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Metabolism Flashcards

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1
Q

2 major hormones that dictate metabolism

A

insulin
glucagon

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2
Q

Fed State

A

energy storage state of metabolism
response to eating
glucose stored in glycogen & fat

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3
Q

Function of the liver in Fed State of metabolism

A

produces glycogen
converts glycogen to fat

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4
Q

Amino acids function in metabolism Fed State

A

protein synthesis OR fat production

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5
Q

Where is glycogen stored?

A

Liver
Skeletal muscle

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6
Q

Where is fat stored?

A

adipose tissue

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7
Q

Adipose tissue (S)

A

dense | large energy source
glucose–>fat storage

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8
Q

What is the building block for fat storage in adipose tissue?

A

triglycerides

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9
Q

Basal State

A

between meals | maintains BG
down glucose –> down insulin, up glucagon
breakdown fat/glycogen

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10
Q

What occurs in the liver during the basal state?

A

Breaks down glycogen into glucose and exports it into blood
=maintain BG & ship to brain
Also makes glucose to maintain BG

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11
Q

What does adipose tissue do in the basal state?

A

uses fat storage and transports to blood for energy for skeletal muscle & tissues

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12
Q

Starved State

A

no food intake | increase ketosis to maintain BG

GREATER decrease glucose –>
down insulin | up glucagon

depleted glycogen, ketone production increase (glucose-sparing effect)

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13
Q

What happens to the liver do in the starved state?

A

glycogen depleted

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14
Q

What happens with gluconeogenesis in the starved state?

A

turned on = glucose made from fat storage

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15
Q

Glucose Sparing Effect

A

ketones used by the brain which keep animal alive in starved state

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16
Q

Enzyme function

A

dictate metabolic pathways

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17
Q

Active site

A

where enzyme binds to substrate (where rxn occurs)

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18
Q

Cofactors

A

not part of protein
inorganic compound

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19
Q

Function of cofactors

A

provide functional groups and help w/ electron transfer

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20
Q

Coenzymes

A

non-protein, contains vitamins

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21
Q

Coenzyme function

A

provide functional groups

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22
Q

Km

A

enzyme’s affinity for substrate

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23
Q

Catabolic Pathway

A

break down energy

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24
Q

Anabolic Pathway

A

build things (small –> big molecules)

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25
Q

Purpose of Catabolic Pathways

A

generate ATP
transfer electrons

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26
Q

Ways to regulate enzymes

A

Inhibition
Activation
Phosphorylation

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27
Q

Inhibition

A

antagonist
stops reaction

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28
Q

Types of Inhibition

A

irreversible
reversible

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29
Q

Irreversible Inhibition

A

completely stop enzyme
ex: toxins, drugs (COX inhibition)

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30
Q

Reversible Inhibition

A

can turn on/off

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31
Q

Types of Reversible Inhibition

A

competitive
non-competitive

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32
Q

Competitive Inhibition

A

compete for binding site & blocks product from being made
can be overcome by increasing substrate

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33
Q

Non-competitive Inhibition

A

bind to separate site on enzyme and inhibit by conformational change

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34
Q

What is most common way to regulate metabolism?

A

Non-competitive inhibition

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35
Q

Activation (type of enzyme regulation)

A

agonist
allosteric (non-competitive)

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36
Q

Allosteric (type of activation)

A

binds to different site on enzyme –> conformational change
= speeds up enzyme or decrease Km

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37
Q

Phosphorylation

A

adding phosphate group activates or inhibits it

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38
Q

Kinase

A

phosphorylates a protein

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39
Q

Phosphatase

A

dephosphorylates a protein

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40
Q

Gleevec

A

competitive inhibitor
treats CML & GIST
inhibits repro of oncogene –> decrease tumor growth

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41
Q

3 Types of Pathway Regulation

A
  1. Product Inhibition
  2. Feedback Inhibition
  3. Feed-forward regulation
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42
Q

Product Inhibition

A

product inhibits further production of it

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43
Q

Feedback Inhibition

A

product inhibits enzyme earlier on | takes different pathway

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44
Q

Feed-forward Regulation

A

production –> more production

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45
Q

Dry Beri-Beri

A

neurological
thiamine-deficient diet –> decrease PDH (pyruvate dehydrogenase) –> down ATP

