccharides before they are added to the amide nitrogen of asparagine

195
Q

what is the main glycoprotein in mucous

A

mucin (an O glycoprotein)

196
Q

what are the properties of mucins

A

negative charge (due to terminal sialic acid) makes them slippery and attracts water

197
Q

what is the function of mucins

A

lubricate/hydrate
transport through GI, respiratory, and genitourinary tracts
protect epithelial surfaces

198
Q

what are lectins

A

glycoproteins that bind to N linked sugars

199
Q

what are the 2 components of influenza A that bind to host glycoproteins

A

HA binds sialic acid to allow entry into host cell
NA has sialidase activity to allow exit from host cell

200
Q

what is the additional terminal sugar in type A blood antigen

A

N-Acetyl Galactosamine (GalNAc)

201
Q

what is the additional terminal sugar in type B blood antigen

A

galactose

202
Q

what is a cause of protein misfolding in regards to glycoproteins

A

abnormal glycosylation

203
Q

how are glycoproteins transported from golgi to lysosome

A

mannose phosphorylation

204
Q

what is a glycoprotein

A

oligosaccharide linked to a peptide

205
Q

what is the charge of proteoglycans

A

negative

206
Q

what are proteoglycans

A

core protein attached to GAG chains

207
Q

what are GAGs (glycosaminoglycans) also known as

A

mucopolysaccharides

208
Q

what is the structure of GAGs

A

repeating chain of alternating acidic sugar and amino sugar

209
Q

what are the 2 common acidic sugars found in GAGs

A

iduronic acid
glucuronic acid

210
Q

what are the 2 common amino sugars found in GAGs

A

glucosamine
galactosamine

211
Q

what addition can be added to amino and acidic sugars of GAGs

A

they can be sulfated

212
Q

sulfated sugars are found in all GAGs except ___

A

hyaluronic acid

213
Q

GAGs provide __ and __

A

hydration
resilience (hydrophilic)

214
Q

how are GAGs and proteoglycans involved in cartilage formation

A

proteoglycans and type II collagen form cartilage

215
Q

how does penicillin inhibit peptidoglycan synthesis

A

interferes with transpeptidase which helps for bacterial cell walls

216
Q

what type of inheritance is Hunter syndrome

A

X linked through mother

217
Q

what type of inheritance is Hurler syndrome

A

autosomal recessive

218
Q

what are the 3 types of complex lipids

A

phospholipids
glycolipids
lipoproteins

219
Q

how many carbons make up a short chain fatty acid
how many carbons make up a medium chain fatty acid
how many carbons make up a long chain fatty acid
how many carbons make up a very long chain fatty acid

A

short= 3-5
medium= 6-12
long= 14-21
very long= 22 or more

220
Q

what are 3 characteristics of saturated fatty acids

A

dense solids
high melting point
no double bonds

221
Q

what are 3 characteristics of unsaturated fatty acids

A

low density liquids
low melting point
kinked with 1 or more double bonds

222
Q

what are monounsaturated fatty acids

A

unsaturated fatty acid with only 1 double bond

223
Q

what are polyunsaturated fatty acids

A

unsaturated fatty acid with more than one double bond

224
Q

how do polyunsaturated fatty acids increase membrane fluidity

A

due to double bonds introducing kinks

225
Q

is natural double bond configuration of fatty acids cis or trans

A

cis

226
Q

the position of the __ determines the name of an unsaturated fatty acid

A

double bond

227
Q

how does the delta naming system differ from the omega naming system of unsaturated fatty acids

A

delta identifies the double bond position from the carboxyl end
omega identifies the double bind position from the methyl end

228
Q

what are the 2 essential fatty acids

A

linoleic acid
alpha- linolenic acid

229
Q

what does it mean for a fatty acid to be essential

A

we must obtain it from out diet

230
Q

the 2 essential fatty acids, linoleic acid and alpha-linolenic acid, are what type of fatty acids

A

polyunsaturated

231
Q

what are the 3 health benefits of omega-3 essential fatty acids

A

anti-inflammatory
brain/neuron functioning
antithrombosis

232
Q

what does omega-6 essential fatty acids do

A

precursor to make arachidonic acid and eicosanoids
pro-inflammatory and atherosclerosis

233
Q

alpha-linolenic acid is an omega __ fatty acid

A

3

234
Q

linoleic acid is an omega __ fatty acid

A

6

235
Q

what is the role of eicosanoids (arachidonic acid) in inflammation and cell signaling

A

they act as hormones

236
Q

why are trans fats harmful in human health

A

they decrease membrane fluidity and increase the risk for atherosclerosis and coronary heart disease

