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VETS1003 > metabolism > Flashcards

metabolism Flashcards

1
Q

proteins digested into

A

amino acids

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2
Q

polysaccharides digested into

A

monosaccharides

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3
Q

TAG digested into

A

fatty acids

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4
Q

what organ plays a central role in processing and distribution of nutrients, and supplies nutrients to tissues via bloodstream

A

liver

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5
Q

Autotrophs

A

(“self-feeders”) make organic materials from inorganic materials in the environment
* The biosphere’s producers — Plants

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6
Q

Heterotrophs

A

(“other-feeders”) use compounds produced by others
* The biosphere’s consumers — Animals

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7
Q

What is Metabolism

A

Metabolism is the sum of the chemical reactions that convert nutrients
into energy and complex molecules within cells

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8
Q

Metabolism comprises hundreds of chemical reactions, catalysed by _____, organized into discrete ________ which operate in an integrated and coordinated manner

A

enzymes
metabolic pathways

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9
Q

flows of metabolic pathways

A

inputs; outputs; passage along pathways

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10
Q

pools of metabolic pathways

A

amounts of molecules

Filled (supplied) or emptied (by demand) by catabolic and anabolic pathways

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11
Q

space and time of metabolic pathways

A

not all pathways necessarily occur at the same time, or in the same place

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12
Q

3 main energy-containing nutrients

A

carbs, fats and proteins

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13
Q

3 reasons metabolism must be regulated

A
  • to prevent “futile cycles”
  • to respond to physiological needs
  • to respond to changes in energy demand
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14
Q

all metabolic pathways must have overall ____ free energy

A

negative

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15
Q

can anabolic pathways simplu reverse catabolic pathway

A

NO

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16
Q

glycolysis, substrate and product

A

1 glucose –> 2 molecules of pyruvate, makes 2ATP

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17
Q

glycolysis takes place in

A

cytosol

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18
Q

pyruvate can yield (3 things)

A
  • Ethanol — by anaerobic fermentation in yeast
  • Lactate — by reduction in anaerobic conditions in muscle
  • Acetyl CoA — by oxidation in aerobic conditions
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19
Q

acetyl coA is a 2C acetyl croup esterified to

A

co-enzyme A

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20
Q

aceytl coA has a central role in

A

metabolism

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21
Q

acetyl coA is put into CAC and what energy do you get out

A

NADH

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22
Q

what is beta oxidiation

A

breakdown of fat to get NADH; fatty acid trimmed 2 C at a time to get acetyl coA

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23
Q

where does CAC occur

A

mitochondria

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24
Q

where does beta oxidation occur

A

mitochondria

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25
Q

3 main VFA

A

acetate
propionate
butyrate

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26
Q

enzymes from _____ and _____ digest dietary peptides and amino acids (protein)

A

stomach and pancreas

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27
Q

Protein breakdown (hydrolysis back to amino acids) occurs constantly in cells by two main pathways:

A
  • Cytosolic pathway: involves ubiquitin and the proteasome
  • Lysosomal pathway: proteins are taken up by lysosomes and hydrolysed by
    proteases (cathepsins)
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28
Q

amino acids split into

A

amine group –> urea cycle –> urea

and

carbon skeleton –> multiple fates such as ketone bodies, acetyl coA, glucose, CO2

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29
Q

what is purpose of CAC etc making NADH

A

to produce lots of ATP; in oxidative phosphorylation (ETC)

NADH used to pump protons in to out of mitochondria; creates high proton concentration out of cell, then ATP synthase brings protons back in and this energy phosphorylates ADP into ATP

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30
Q

is pyruvate dehydrogenase reversible

A

NO its irreversible

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31
Q

can acetyl coA turn back into glucose

A

NO

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32
Q

gluconeogenesis

A

Plants: 3-phosphoglycerate
(Calvin cycle) → glucose

Animals: non-carbohydrate
precursors → glucose
– important in fasting

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33
Q

fats breakdown vs fatty acid synthesis

A

breakdown (beta oxidation)
location: mitochondria
coenzyme: NAD+/ FAD
enzymes: 4

synthesis
location: cytoplasm
coenzyme: NADPH
enzymes: 2

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34
Q

protein synthesis

A

Ribosomes translate mRNA and synthesize protein

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35
Q

enzymes lower

A

activation energy

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36
Q

mammalian genome has ~____ genes that code for proteins

A

30 000

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37
Q

in eukaryotes can one gene code for several proteins

A

yes
* post-translational modification
* alternate splicing of different exons in the mRNA transcript