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46
Q

Wet Beri-Beri

A

cardiac
thiamine buildup –> heart failure

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47
Q

Thiamine

A

coenzyme for vitamin for PDH

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48
Q

Polioencephalomalacia

A

disease in cattle
high grain diet increase thiaminase bacteria in rumen
–> anorexia, lethargy, “star-gazers”, pressing

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49
Q

TCA Cycle Purpose

A

starting point for carb/fat/protein oxidation
transfer electrons –> ATP in ETC

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50
Q

Location of TCA Cycle

A

Mitochondrial matrix

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51
Q

TCA cycle substrate

A

Acetyl CoA

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52
Q

TCA cycle products

A

Primary: NADH + H+
Secondary: FADH2 + GTP

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53
Q

TCA regulatory enzyme

A

dehydrogenases:
IDH | a-KGDH | MDH

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54
Q

How is TCA turned on?

A

high energy demand (down ATP, up ADP)
ETC activates causes down NADH = TCA ON

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55
Q

What turns off TCA?

A

Low energy demand (up ATP, down ADP)
ETC slows, NADH rises, dehydrogenases inhibited = TCA OFF

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56
Q

ETC purpose

A

generate ATP from oxidizing carbs/fats/proteins

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57
Q

ETC Substrate

A

NADH + H+, FADH2

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58
Q

ETC Product

A

ATP, H2O

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59
Q

ETC reg enzyme

A

ATP synthase

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60
Q

What turns on ETC?

A

high energy demand (down ATP, up ADP)
NADH + H+ donate electrons

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61
Q

Location of ETC

A

inner mitochondrial matrix
(Impermeable membrane)

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62
Q

Complex II: Succinate Dehydrogenase

A

complex in ETC
binds FAD (from TCA cycle)
skips “pumping”, produces ATP but LESS than ATP synthase

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63
Q

Pyruvate Dehydrogenase (PDH)

A

protein complex
Pyruvate –> Acetyl CoA (outside TCA)
converts so it can enter mito matrix

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64
Q

What is PDH stimulated by?

A

Ca2+ | ADP | insulin
dephosphorylation activates

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65
Q

What is PDH inhibited by?

A

NADH | Acetyl CoA (product)
phosphorylation inactivates

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66
Q

What do coenzymes rely on for proper function?

A

B vitamins (1,2,3,5)

67
Q

Glycolysis substrate

A

glucose

68
Q

Glycolysis product

A

pyruvate or lactate

69
Q

Glycolysis reg enzyme

A

PFK-1

70
Q

Glycolysis purpose in peripheral tissues

A

break down glucose for energy

71
Q

Glycolysis purpose in liver

A

glucose –> pyruvate for fat synthesis

72
Q

What turns on glycolysis in peripheral tissues?

A

energy demand (up AMP, up PFK1)

73
Q

What turns on glycolysis in liver?

A

up insulin –> up PFK 2 –> active PFK1

74
Q

Glycolysis in liver (substrate/product)

A

glucose (substrate) –>
pyruvate + acetyl coA (product)

75
Q

Gluconeogenesis subtrate

A

lactate | glycerol | alanine

76
Q

Gluconeogenesis product

A

glucose

77
Q

Gluconeogenesis purpose

A

maintain BG
convert non-glucose precursors into glucose

78
Q

Gluconeogenesis reg enzyme

A

pyruvate carboxylase

79
Q

What activates gluconeogenesis?

A

excess Acetyl CoA from B-oxidation

80
Q

Glycogen Synthesis substrate

A

UDP-glucose

81
Q

Glycogen Synthesis product

A

glycogen

82
Q

Glycogen Synthesis purpose

A

store glucose

83
Q

Glycogen Synthesis reg enzyme

A

glycogen synthase

84
Q

What activates glycogen synthesis?

A

insulin dephosphorylates glycogen synthase = ON

85
Q

What deactivates glycogen synthesis?

A

glucagon phosphorylates glycogen synthase = OFF

86
Q

Glycogenolysis substrate

A

glycogen

87
Q

Glycogenolysis product

A

glucose-6-phosphate

88
Q

Purpose of Glycogenolysis in peripheral tissues

A

glycogen –> glucose for glycolysis –> energy!

