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ISBM > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

mammalian fates of pyruvate with associated enzymes

A
  1. Reduction to lactate via LDH (cytosolic rxn)
  2. Carboxylation to OAA via pyruvate carboxylase (mito. rxn)
  3. Acetyl-CoA via PDH
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2
Q

what molecule allows the movement of pyruvate into the mito. matrix

A

MPC

located in the inner mito membrane

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3
Q

How is pyruvate converted to acteyl-CoA

A

via pyruvate dehydrogenase

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4
Q

where does the PDH reaction take place?

A

mitochondria

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5
Q

if the oxidation of pyruvate —> acteyl- CoA via PDH reversible or irreversible?

A

irreversible!!!

delta G -33. kJ/mol

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6
Q

what 3 enzymes make PDH complex

A
  1. PDH (E1)
  2. Dihydrolipoyl transacetylase (E2)
  3. Dihydrolipoly dehydrogenase (E3)
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7
Q

fxn of PDH (E1)

A

decarboxylation of pyruvate

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8
Q

fxn of Dihydrolipoyl transacetylase (E2)

A

addition of coenzyme-A

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9
Q

how is PDH complex regulated

???????

A

autophosphorylation

high ATP = phosphorylated enzyme complex= consume ATP = inhibition of PDH

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10
Q

what is the storage form of FAs

A

triglycerides (TAG)

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11
Q

medium chain FA consists of how many Carbon atoms

A

6-12 atoms

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12
Q

what hormones foster the liberation of FA

A

Epinephrine and glucagon

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13
Q

how is FA mobilized/transported?

A
  • FA liberated from adiopoytes diffuse in ECF and into plasma and associate with albumin
    *always some free FA in solution but most associated with albumin
    (albumin helps with transportation)
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14
Q

What are the functions of PDH

A
  1. decarboxylation (removes 1 carbon atom and results in release of CO2)
  2. Oxidation of pyruvate (results in reducing power in form of NADH)
  3. Coenzyme A is introduced and forms a high energy bond (primes pyruvate)
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15
Q

where does the PDH reaction take place?

A

mitochondria

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16
Q

what 5 cofactors particpate in the rxn of PDH

A
  1. thiamine pyrophosphate aka TPP (vit. B1)
  2. Lipoate
  3. FAD
  4. NAD
  5. Coenzyme-A
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17
Q

what contents are in the mito. matrix (7)

A
  1. PDH complex
  2. citric acid cycle enzymes
  3. FA beta-oxidation enzymes
  4. AA oxidation enzymes
  5. DNA, ribosomes
  6. Many more enzymes
  7. ATP, ADP, P, Mg2+, CA2+, K+
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18
Q

fxn of Dihydrolipoly dehydrogenase (E3)

A

oxidation of NADH from electrons on FADH2

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19
Q

what is the most highly reduce form of metabolic fuel

A

fatty acids

* provide >50% of energy requirements of liver and skeletal muscle

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20
Q

what is the storage form of FAs

A

triglycerides (TAG)

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21
Q

what is the backbone for glycerol

A

triglycerides

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22
Q

___% of TAG’s energy is derived from the oxidation of the FA chains
the rest is from ____

A

95% from oxidation of the FA chains

5% from glyercol

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23
Q

how is a triacylglycerol formed?

A

glyercol + FA via a ester linkage in a dehydration rxn

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24
Q

how do Epinephrine and glucagon foster the liberation of FA from the TAG?

A

through secondary messengers: cAMP
G protein-hormone binding –> (+) adenylate cyclase –> (+) cAMP release –> (+) PKA –> (+) phosphorylates triacylglycerol lipase

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25
Q

what form of triacylglycerol lipase is inactive

A

dephosphorylated form

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26
Q

describe the rxn of beta oxidation

A
  1. C16 fatty acid palmitic acid (aka palmitocyl CoA, aka a primed fatty acytl-CoA) undergoes oxidation at alpha and beta carbon—> FADH2
  2. then a hydroylsis rxn
  3. further oxidation on beta carbon –> NADH
  4. last enzyme: thiolase- catalyzes a bidirectional rxn with the addition of coenzyme A
  5. product is acteyl-CoA + another fatty acyl-CoA that reenters same pathway (spiral pathway)
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27
Q

where does the priming of FA the place in a cell?

A

cyptoplasm

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28
Q

what form does FA exists in in the cytoplasm

A

fatty actyl-CoA

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29
Q

how is FA primed?