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38
Q

To control the amount of a protein in a cell

A

– control gene expression
(stable vs inducible genes: transcription factors controlled by metabolites, hormones, etc) and
- control protein degradation
Some proteins live long, some ~few minutes

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39
Q

Covalent modification alters protein _____ → regulates activity

A

conformation

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40
Q

what is a reversible way of regulated proteins

A

Common important modification: phosphorylation (addition of phosphate group) of serine, threonine or tyrosine side chains

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41
Q

protein kinases

A

phosphorylates proteins; adds a phosphate group, which changes the structure of proteins therefore changing the activity of that
protein

Each has a specific target protein (substrate) that it phosphorylates, & specific effectors; some have broad, some
narrow, specificity

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42
Q

what is an irreversible way to regulate proteins

A

activation of a precursor: ie inactive forms of proteins exist and then can be activated (irreversible)

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43
Q

protein kinase examples and what they are activated by

A
  • protein kinase A; activated by cAMP
  • phosphorylase kinase; activated by protein kinase A and Ca2+
  • protein kinase C; activated by Ca2+
  • protein tyrosine kinases; activated by insulin receptorsand others
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44
Q

protein phosphatases

A

enzyme that cuts off phosphate groups from proteins (opposite of protein kinases)

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45
Q

protein control of activity by non-covalent binding of

A

effector; may enhance or inhibit activity (allosteric regulation like a built in regulatory network, feedback)

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46
Q
  • Allosteric activation, inhibition
  • Competitive inhibition

timescale:

A

less than 1 second

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47
Q
  • Activation of preformed precursor proteins
  • Activation/inactivation by reversible covalent
    modification

time scale

A

seconds to minutes

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48
Q
  • Synthesis of new protein in response to signals (e.g. hormones)

timescale

A

minutes to hours

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49
Q
  • Major changes to the overall protein profile of a tissue (e.g. in response to dietary changes, exercise); rebalancing of synthesis and breakdown

time scale

A

days to weeks

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50
Q

Erythrocytes

A

carry O2 from lungs to tissues and CO2 from tissues to lungs

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51
Q

Plasma

A

carries nutrients (glucose, amino acids, nucleosides, etc) around the body for uptake by tissues; and

Carries metabolites/waste products to (e.g. toxins, glutamine) and from (e.g.
urea) liver; urea goes to kidney for excretion. Also carries hormones

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52
Q

blood delivers what nutrients to brain

A

glucose, ketone bodies

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53
Q

blood delivers what nutrients to cardiac muscle

A

glucose, FA, ketone bodies

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54
Q

blood delivers what nutrients to skeletal muscle

A

glucose, FA, ketone bodies, amino acids

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55
Q

plasma proteins are involved in

A

blood coagulation and fibrinolysis

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56
Q

albumin (plasma protein)

A

carries fatty acids and many other molecules

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57
Q

lipoprotein (plasma protein)

A

carry TAGs and cholesterol esters

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58
Q

Most plasma proteins are synthesized in the

A

liver

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59
Q

After absorption from the gut, sugars (monogastrics; mainly glucose) and amino acids, VFAs, and some TAG, pass via the blood to the

A

liver

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60
Q

most TAG is stored in

A

adipose tissue via lymphatic system
(some in liver)

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61
Q

Hepatocytes transform nutrients into

A

fuels and precursors for other tissues

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62
Q

Kinds & amounts of nutrients supplied by the
liver vary with

A

diet and the time between feeds

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63
Q

liver: Demand by non-hepatic tissues depends on

A

the organ and on the activity of the animal

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64
Q

why does the liver have remarkable metabolic flexibility

A
  • Builds up stores when fuel is plentiful; releases when needed
  • Interacts with other organs via the blood, helped by hormones
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65
Q

GLUT2

A

glucose transporter ensures that hepatic glucose
concentration is the same as in blood

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66
Q

Glucose is phosphorylated by _____ to glucose-6-phosphate when it gets into liver

A

glucokinase (glucose-6-phosphate is negative and large and basically traps the glucose inside the liver cell)

then turned to glycogen

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67
Q

liver stores glucose as

A

glycogen

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68
Q

adipose tissue stores ____ and supplies ____

A

TAGS
fatty acids

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69
Q

adipose tissue is ___% of young mammals weight

A

15-25%

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70
Q

do all animals need blood glucose

A

YES; RBCs and brain rely on it!