237
Q

what are triglycerides

A

storage form of fatty acids
nonpolar

238
Q

how do triacylglycerols (triglycerides) store energy

A

as fats and oils

239
Q

what are the 3 types of membrane lipids

A

sterols
glycolipids
phospholipids

240
Q

are membrane lipids hydrophilic, hydrophobic, or amphiphatic

A

amphipathic
nonpolar -phobic tail, -philic polar hear

241
Q

what is cholesterol an important component of

A

cell membrane

242
Q

bile salts are what type of molecule

A

cholesterol

243
Q

what is the function of bile salts

A

assist in emulsification (micelle formation)
digestion
absorption of dietary lipids

244
Q

bile salts are made of bile __

A

acids

245
Q

what is the head group of the glycerophospholipid cephalin

A

ethanol amine

246
Q

what is the head group of the glycerophospholipid phosphatidylserine

A

serine

247
Q

what is the head group of the glycerophospholipid phosphatidalcholine (lecithin)

A

choline

248
Q

cholesterol is a __

A

sterol

249
Q

how do phytosterols in plants prevent the absorption of cholesterol from food

A

they compete with cholesterol for absorption site, inhibiting cholesterol absorption

250
Q

which fat soluble vitamins contain a isoprene backbone

A

A
E
K

251
Q

what 3 antibiotics are lipids (polyketides)

A

erythromycin
tetracyclin
doxycycline

252
Q

what 2 molecules accumulate in Hunter syndrome

A

dermatan sulfate
heparan sulfate

253
Q

what 2 molecules accumulate in Hurler syndrome

A

dermatan sulfate
heparin sulfate

254
Q

what do lipoproteins transport

A

triglycerides
cholesterol
fat soluble vitamins (ADEK)

255
Q

where are chylomicrons made

A

enterocytes

256
Q

what is the function of chylomicrons

A

transport dietary lipids from the small intestine to muscle/adipose tissue

257
Q

what are the 4 dietary lipids

A

triglycerides
cholesterol
vitamins
phospholipids

258
Q

what is the essential apoprotein of chylomicrons

A

apo-B48

259
Q

what apoproteins are present on chylomicrons

A

apo-B48
apoC-II
apo-E

260
Q

where do chylomicrons get apoC-II and apo-E from

A

HDL

261
Q

what is the function of apoC-II

A

activate lipoprotein lipase

262
Q

what is the function of apo-E

A

mediate uptake of chylomicron and VLDL remnants in the liver

263
Q

what is the function of lipoprotein lipase

A

convert triacylglycerides to 3 fatty acids+glycerol

264
Q

what occurs with a defect in lipoprotein lipase or ApoC-II

A

increase plasma chylomicrons (hyperchylomicronemia)

265
Q

what occurs with a defect in apo-E

A

increased remnants of chylomicrons and VLDL
(dysbetalipoproteinemia)

266
Q

what is the effect of insulin on lipoprotein lipase

A

upregulates in fed state

267
Q

where is VLDL made

A

hepatocytes

268
Q

what is the function of VLDL

A

transport endogenous lipids (triacylglycerides, vitamins, and cholesterol) from the liver to tissues

269
Q

what is the main integral protein for VLDL

A

apo-B100

270
Q

what apoproteins are present on VLDL

A

apo-B100
apoC-II
apo-E

271
Q

VLDL is can be converted to __ or __

A

IDL
LDL

272
Q

what lipoprotein (VLDL, LDL, or HDL) delivers cholesterol to all cells

A

LDL

273
Q

how does LDL deliver cholesterol to tissues

A

using apo-B-LDL receptor

274
Q

how does LDL fom

A

derived from IDL

275
Q

what is the function of LDL

A

transport and deliver cholesterol from liver to tissues

276
Q

what is the only apoprotein on LDL

A

apo-B100

277
Q

lipoprotein a is only find in patients with

A

hypercholesterolemia (modified form of LDL)

278
Q

how can apo-A of lipoprotein A increase thrombosis

A

it’s a competitive inhibitor of plasminogen, inhibiting fibrinolysis

279
Q

where is HDL made

A

in the liver

280
Q

what is the function of HDL

A

bring cholesterol from tissues to liver
(“good”)

281
Q

what apoprotein is needed for HDL

A

apoA-I

282
Q

what are the apoproteins present on HDL

A

apoA-I
apoC-II
apoE

283
Q

what does apoA-I do

A

activate LCAT which converts cholesterol–> cholesterol ester+lysolecithin

284
Q

what is the function of apoA-I

A

trap and pack cholesterol esters

285
Q

how do exogenous lipids differ from endogenous lipid

A

exogenous- dietary lipids digested by lipases and absorbed in the small intestine
endogenous- synthesized from excess glucose/AA in the liver