A
  • ATP requirement which will prime FA
  • generate a phosphorylated intermediate
  • then form addition of coenzyme A to adenosine

*fatty acyl-CoA synthase is responsible for these 2 rxns

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30
Q

what is the end product of odd chain FA oxidation

A

propionyl-CoA

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31
Q

what does propionyl-CoA get converted into

A

succinyl Co-A with use of ATP

  • TCA cycle intermediate
  • feeds into TCA cycle directly
  • drives substrate level phosphoryation
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32
Q

what contents are in the mito. outer membrane

A

freely permeable to small molecules and ions

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33
Q

what contents are in the mito. inner membrane

A
  • very selective
    1. respiratory electron carriers (complexes I-IV)
    2. ADP-ATP translocases
    3. ATP synthase
    4. Other membrae transporters
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34
Q

what is the rate limiting step in FA oxidation

A

carnitine shuttle

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35
Q

CPT is allosterically inhibited by what

A

malonyl-CoA

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36
Q

how are FA chains transported across the inner mito membrane

A
  1. small and medium FA chains diffuse across membrane w/o carriers
  2. long FA chains use carnitine and pore proteins to cross *bidirectional diffusion via concentration gradient)
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37
Q

what is the general flow of TCA cycle

A 
Acetyl-CoA + OAA ---> Citrate
citrate
isocitrate
(CO2 + NADH)
alpha-ketoglutarate
(CO2 + NADH)
succinyl-CoA
(GTP--> ATP)
Succinate
(FADH2)
Fumarate
Malate
(NADH)
OAA + acetyl-CoA
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38
Q

where is carnitine acyltransferase II located

A

inner leaflet of inner mito membrane (matrix)

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39
Q

this mechanism is important for moving fatty acyl CoA molecule from cytoplasm into matrix of mitochondria

A

carnitine shuttle

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40
Q

how does fatty acyl-CoA move into mitochondria

A
  1. fatty acyl CoA is able to diffuse across outer membrane of mitochondria into the inter membrane space where it is acted upon by two things:
  2. CPT1-covalently adds carnitine, substituting it for coenzyme A molecule–> results in fatty acyl carnitine
  3. fatty acyl carnitine moves through pore
  4. CPT2- undoes the previous action. Uses fatty acyl carnitine and coenzyme A as substrate to make fatty acyl CoA.
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41
Q

covalently adds carnitine, substituting it for coenzyme A molecule–> results in fatty acyl carnitine

A

CPT1 (carnitine acyl transferase I )

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42
Q

Uses fatty acyl carnitine and coenzyme A as substrate to make fatty acyl CoA

A

CPTs (carnitine acyl transferase II)

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43
Q

what happens after fatty acyl CoA is in the matrix

A

beta oxidation

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44
Q

what regulates beta oxidation

A
  • diffusion of acyl carnitine into matrix

- availability of cofactors like NAD

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45
Q

what happens to the NADH/NAD ratio as we engage in Beta oxidation

A

increase the ratio

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46
Q

overall, is beta oxidation reversible?

A

no, irreversible

*acetyltransferase is reversible enzyme

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47
Q

Series of oxidative reactions that occur over and over using oxidized cofactors until we are left with two fragment carbons- acetyl CoA.

A

beta oxidation

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48
Q

describe the rxn of beta oxidation

A
  1. C16 fatty acid palmitic acid (aka palmitocyl CoA, aka a primed fatty acytl-CoA) undergoes oxidation at alpha and beta carbon—> FADH2
  2. then a hydroylsis rxn
  3. further oxidation on beta carbon –> NADH
  4. last enzyme: thiolase- catalyzes a bidirectional rxn with the addition of coenzyme A
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49
Q

classic example of a spiral pathway

A

beta-oxidation

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50
Q

what are the products of beta-oxidation

A
  1. fatty acyl Co-A
  2. NADH
  3. FADH2
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51
Q

how are odd chained FA oxidized

A

beta oxidation

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52
Q

what is the end product of odd chain FA oxidation

A

propionyl-CoA

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53
Q

what does propionyl-CoA get converted into

A

succinyl Co-A with use of ATP

  • TCA cycle intermediate
  • feeds into TCA cycle directly
  • drives substrate level phosphoryation
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54
Q

what are the fates of acetyl-CoA

A
  1. into TCA cycle –> citric acid
  2. production of ketone bodies
  3. Cholesterol biosynthesis
  4. Fatty acid synthesis (de novo lipogenesis)
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55
Q

how many rxns occur in the TCA cycle

A

8 rxns

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56
Q

what is the rate limiting step in TCA cycle?