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71
Q

cats and ruminants blood glucose

A

blood glucose doesn’t come from the gut

cats: * No correlation with food ingested in the previous 2h * Both normal cats and diabetic cats

ruminants: * ~80–90% of absorbed VFAs are taken up by the liver * Major consequences for hormonal control

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72
Q

rumen microbes ferment

A

cellulose –> VFAs

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73
Q

horse digestion

A

digestible carbs –> stomach –> glucose
fat –> small instestine –> FAs
fermentable fiber –> large intestine –> VFAs

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74
Q

rumen microbes

A

Cellulytic bacteria, protozoa hydrolyze cellulose

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75
Q

rumen microbes turn cellulose

A

–> cellobiose –> glucose –> VFAs

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76
Q

fate of VFAs

A

bloodstream –> oxidized –> energy
also –> amino acids and vitamins

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77
Q

acetate

A

VFA, for energy and FA synthesis

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78
Q

propionate

A

VFA, forms glucose in gluconeogensis

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79
Q

butyrate

A

VFA, for energy and FA synthesis, some metabolized in rumen wall and liver then to tissues

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80
Q

VFA absorption

A

Passive diffusion
* 75% reticulo-rumen
* 20% omasum and abomasum
* 5% small intestine

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81
Q

bloat

A

lush pasture –> increase sugar –> increase gas

82
Q

cats blood glucose comes from

A

glucogenic amino acids (amino acids from diet that have gone through gluconeogenesis)

83
Q

horses and ruminants blood glucose come from

A

VFAs and glucogenic amino acids (amino acids that have undergone gluconeogenesis)

84
Q

gluconeogenesis is active during

A

fasting

85
Q

3 main substrates of gluconeogenesis

A
  • Amino acids (from muscle protein breakdown)
  • Glycerol (from fat breakdown)
  • Lactate (from anaerobic glycolysis).
86
Q

can fatty acids produce glucose

A

no!

87
Q

what is the primary energy substrate

A

carbs –>
monogastrics: glucose,
ruminants; VFAs

88
Q

what is primary substrate for fat synthesis

A

carbs –>
monogastrics; glucose
ruminants; acetate

89
Q

extent of glucose absorption from gut

A

monogastrics; extensive
ruminants; little to none

90
Q

cellular demand for glucose

A

non-ruminants= high
ruminants and cats= high

91
Q

importance of gluconeogenesis

A

monogastrics= less importants
ruminants and cats= very important

92
Q

intense exercise effects on cell

A
  • cells need to generate lots of ATP
  • means its taking glucose-6-phosphate and taking in through glycolysis to generate ATP
  • J large
93
Q

resting state (idling) effect on cells

A
  • not much glycolysis is happening
  • also not much gluconeogenesis happening
  • these relatively balanced
  • J is small and balanced
94
Q

J= vf=vr

A

vf= glycolysis
vr= gluconeogenesis

95
Q

is we had both fructose 6-phosphate (the enzyme for glycolysis)

and fructose 1,6 biphosphate (enzyme for gluconeogenesis) both active at same time in cell what would we get

A

futile cycle (constant unnecessary back and forth) making and burning ATP, no gain

96
Q

how does substrate cycling (ie futile cycles) allow fine control of metabolism

A
  • Substrate cycling with no flux through glycolysis uses up ATP for no apparent result BUT:
  • Heat is generated
  • The ADP produced needs to be reconverted to ATP
97
Q

in mitochondria ____ and ____ are tightly coupled

A

oxidation and phosphorylation

98
Q

in mitochondria, NADH and FADH2 cannot be oxidized unless ____ is present

A

ADP

99
Q

when would uncoupling of oxidation from phosphorylation occur

A

Uncoupling occurs in the brown adipose tissue of animals that live in very cold climates (non-shivering thermogenesis)

neonates have lots of brown adipose tissue

100
Q

describe uncoupling of oxidation from phosphorylation in mitochondria

A

protons being pumped out like usual but instead of flowing back through through ATP synthase and phosphorylating ADP –> ATP, instead a protein is there that allows protons to flow freely through different pore

this generates heat!!