89
Q

Purpose of glycogenolysis in liver

A

glycogen –> glucose to export in blood

90
Q

Glycogenolysis reg enzyme

A

Phosphorylase

91
Q

What turns on glycogenolysis?

A

glucagon phosphorylates phosphorylates phosphorylase = ON

92
Q

What turns off glycogenolysis?

A

insulin dephosphorylates phosphorylase = OFF

93
Q

B-oxidation substrate

A

fatty acids

94
Q

B-oxidation product

A

Acetyl CoA

95
Q

B-oxidation purpose

A

oxidize fatty acids –> NADH + H+ –> ATP

96
Q

B-oxidation reg enzyme

A

CPT-1

97
Q

What turns off B-oxidation?

A

fatty acid synthesis which increases malonyl coA = OFF

98
Q

Fatty Acid Synthesis substrate

A

Acetyl CoA –> Malonyl CoA

99
Q

Fatty Acid Synthesis product

A

palmitate

100
Q

Fatty Acid Synthesis purpose

A

make fatty acids to store excess glucose
make carbon chain from amino acids as triglycerides in adipose tissue & liver

101
Q

Fatty Acid Synthesis reg enzyme

A

Acetyl CoA Carboxylase (ACC)

102
Q

What activates FA synthesis?

A

up BG, up insulin, dephosphorylates ACC = ON

103
Q

What deactivates FA synthesis?

A

down BG, down insulin, down ACC
down Malonyl CoA = on B-oxidation = OFF

104
Q

Ketone Formation substrate

A

Acetyl CoA (excess)

105
Q

Ketone Formation product

A

ketones:
B-hydroxybutyrate
Acetone
Acetate

106
Q

Purpose of Ketone Formation

A

generate blood-soluble ketones from excess Acetyl CoA when B-oxidation is high

107
Q

Ketone Formation reg enzyme

A

Acetyl CoA carboxylase (indirectly)

108
Q

What turns on ketone formation

A

up B-oxidation –> excess Acetyl CoA = ON

109
Q

Hexokinase

A

enzyme that traps glucose in cell (by converting to glu-6-phosphate)
IMMEDATE trapping!

110
Q

Location of Hexokinase

A

most tissues

111
Q

Glucokinase

A

enzyme in glycolysis that traps glucose in cell by converting to glu-6-phosphate
NOT immediate! need high glu levels (like after meal)

112
Q

Glycolysis location

A

cytosol

113
Q

Shuttle systems

A

“shuttle” electrons from cytosol to mitochondrial matrix in glycolysis (so it can get into cell)

114
Q

Malate-aspartate shuttle

A

more efficient shuttle
makes malate which can get electrons into matrix for TCA

115
Q

Glycerol phosphate shuttle

A

less efficient shuttle
transfers NADH electrons –> glycerol phosphate dehydrogenase to get into mitochondrial matrix

116
Q

Anaerobic Glycolysis

A

fastest way to generate ATP
rely on endogenous glycogen (in cell)

117
Q

Purpose of Anaerobic Glycolysis

A

regenerate NAD so glycolysis can continue

118
Q

Ruminant Gluconeogenesis

A

rumen can break down cellulose–>glucose
breaks down further then remakes it

119
Q

Propionate

A

major precursor for ruminant gluconeogenesis
major source of glucose

120
Q

Feline Gluconeogenesis

A

obligate carnivores
can’t handle carbs
convert proteins –> amino acids –> glu (via gluconeogenesis)

121
Q

Cori Cycle

A

integrates glycolysis + gluconeogenesis
liver + lactate –> glucose –> tissues

122
Q

Branching Enzyme

A

enzyme in glycogen synthesis
clips glucose chain & moves it so new chain can be formed = branching

123
Q

Purpose of glycogen branching

A

increase SA, quicker process, more soluble

124
Q

Debranching enzyme

A

enzyme in glycogenolysis
removes branch so further branching

125
Q

Glycogen phosphorylase

A

releases glucose from free ends
in glycogenolysis

126
Q

What activates glycogen phosphorylase?