A

incorportation of acteyl-CoA into citrate via citrate synthase to make a 6 Carbon substance

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57
Q

carries out 1st oxidation in TCA and decarboxylation rxn

A

isocitrate dehydrogenase

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58
Q

what TCA enzyme carries out substrate level phosphorylation

A

succinate thiokinase

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59
Q

what products are produce in TCA cycle (not substrates)

A

3 NADH
FADH2
2 CO2

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60
Q

negative allosteric influences of PDH

A
  1. high acetyl-CoA
  2. high NADH
  3. High ATP/ high AC
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61
Q

positive allosteric influences of PDH

A
  1. high ADP or AMP
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62
Q

postive allosteric influences on pyruvate carboxylase

A
  1. high acetyl-CoA
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63
Q

how is PDH able to autophosphorylate

A

if AC is low it will de-phosphorylate itself to become active

  • high AC = phosphorylated = inactive
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64
Q

Citrate synthase, isocitrate DH, and Alpha-ketoglutarate DH are all neg. influenced by what?

A

high NADH

*in high energy state and don’t need more energy

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65
Q

neg. influences of citrate synthase

A
  1. high ATP

2. high NADH

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66
Q

important side-products of TCA cycle

A
  1. citrate
  2. alpha-ketogluterate
  3. succinyl-CoA
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67
Q

this can undergo transamination to produce glutamate and other AAs. Purines come from here

A

alpha-ketogluterate

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68
Q

can be used to make porphrins like heme. These are what give thins like hemoglobin and myoglobin their transport properties

A

succinyl-CoA

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69
Q

Citrate is allowed to leak out of mitochondria, enter the intermembrane space, freely diffuse into the cytoplasm on its concentration gradient.
what is its effects in the cytoplasm?

A

in the cytoplasm it has negative effect on PFK1 and pyruvate kinase, so it down regulates glycolysis

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70
Q

when will the diffusion of citrate into the cytoplasm increase

A

with increase AC

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71
Q

used to move acetyl CoA out into the cytoplasm

A

citrate

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72
Q

cleaves citrate into OAA and acetyl CoA

A

citrate lyase

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73
Q

where does FA synthesis and FA break down occur

A

FA synthesis: cytoplasm

FA breakdown: mito

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74
Q

replenishing rxns, that offer up opportunity for substances to feed into TCA cycle

A

anapleurotic rxns

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75
Q
  • reduced acetoacetate

- principle ketone body

A

beta-hydroxybutyrate

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76
Q

where are ketones produced

A

hepatocytes

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77
Q

what is the starting material for ketone synthesis

A

2 acetyl-CoA

78
Q

what enzyme condenses two acetyl CoA molecules together to give us acetyl acetyl CoA

A

thiolase

79
Q

why is B-hydroxybutyrate the principle ketone

A

we are in a state of high reducing power (NADH/NAD+ ratio)

80
Q

what enzyme removes acetyl-CoA as a byproduct and leaves you with acetoacetate

A

HMG-CoA lyase

81
Q

what drive ketone body production?

A
  1. a lot of reducing power (NADH)

2. a lot of acetyl-CoA (**overflow pathway)

82
Q

how are ketones utilized?

A

degrade them back into actyl-CoA
(degrade ketone bodies by oxidizing B-Hydroxybutyrate into acetoacetate then finally thiolase is responsible for generating acetyl-CoA)

83
Q

what tissues can utilize acetyl-CoA

A

any tissue with mito

ex. CNS, heart, skeletal muscle, kidney

84
Q

what will happen to ketone bodies in a starved state

A

increase

85
Q

where/when do the oxidative pathways of carbohydrates, lipids and amino acids converge

A

ETS during respiration

86
Q

is ubiquinone fully reduced or fully oxidized

is ubiquinol fully reduced or fully oxidized

A

Ubiquinone is fully oxidized and ubiquinol is fully reduced

87
Q

contain cysteine residues that are important because they possess a sulfur moiety and these sulfur moieties are responsible for binding iron within a wide array of matrix forms. The key here is that iron is capable of being readily oxidized and reduced. Fe2+ —-Fe3+ ferrous to ferric state that is freely reversible

A

iron sulfur proteins (Fe-S)