101
Q

highest to lowest capacity for ATP production

OPPOSITE OF fastest to slowest ways to make ATP

A
  • Aerobic lipid metabolism (slowest but most ATP)
    Fatty Acid –> Acetate –> CO2 + H2O
  • Aerobic carbohydrate metabolism
    Glucose –> Pyruvate –>CO2 + H2O
  • Anaerobic glycolysis
    Glucose –> Pyruvate –> Lactate
  • Substrate-level phosphorylation (fastest but least ATP)
    Phosphocreatine + ADP –> Creatine + ATP
102
Q

fastest to slowest ways to make ATP

OPPOSITE OF highest to lowest capacity for ATP production

A
  • Substrate-level phosphorylation (fastest but least ATP)
    Phosphocreatine + ADP –> Creatine + ATP
  • Anaerobic glycolysis
    Glucose –> Pyruvate –> Lactate
  • Aerobic carbohydrate metabolism
    Glucose –> Pyruvate –> CO2 + H2O
  • Aerobic lipid metabolism (slowest but most ATP)
    Fatty Acid –> Acetate –> CO2 + H2O
103
Q

at rest muscles use ___% of O2
working they use up to ___%

A

50
90

104
Q

contracting muscles

A

ATP splits, → energy → fibre contracts

Transfers high-energy Pi → contracting element

ATP → ADP + Pi

** need to be able to regenerate ATP

105
Q

3 sources of ATP for muscle contraction

A
  • Phosphocreatine (PC)
  • Glycolysis
  • Oxidative phosphorylation
106
Q

Phosphocreatine (PC) positives and negatives as a source for ATP for muscle contraction

A

positives
* Very quick: 4–5s > aerobic
* One step → energy
Negatives
* Little PC stored, used up quickly

107
Q

rest to exercise oxygen transition

A

*O2 uptake ↑↑ → steady state ~1–4 mins
* O2 deficit as work begins
* Lag in O2 uptake
∴ Anaerobic glycolysis → ATP
* Steady state: aerobic metabolism ® ATP

108
Q

very quick exercise (couple of seconds)

A

phosphocreatine as source of ATP

109
Q

short burst of exercise (couple of mins) source of ATP

A

anaerobic metabolism (ie glycolysis)

110
Q

long exercise (hours) source of ATP

A

aerobic metabolism

111
Q

carb sources during exercises

A
  • blood glucose
  • muscle glycogen
112
Q

fat sources during exercise

A
  • plasma FA (from adipose tissue lipolysis)
  • intramuscular triglycerides
113
Q

protein sources during exercise

A

small contribution to total energy

114
Q

blood lactate sources during exercise

A

gluconeogenesis via cori cycle

115
Q

cori cycle

A

muscle –> lactate –> liver gluconeogenesis –> glucose –> muscle

116
Q

metabolic cooperation between liver and skeletal muscle

A

muscle: glycolysis –> ATP –> contraction –> lactate into blood

liver: ATP used –> glucose –> blood (more expensive)

cori cycle: muscle –> lactate –> liver gluconeogenesis –> glucose –> muscle

ie muscle uses glucose and creates lactate
liver uses lactate and creates glucose

117
Q

what is primary fuel in low-intensity exercise

A

fats (needs aerobic conditions ie needs oxygen)

118
Q

what is primary fuel in hgih-intensity exercise

A

carbs

119
Q

crossover concept: Fat → carb as exercise ↑↑, why

A
  • Recruit fast muscle fibers
  • ↑ blood epinephrine
120
Q

in prolonged exercise; CHO

A

–> fat metabolism

121
Q

advantages of TAG for storing energy (4)

A
  • Highly reduced: More energy
  • Nonpolar: Anhydrous fat droplets: compact
  • More space: Larger total energy store
  • Insulation
122
Q

disadvantages of TAG as energy store

A
  • hydrolysis –> FA
  • not flexible as energy source ie some tissue can’t use (brain and RBCs)
  • cannot form glucose
  • not water soluble; inconvenient to move around body
123
Q

advantages of polysaccharides (glycogen and starch) for energy storage

A
  • most flexible energy source
  • very polar, soluble
  • hydrolysis –> glucose
  • glucose stored as glycogen can be very branched and compact
124
Q

disadvantages of polysaccharides (glycogen, starch) for energy storage

A
  • bulky since hydrated
  • energy content less than TAGS (since its partly oxidized due to have OH groups compared to TAG which have fully reduced FA)
125
Q

glycogen is a polymer of

A

glucose

126
Q

glycogen: a chain of

A

glucose
can be branched; lots of end points so many places glucose can be added or removed
pretty bulky