A

phosphorylation of glycogen phosphorylase

127
Q

Glycogen Metabolism in Liver

A

glucagon binds to G protein
stim phosphorylation of phosphorylase = active

Glu-6-P dephosphorylates –> export in blood
exports for needs of body

128
Q

Glycogen metabolism in muscle

A

NO glucagon signaling
stimulated by EPI
uses energy via glycolysis for its own
important in muscle endurance

129
Q

Glycogen Storage Disease

A

can’t maintain BG
glucose-6-phosphatase mutation = can’t export glucose

130
Q

What type of fatty acids does the body make? (and saturated/unsaturated?)

A

palmitic acid (16 carbons)
saturated

131
Q

What is the purpose of saturated fatty acids?

A

all single bonds, store as many electrons as possible

132
Q

Where does fatty acid synthesis occur?

A

cytoplasm

133
Q

Is fatty acid synthesis reductive or oxidative?

A

reductive (giving electrons for storage)

134
Q

What causes Type I Diabetes?

A
135
Q

B cells

A

cells that produce insulin

136
Q

How do B-cells produce insulin?

A

glucose influx via GLUT2
glycolysis makes ATP
ATP inhibits K+ sensitive channel
Depolarization of VG Ca2+ channel
Ca2+ triggers exocytosis
B cell vesicles diffuse out insulin

137
Q

What causes insulin receptor to activate?

A

phosphorylation of receptor

138
Q

Tyrosine Kinase Receptor

A

insulin receptor

139
Q

Two ways insulin causes glucose uptake into cell

A

direct
indirect

140
Q

Direct glucose uptake by insulin

A

glucose taken up via transporters

141
Q

Indirect glucose uptake by insulin

A

stimulation of glycolysis / glycogen synthesis
(help clear glucose from blood=uptake)

142
Q

What receptor leads to insulin stimulated by glucose uptake directly?

A

GLUT 4

143
Q

What causes Type 1 Diabetes?

A

insufficient insulin
low BG b/c not enough insulin
autoimmune B-cell destruction

144
Q

What causes Type 2 Diabetes?

A

insulin resistance
plenty of insulin
response muted (no glucose uptake)

145
Q

What species is Type I diabetes most common?

A

dogs

146
Q

What species is Type II diabetes most common?

A

cats

147
Q

Type I Diabetes Non-Ketotic symptoms

A

polyuria | polydipsia (drink)
weight loss | cataracts

148
Q

How do B-cells get destroyed in Type I diabetes?

A

T-cells/macrophage attack B-cells
decrease insulin overtime

149
Q

Ketoacidosis + symptoms

A

occurs in diabetes w/o treatment
symptoms: depression, anorexia, dehydration, labored breathing, death

150
Q

Ketoacidiosis pathology

A

vessels constrict in kidneys –> shut down CNS

151
Q

Ketoacidosis treatment

A

insulin + fluids

152
Q

What is an underlying cause of T2DM?

A

obesity

153
Q

Mechanism of T2DM

A

no signal to IRS1 means no GLUT4 vesicle for glucose to come in

154
Q

Ceramides

A

lipotoxicity (“toxic lipids”)
which inhibit receptor signals for glucose uptake

155
Q

Stages of T2DM

A

early stage
postprandial hyperglycemia
falling insulin
normal to low insulin (late stage)

156
Q

Eary stage T2DM

A

up insulin, body tries to compensate
“pre-diabetes”

157
Q

Postprandial hyperglycemia stage Type 2

A

Type 2 progresses
lose more receptors, really up insulin

158
Q

Falling insulin stage Type 2

A

insulin decreases B cells die
up glucose @ rest (w/o meal)
up gluconeogenesis & glycogenolysis

159
Q

Normal to Low insulin stage Type 2

A

cannot produce insulin (transition to closer to Type 1)

160
Q

Amyloid

A

becomes toxic when builds up in B-cells
leads to loss of insulin production

161
Q

What causes B-cell exhaustion?

A

up free FA & glucose –> ER stress

162
Q

What is different with insulin signaling between dogs & cats?

A

cats fewer receptors than dogs
obligate carnivores –> don’t clear glucose as quickly and have fewer receptors

163
Q

AMP kinase (AMPK)

A

enzyme on when energy demand is high (up AMP)
target for T2DM treatment in humans (NOT cats!)

Cell Biology (6 decks)

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