*more e- in ETS

88
Q

These molecules posses a porphyrin ring structure (recall that the production of porphyrin ring structures is a side reaction of the TCA cycle!). The ring structure relies on the presence of iron that is able to be freely oxidized or reduced

A

Cytochromes a, b, c

*more e- in ETS

89
Q

This molecule has two ketone moieties where oxygens are able to accept or lose electrons and a proton. So it can be oxidized or reduced

A

Ubiquinone- CoQ 10

*more e- in ETS

90
Q

how do e- move in the ETS

A
  1. Fe-S proteins
  2. cytochromes a, b, c
  3. ubiquinone
91
Q

how much ATP does NADH and FADH2 produce

A 
NADH= 3 ATP
FADH2= 2 ATP
92
Q

why does NADH produce more ATP than FADH2

A

Because NADH started with Complex I, it had more chances to pumps more protons across the gradient, which powers the ATP synthase and gives us 3 ATP per molecule of NADH. FADH2 produces 2 ATP during the ETC because it gives up its electron to Complex II, bypassing Complex I.

93
Q

CO and CN blocks the movement of electrons where in the ETS

A

complex 4

94
Q

amytal and rotenone (sedatives) blocks the movement of electrons where in the ETS

A

complex I

95
Q

where are the subunits of ATP synthase located

A

F0- inner membrane

F1- in matrix (made of alpha and beta subunits that allow the gamma subunit to rotate)

96
Q

what drives the production of ATP with ATP synthase

A

the proton motive force drives oxidation phosphorylation of ADP to ATP

97
Q

explain the chemiosomotic theory/coupling

A

separation of H+ and e- creates a chemical gradient as well as a electrical potential gradient that is used to drive ATP synthase

Chemical gradient = (basic in matrix due to e-)
Electrical potential= (- charge in matrix)

98
Q

how much ATP is generated in glucose oxidation and palmitoyl coA oxidation

A

glucose oxidation= 38 ATP
palmitoyl coA oxidation= 131 ATP

*FA is a greater source of energy

99
Q

main pathways of AA

A
  1. synthesis of non-essential AA via transamination
  2. synthesis of non-protein derivatives
  3. production and handling of NH4+ via oxidative deamination
100
Q

what is alanines counter part?

A

pyruvate

101
Q

how can alanine be used in TCA cycle/ gluconeogenesis

A
  1. alanine + alpha ketoglutarate = glutamate and pyruvate via transamination (OCCURS IN THE LIVER!!)
  2. pyruvate can be used to make acetyl-coA which can be used in TCA cycle
102
Q

what can we do in alpha ketoglutarate levels are low in the TCA cycle

A

we can transaminate pyruvate making alpha ketogluterate and alanine from pyruvate

103
Q

what are the precursors of creatine

A

arginine and glycine

form ornithine intermediate- in urea cycle

104
Q

how is GABA neurotransmitter formed

A

decarboxylation of glutamate via PLP and loss of CO2

105
Q

what is the precursor of seratonin

A

tryptophan via decarboxylation

106
Q

what is the precurosr of dopamine, norepi, and epi

A

tyrosine

107
Q

how is histamine formed

A

histidine via decarboxylase

108
Q

____ is a regulator of HCL production in the GI tract

A

histamine

109
Q

how much ATP does it cost to bottle up 2 Nitrogens

A

3 ATP

110
Q

FA are found in the blood is mainly what form

A

bound to albumin

aka non esterified fatty acids- NEFAs

111
Q

FA are found in tissue are mainly in what form

A

bound to coenzyme A
aka fatty acyl-CoA
* in their prime form ready for use!

112
Q

no double bonds

A

saturated FA

113
Q

: one double bond

A

monounsaturated FA

114
Q

more than one double bond, best for health ie omega 3 fatty acids

A

polyunsaturated FA

115
Q

Mammals lack enzymes needed to _________ so we must obtain these FAs from ______

A

introduce double bonds beyond C-9

our diet- plant sources

116
Q

example of FA that we need to obtain from diet

A

Linoleic acid (omega 6)

Linolenic acid (omega 3)

117
Q

Essential fatty acids can be used as precursors for:

A
  • other unsaturated fatty acids
  • structural lipids
  • lipids involved in cell signaling
118
Q

when you consume lipids they are

A

digested, absorbed, resynthesized into TAGs and then diffuse into lymphatics

119
Q

sources of FA

A

diet
lipolysis (break down TAG)
De novo lipogenesis

120
Q

the synthesis of new fatty acids from a non-fatty acid source

A

De novo lipogenesis (DNL)