286
Q

what enzymes account for the first breakdown of lipids

A

esterases

287
Q

what type of fatty acids are readily absorbed into portal circulation without being emulsified

A

short and medium chain

288
Q

what are the 2 substances make up micelles

A

digested lipids and bile salts

289
Q

what are 5 substances that can be found in micelles

A

long chain fatty acids
monacylglycerols
cholesterol esters
phospholipids
vitamins ADEK

290
Q

what is the structure of a micelle

A

outer layer- hydrophilic head, hydrophilic tail of phospholipid
inner core- hydrophobic lipids

291
Q

what is the function of a micelle

A

transport of fatty acids

292
Q

where are fatty acids esterified

A

SER

293
Q

how are fatty acids activated
what enzyme is involved

A

fatty acyl-CoA synthase adds CoA (vitB5) to fatty acids

294
Q

what makes up a chylomicron

A

dietary lipid+apolipoprotein

295
Q

where does chylomicron formation occur

A

golgi

296
Q

how is microsomal triacylglycerol transfer protein (MTTP) involved in chylomicron formation

A

loads apo-B48 and lipids on chylomicron

297
Q

where are chylomicrons released into for transport

A

lymph

298
Q

what is the structure of a chylomicron

A

core- triacylglycerols, cholesterol esters, vit ADEK)
outer layer- phospholipids, apo-B48

299
Q

where is apo-B48 formed

A

rER

300
Q

how does the drug orlistat (xenical) work

A

inhibits pancreatic and gastric lipase, preventing digestion and absorption of dietary fats
anti-obesity drug

301
Q

what is the major side effect of orlistat (xenical)

A

steatorrhea (oily, loose stool)

302
Q

how does the drug olestra work

A

it’s an artificial undigestible fat made of sucrose polymer so it isn’t degraded by gastric or pancreatic lipases

303
Q

what are the side effects of olestra

A

diarrhea
abdominal cramps
steatorrhea

304
Q

what are 2 foods with medium chain fatty acids

A

coconut oil
milk

305
Q

what foods is omega 6 found in

A

sunflower, corn, and soybean oils

306
Q

what foods is omega 3 found in

A

fish
flaxseen
walnuts
canola oil
soybean oil

307
Q

what are the effects of cholecystokinin release

A

contraction/bile release from gallbladder
digestive enzyme release from pancreas
decreased gut motility to increase chyme contact with enzymes

308
Q

when is secretin released from duodenal cells

A

in response to low pH of chyme entering the small intestine

309
Q

how does secretin act

A

on pancreas to release bicarbonate ions leading to neutralization of the low pH chyme

310
Q

MTTP is required in synthesis of __ and __

A

chylomicrons
VLDL

311
Q

what are the 2 major carriers of triacylglycerols

A

chylomicrons
VLDL

312
Q

list the plasma lipoproteins from highest density to lowest density

A

HDL
LDL
IDL
VLDL
chylomicron

313
Q

list the plasma lipoproteins from largest to smallest

A

chylomicron
VLDL
IDL
LDL
HDL

314
Q

list the plasma lipoproteins from highest triglyceride content to lowest triglyceride content

A

chylomicron
VLDL
LDL
HDL

315
Q

list the plasma lipoproteins from highest cholesterol content to lowest cholesterol content

A

LDL
HDL
VLDL
chylomicron

316
Q

list the plasma lipoproteins from highest protein content to lowest protein content

A

HDL
LDL
VLDL
chylomicron

317
Q

what is the rate limiting enzyme of bile acid synthesis

A

7-alpha hydroxylase (+vit c)

318
Q

a deficiency in 7-alpha hydroxylase can lead to ___

A

gallstones

319
Q

what is the rate limiting step of cholesterol synthesis

A

HMG CoA–>mevalonate
by HMG CoA reductase

320
Q

the transcriptional rate of HMG CoA reductase is controlled by __

A

SCAP not bound to cholesterol
=SREBP to nucleus for transcription of HMG CoA reductase gene