*occurs primarily during overfeeding, especially when our diet has little fat in it and high in carbs

121
Q

The fatty acids are being produced from ____ and where does it occur

A

Acetyl CoA

in liver, adipose tissue and mammary glands

122
Q

Denovolipogenesis is stimulated by ___ and inhibited by ___

A

-stimulated by insulin due to high levels of glucose and

  • inhibited by glucagon
  • inhibited by unesterified FA may inhibit FA synthesis (eg. In starvation)
123
Q

explain how insulin can stimulate DNL and glycolysis

A

due to spill over of Acetyl CoA- Acetyl CoA at cross roads: it can enter the TCA cycle, but if adenylate charge or reducing power are elevated ketone bodies will be formed AND it will be used to produce fatty acids from in the cytoplasm

124
Q

Steps of FA synthesis

A
  1. acetyl-CoA added to small arm of FA synthase
  2. Malonyl-CoA added to long arm (acyl carrier protein)
  3. Malonyl-CoA is decarboxylated and releases CO2
  4. Condensation of acetyl-CoA and Malonyl-CoA remnant –> attach to aceyl carrier protein arm
  5. Reduction via NADH to a 4 C compound
  6. Translocation of the molecule onto acetyl coA arm (this opens the acetyl carrier protein for the addition of another malonyl-CoA)
  7. repeat until FA
125
Q

what is the rate limiting step in the synthesis of FAs

A

Acetyl-CoA carboxylase (ACC) incorporates CO2 in the form of bicarbonate onto acetyl-CoA —> Malonyl-CoA

*ACC is subject to phosphorylation and requires biotin as a cofactor

126
Q

what is the main contributor to FA synthesis

A

malonyl-CoA

127
Q

allosteric regulators of DNL

A
  1. need NADPH
  2. Citrate is a + allosteric to ACC
  3. Palmitic acid/palmatyl-CoA (product of DNL) is a - allosteric influence to ACC And FAS
  4. malonyl-CoA is a - allosteric influence of CPT1 (prevent our new FFA from beta oxidation)
  5. epi and glucagon (activate PKA which phosphorylates ACC and turns it off = less malonyl-coA)
  6. insulin
128
Q

how does insulin regulate DNL

A

activates PPP 1 which:

  1. dephosphorylates TAG lipase turning it off= preventing FA breakdown
  2. (+) ACC via dephosphorylation
  3. increases gene expression of ACC and FAS therefore promoting FA and TAG synthesis
129
Q

how are TAGs and phospholipids made from new FFA

A
  1. get FA and glycerol into their energized states= “G3P” + “fatty acyl-CoA” = Phosphatidate
  2. phosphatidate can become a TAG or phospholipid
  3. to become TAG: lose a phosphate and add an acetyl-CoA
    to become phospholipid: gains additional characteristics
130
Q

carriers that transport hydrophobic substances (sort of like albumin).

A

lipoproteins

131
Q

explain the structure of a lipoprotein

A

they all possess an arrangement of phospholipids and cholesterol as well as proteins embedded in the phospholipids. They also possess a neutral core that holds hydrophobic substances (ex. TAG, cholesteryl-esters)

132
Q

what occurs when you are in the post-prandial state

A

The fatty acids that you produce though digestion are going to be absorbed across the GI epithelium, re-synthesized into TAGs, and then are packaged in the form of lipoproteins called CHYLOMICRONS which are made by GI tract

133
Q

what occurs when you are in the post-absorptive state?

A

the liver is responsible for making and secreting a different lipoprotein that is responsible for carrying our triglyceride population. These are called VLDL very low density lipoproteins

134
Q

the main carriers of TAGs in the blood

A

chylomicrons and VLDLs

135
Q

what lipoprotein has the most TAGs and the most Protein

A

most TAG= chylomicrons

most protein- HDL

136
Q

what is required for VLDL assembly

A

ApoB

137
Q

Driving forces of VLDL production

A
  1. synthesis of ApoB (stimulated by insulin)*** rate limiting step!
  2. FA availbility in the liver (DNL, FA, and chylo uptake)
138
Q

what breaks down TAGs assocaited with VLDLs or chylomicrons

A

LDL (Lipoprotein lipase)

*sits on the surface on the tissues that use fatty acids for their energy requirements

139
Q

the mechanism for providing TG delivery to tissues that utilize TG and FA as a source of energy

A

LPL

*activated by insulin when it is dephosphorylated by PPP1 and also requires ApoC

140
Q

how do LPLs work

A
  1. Binds to the cell surface by proteoglycans
  2. Heparin releases these interactions
  3. Requires ApoC II for activation (Several Apo CII per VLDL for maximum lipolysis)
141
Q

metabolism of endogenous fat

A

VLDLs

142
Q

metabolism of dietary fats

A

chylomicrons

143
Q

why is HDL considered good cholesterol

A

HDL can pick up cholesterol from peripheral sources –> cholesterol is moved from cell membranes into HDLs to the liver in a process called REVERSE CHOLESTEROL TRANSPORT
*liver can then use it to make bile salts and send it to gut where it can then be excreted or picked up via chylos

144
Q

how does cholesterol exisit in tissue

A
  1. free cholesterol/ un-esterified form

2. Cholesterol esters “storage form”

145
Q

how does cholesterol exisit in the blood

A

cholesterol esters (on VLDLs or chylomicrons)

146
Q

how does cholesterol exist in the liver

A
  1. free cholesterol

2. bile salts - used for the emuslificaiton of fats

147
Q

sources of cholesterol

A
  1. diet
  2. de novo synthesis (in liver)
    3 reverse cholesterol transport
148
Q

uses of cholesterol

A
  1. secretion of HDL and VLDLs
  2. free cholesterol secreted in bile
  3. make bile salts/ steroids
  4. make phospholipid bilayer
149
Q

cholesterol is a precursor for what?

A

steroid hormones
Vit. D
Bile salts/acids

150
Q

what is the RLS in cholesterol synthesis

A

HMG-CoA reductase converting acetoacetyl-CoA into mevalonate
(requires 2 NADPH)

**Statins target this step!

151
Q

phases of cholesterol synthesis

A
  1. make mevalonic acid via HMG-CoA reductase (**RLS)
  2. mevalonic acid to activated isoprene units
  3. isoprene units to farnesyl-PP and onto squalene
  4. Squalene to Ianosterol and cholesterol

**Requires 18 ATP per 1 cholesterol molecule

152
Q

regulators of HMG-CoA reductase

A
  1. insulin= +PPP1= + HMGR
  2. Epi/glucogon= +PKA = - HMGR
  3. gene expression SREBP-2
153
Q

how does cholesterol considered “bad”

A
  • LDLs are oxidized and then taken up by macrophages. These macrophages are called foam cells and they sit in the vasculature just under the endothelial layer where they enhance plaque formation due to the inflammation of the endothelium.
  • an inflamed endothelium from these foam cells eating up LDLs would cause disruptive flow or even endothelial damage.
154
Q

Endocrine Function

A

A source cell secretes a hormone, hormone enters the blood and effects another cell (ie beta cells of pancreas secrete insulin which affects adipocytes, liver and muscle)

155
Q

Neurocrine Function

A

Our source cell is a neuron which can synthesize and release a neurocrine hormone into the ECF, hormone goes into blood and affects other cells with receptors. The stimulus for the release will be depolorization of the nerve cell leading to vesicular fusion at the axon end

156
Q

what type of fxn do ADH and oxytocon have

A

neurocine fxn

157
Q

what type of fxn do prostaglandins have

A

paracrine

158
Q

source cell secretes a substance that diffuses out and ends up acting on the source cell itself.

A

autocrine

159
Q

Locally produced and locally active. Example, the source cell secretes a substance that diffuses locally- short half life of substance. Actions of this hormone are on cells close by.

A

paracrine

160
Q

types of hormones

A
  1. peptides (largest)
  2. lipids (steroids)
  3. amino acid analogs (TH)
161
Q

synthesis of peptide hormone

A

DNA–>mRNA–> preprohromone–> modification (signal sequence for secretion)–> signal is removed at ER and binds to co-peptide–> prohormone–> golgi processing–> hormone stored in granules

162
Q

ACTH (peptide hormone) effects

A
  1. Immediate: steriodgenesis activator peptide
  2. Subsequent: steroid hormone including protein
  3. Long term: IGF-2
163
Q

steroid hormones are derived from what

A

cholesterol

164
Q

what is the main difference between steroid hormone synthesis and peptide hormone synthesis

A

steroid hormones are synthesized de-novo, they aren’t stored

*therefore has slower actions

165
Q

thyroid hormones are derived from waht

A

tyrosine

166
Q

what does T3 and T4 regulate?