321
Q

where does cholesterol synthesis occur

A

smooth ER

322
Q

what causes atherosclerosis

A

increase in ox-LDL (oxidized LDL leads to foam cell deposition in vessels

323
Q

what is the rate limiting step of beta oxidation

A

acyl CoA dehydrogenase

324
Q

what is the rate limiting step of fatty acid oxidation

A

carnitine acyltransferase I

325
Q

what is the rate limiting enzyme of fatty acid synthesis

A

acetyl CoA carboxylase

326
Q

where does fatty acid synthesis occur

A

cytoplasm

327
Q

where does beta oxidation occur

A

mitochondria

328
Q

in the citrate shuttle of fatty acid synthesis, what enzyme produces NADPH

A

malic enzyme

329
Q

what is absence or defective in abetalipoprotein

A

MTTP

330
Q

what is abetalipoprotein

A

absence beta lipoproteins (chylomicrons, VLDL, LDL)
very low cholesterol and TAG
usually due to absence of MTTTP

331
Q

what is deficient in hyperchylomicronemia (type I familial hyperbetalipoproteinemia)

A

ApoCII or LDL

332
Q

what is deficient in hypercholesterolemia (type II familial hyperbetalipoproteinemia)

A

ApoB100 or LDL receptor

333
Q

what is the lab diagnosis for abetalipoproteinemia

A

very low plasma TAG and cholesterol

334
Q

what is the optimum level for triglycerides

A

<150 mg/dL

335
Q

what is the optimum level for total cholesterol

A

<200 mg/dL

336
Q

what is the optimum level for LDL cholesterol

A

<100 mg/dL

337
Q

what is the optimum level for HDL cholesterol

A

60 or greater
(low= <40)

338
Q

what is the optimum ratio of LDL:HDL

A

< 3.0
(LDL should be 3x less than HDL)

339
Q

deficiency in lipids or fat soluble vitamins in children leads to what symptoms

A

growth failure and mental retardation
neurological problems

340
Q

what are the main signs of hypercholesteremia

A

yellowed plaques of skin (xanthoma)
near tendons, palms, and eyes
chest pain/easy fatigue

341
Q

what are the main signs of hypertriglyceridemia

A

eruptive xanthoma (reddish papules)
pancreatitis
obesity
upper abdominal pain

342
Q

in hyperlipidemia, what lipoprotein level is decreased

A

HDL

343
Q

in familial hyperlipidemia, there is an increase in what in each:
type I
type II
type III
type IV

A

I= chylomicron and TAG
II= LDL
III= chylomicron and VLDL remnants
IV= VLDL

344
Q

what is the optimum triglyceride (VLDL) level

A

<150

345
Q

what is the optimum total cholesterol level

A

<200

346
Q

what is the optimum LDL level

A

<100

347
Q

what is the optimum HDL level

A

> /= 60

348
Q

what is the optimum LDL:HDL ration

A

<3

349
Q

what is the function of dipalmitoylphosphatidyl choline (DPPC)

A

part of surfactant that line inner surface of alveoli to lower surface tension, preventing collapse

350
Q

how does surfactant work

A

decrease hydrogen binding, preventing alveolar collapse

351
Q

prior to birth, what hormone is used to induce production of surfactant (DPPC)

A

cortisol

352
Q

in pre-mature born babies, DPPC levels are low. what has to be administered as a result

A

DPPC by intratracheal injection

353
Q

what is the function of cardiolipin

A

found in inner mitochondrial membrane where it maintains the structure and function of ETC

354
Q

if the L:S ration is <2 in premature babies, what is the result

A

immature pneumocytes, lung collapse due to less DPPC in alveoli

355
Q

where are ether glycerophospholipids formed

A

peroxisomes

356
Q

what are the bonds found in ether glycerophospholipids

A

C1 of glycerol forms an ether with alkyl or alkenyl hydrocarbon

357
Q

what type of molecule is platelet activating factor

A

ether glycerophospholipid derived from phosphatidylcholine (lecithin)

358
Q

what is multiple sclerosis

A

autoimmune demyelination of motor neurons

359
Q

where are glycolipids mostly found in the plasma membrane

A

outer leaflet of bilayer facing extracellular syrface

360
Q

what are 3 types of sphingoglycolipids

A

cerebroside
globoside
ganglioside

361
Q

glucocerebrosides occur in the plasma membrane of ___ cells
glucocerebrosides occur in the plasma membrane of __ cells

A

non-neuronal
neuronal

362
Q

do globosides contain NANA (sialic acid)

A

no

363
Q

what are gangliosides

A

glycosphingolipid with 1 or more sialic acid

364
Q

saccharolipids are made up of ____

A

fatty acids esteridied to a sugar backbone without glycerol/sphingo backbone

365
Q

what are 2 examples of bacterial liposaccharides (glycolipids)

A

cholera and tetanus toxins

366
Q

where are phospholipids degraded

A

lysosomes

367
Q

glycerophospholipids are degraded by what enzyme

A

phospholipases

368
Q

where are sphingolipids degraded

A

lysosome

Metabolism/Nutrition (6 decks)

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