A

mitochondrial activity
TCA cycle
ETS
Na+/ K+ pump

167
Q

______ in more sensitive to hormone concentration than a binding curve indicates

A

physiological response

168
Q

Due to a PROLONGED REDUCED circulating hormonal concentration (or receptor blockade)

A

up-regulation of HR

*increase in cell-surface receptor numbers

169
Q

Due to a PROLONGED INCREASE circulating hormonal concentration

A

Down regulation of HR

*reduction of cell-surface receptor numbers

170
Q

Over stimulation of cells→ adrenal tumor → increases Epi and NE

A

example of down regulation of HR

171
Q

Loss of hormonal regulation, chronically block the receptors → beta blockers = increase the number of beta blockers in the cell

A

example of up regulation of HR

172
Q

Secondary effects- degree of change brought about

A

power

173
Q

less of it needed to bring about change so very low Km

A

potency

174
Q

hormones that are regulated by sleep cycle

A

hGH- increased after REM
prolactin- spike after sleep
ACTH- increase after waking= increase in cortisol
*high coritosl in morning

175
Q

The pancreas has exocrine portions called

A

islets of langerhorns

176
Q

These make and store and release glucagon

A

alpha cells of pancreas

177
Q

These make and store and release insulin

A

beta cells of pancreas

178
Q

A, B, C peptide are all connected with no disulfide bonds

-made in RER

A

Pre-proinsulin

179
Q

A, B, C peptide are all connected with disulfide bonds

A

proinsulin

180
Q

C peptide is cleaved by the Golgi apparatus leaving insulin molecule

A

insulin

181
Q

insulin is screted in response to 5 factors and inhibited by 2

A
  1. increased plasma glucose
  2. increased plasma AA
  3. hormones from GI tract (GIP)
  4. parasympathetic neurons (release of actylcholine)
  5. epi/glucagon

inhibited:

  1. sympathetic neurons
  2. [high epi] = alpha-adronergic receptors
182
Q

explain how glucose stimulated insulin release

A
  1. glycolysis is stimulated which produces reducing power
  2. reducing power closes K+ channels trapping K+ in cells
  3. opens Ca2+ channels and (Ca2+ goes into cell)
  4. membrane depolarization (more + inside)
  5. stimulates exocytotic activity of stored hormones
183
Q

when does epi/glucagon stimulate insulin release

A

when [epi] are low= binds to beta-adronergic receptors=(+) PKA= increase insulin

[high epi]= binds to alpha-adronergic receptors= decrease insulin

184
Q

how does acteyl-choline stimulate insulin release

A

+ Gq protein–> + phospholipase C –> + IP–> increase efflux of Ca2+ from ER to cytoplasm–> depolarization of cell–> increase insulin

185
Q

why do you get more insulin release when you takei n glucose orally

A

GIP stimulates insulin release

*GIP is in the GI tract

186
Q

how does glucose impact a membrane potential

A

increase in membrane potential (CLEAR DEPOLARIZATION)

*result of K+ and Ca2+

187
Q

insulins main effects:

A
  1. glucose uptake
  2. glycogen synthesis and DNL
  3. glucose oxidation
  4. promoting FA synthesis
  5. increase AA uptake and protein synthesis

*brought about by phosphorylation/dephosphorylation and gene expression

188
Q

DNL signals

A
  1. increased insulin and glucose
  2. inhibited by unesterified FA
  3. inhibited by glucagon`
189
Q

regulation of ACC activity

A
  1. increase in insulin (dephosphorylation)
  2. increase citrate (allosterically)
  3. decrease in glucoagon and epi (phosphorylation by cAMP dependent PKA)
  4. decrease Palmitoyl CoA
190
Q

malonyl CoA is ___ whne ACC is activated

A

elevated

191
Q

Response of a diabetic person to exogenous insulin in regards to insulin, glucagon, glucose, B-OH-butyrate, BUN

A 
Increase in insulin
Decrease in glucagon
Decrease in glucose
Decrease in B-OH-butyrate
Decrease in urine nitrogen
192
Q

Glucagon release is stimulated by:

A
  1. decreased plasma glucose
  2. increased plasma AA**
  3. sympathetic neurons and circulating epi
  4. parasympatheic neurons

ISBM (8 decks)

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