127
Q

glycogen synthesis

A

glucose phosphorylated; traps it inside cell

added to UTP: activates it into UDP-glucose (activated glucose)

then added to existing chain of glycogen (chain of glucose)

each of these steps has an enzyme that catalyses it

can debranch this chain if there is a demand of glucose (enzyme glycogen phosphorylase does this)

128
Q

glucose homeostasis during exercise is mediated by hormones like

A
  • noradrenalin (NE), epinephrine (E)
  • insulin, glucagon
  • thyroxine, cortisol (growth hormone)
129
Q

hormones

A

small molecules of intercellular communication

130
Q

3 modes of action of hormones

A
  • autocrine; act upon themselves
  • paracrine; acts locally
  • endocrine; everywhere else, ie acts far away via bloodstream
131
Q

hormone classes based on chemical structure

A
  • steroid hormones
  • peptides
  • amino acid derivatives
132
Q

hormones alter metabolism in ____ cells

A

target

133
Q

in presence of high blood glucose (lots of glucose in blood) _____ is released by pancreas

A

insulin

134
Q

what does insulin do

A

when there is high blood glucose, insulin counteracts this by lowering the concentration of glucose in blood

does that by telling organs to take up glucose (stimulates liver, skeletal muscle and adipose tissue to take up glucose into their cells)

135
Q

what does liver do when stimulates by insulin

A

takes up glucose from the blood into its cells and stores it as glycogen

  • increases glucokinase; enzyme that does glucose uptake
  • increases glycogen synthase; enzyme that does glycogen synthesis
  • inhibits glycogen phosphorylase; enzyme that does glycogen breakdown
136
Q

what does skeletal muscle do when stimulated by insulin

A

takes up glucose from blood, store it as glycogen

  • increases glucose transporter; enzyme that does glucose uptake
  • increases glycogen synthase; enzyme that does glycogen synthesis
  • inhibits glycogen phosphorylase; enzyme that does glycogen breakdown
137
Q

what does adipose tissue do when stimulated by insulin

A

takes up glucose from the blood, it is turned into fatty acids and glycerol, and stored as TAG (fat)

138
Q

when there is low blood glucose, ____ is released from pancreas

A

glucagon

139
Q

what does glucagon do when released from pancreas

A
  • released when there is low blood glucose
  • purpose is to raise glucose concentration in blood
  • does this by stimulates liver, skeletal muscle and adipose tissue to release glucose
140
Q

what does liver do when stimulates by glycogen

A
  • glycogen is depolymerized back into glucose, which is excreted from liver cells into blood
  • activates glycogen phosphorylase; enzyme that stimulates glycogen breakdown
  • inhibits glycogen synthase; enzyme that does glycogen synthesis
  • inhibits phosphofructokinase-1; enzyme involved in glycolysis
  • increases enzymes involved in gluconeogenesis
141
Q

what does adipose tissue do when stimulates by glycogen

A

release of fatty acids and glycerol from fat –> back into blood

doesn’t effect glucose concentration directly but then other things such as muscle can use these fats instead of using glucose (alternative energy source)

142
Q

Blood glucose concentration is tightly controlled To prevent

A

hyperglycaemia and hypoglycaemia

143
Q

Blood glucose ____ after meals

A

increases

144
Q

Blood glucose ____ as cells take it up and metabolise it

A

decerases

145
Q

insulin and glucagon are synthesized in

A

islets of langerhans; small cell clusters in pancreas

146
Q

insulin _____ glucose storage

A

increases (ie stimulates the take up of glucose from the blood and therefore decreases blood glucose)

147
Q

glucagon _____ blood glucose

A

increases

148
Q

type 1 diabetes

A

auto-immune disease; pancreas does not produce enough insulin

149
Q

type 2 diabetes

A

pancreas produce insulin normally but it is ineffective

150
Q

insulin increases

glucagon increases

A

glucose storage

blood glucose

151
Q

glucose is ____ so it needs help to cross cell membrane; this is done by:

A

polar
glucose transporters: GLUT proteins

152
Q

GLUT 1

A

widespread glucose transporter protein

153
Q

GLUT 2,3,4,5,7

A

tissue-specific glucose transporter proteins

154
Q

are both insulin and glucagon always present in circulation

A

yes, at different concentrations; always some futile cycle happening

155
Q

GLUT2; where and rate

A

liver, endocrine pancreas

rate of glucose uptake proportional to glucose concentration

156
Q

GLUT 3 where

A

brain, nerves; high glucose demand

157
Q

GLUT4 where

A

insulin-sensitive transporter; only in muscle and adipose tissue

158
Q

insulin ____ liver glycolysis

A

promotes

insulin is released when blood glucose concentration is high and so it also speeds glycolysis in order for more glucose to be used up during glycolysis in order to decrease blood glucose concentration

activates key enzymes in glycolysis by dephosphorylating the enzymes

159
Q

what does insulin do to the enzymes in glycolysis to promote glycolysis

A

dephosphorylates them (removes a phosphate group) which activates them

160
Q

glucagon ___ liver glycolysis

A

slows

glucagon is released when blood glucose concentration is low and so it also slows glycolysis in order for less glucose to be used up during glycolysis in order to increase blood glucose concentration

does thus by phosphorylating the key enzymes involved

161
Q

what does glucagon do to the enzymes involved in glycolysis to slow the process

A

phosphorylates the key enzymes (addition of a phosphate group) in order to deactivate them

162
Q

glycogen synthase and glycogen phosphorylase

A

glycogen synthase: synthesizes glycogen by allowing activated glucose to be added to the glycogen chain

glycogen phosphorylase; takes a glucose off the glycogen chain and adds a phosphate group back on: turns it into glucose-1-phosphate

glucose on terminal groups (end of the glycogen chain on any of branch points) where these enzymes can act

163
Q

insulin effect on glycogen synthase and glycogen phosphorylase

A

increase glycogen synthase; ie adds glucose to glycogen and increases glucagon storage

164
Q

insulin _____ glucagon secretion

A

suppresses

165
Q

mechanism of insulin action

A
  • Insulin binds to its receptor, a protein tyrosine kinase, never actually gets inside cell
  • change in structure and conformation of receptor inside cell
  • changes phosphorylation status of insulin receptor
  • downstream events via second messengers

glucagon same shid

166
Q

insulin release is triggered by

A

glucose metabolism; ie high blood glucose

167
Q

insulin _____ glycogen synthase and _____ glycogen phosphorylase

A

increases
decreases

glycogen stores glucose; insulin when blood glucose is high; activates glycogen synthase to store more glucose to decrease blood glucose

168
Q

second messengers

A

small molecules that transmit signals

169
Q

G protein coupled receptors produces

A

IP3

170
Q

normal blood glucose in
monogastrics
ruminants
birds

A

monogastrics: 5mM
ruminants; 3mM
birds; 14mM

171
Q

cats and horses blood blucose

A
  • little to no glucose from feed
  • rely on gluconeogenesis for blood glucose
172
Q

in ruminants describe glucagon and insulin after a feed

A
  • BOTH glucagon and insulin increase w feeding; highest 2-4 hours w feed
  • BOTH decrease in starvation
  • effect on insulin on liver is MARGINAL in these animals
  • high glucagon stimulates gluconeogenesis (liver); stimulated from VFAs
173
Q

IP3 and DAG are both

A

second messengers

174
Q

is IP3 polar

A

yes very, therefore in cytosol

175
Q

is DAG polar

A

no, therefore in membranes

176
Q

second messenger vs intracellular signalling

A
  • 2nd messenger; peptide or amine hormones, like insulin/ glucagon which are proteins; too large to enter cell, attach to receptor outside of cell and rely on second messengers inside cell : alter activity of preexisting enzyme, small impact, fast
  • intracellular; steroid or thyroid hormones, can enter cells and hormone-receptor complex acts in nucleus: alter amount of newly synthesized proteins (alter transcription of specific genes), big impact, slow
177
Q

epinephrine (adrenaline)

A
  • increase heart rate
  • blood pressure
  • dilation of respiratory passages
  • increases glycogen breakdown
  • decreases glycogen synthesis
  • increase glyconeogenesis
  • increase glycolysis (this one doesn’t make sense, everything else similar to glucagon)
  • increase glucagon secretion
  • decreases insulin secretion
178
Q

cortisol

A
  • liver: increase gluconeogenesis
  • muscle: proteolysis: stimulates release of amino acids
  • adipose: stimulates hydrolysis of TAG into fatty acids
  • counterbalances insulin
179
Q

T3 controls

A

basal metabolic rate (BMR)

180
Q

T3 binds to

A

transcription factor RXR/THR –> promoter of some genes

stimulates expression in some genes; alters transcription

181
Q

mammalian fuel reserves

A

glycogen (liver and muscle)
TAG (adipose)
protein (muscle)

182
Q

glycaemic index of food

A

rate at which glucose concentration in blood increases after eating that food

183
Q

low glycaemic index diets

A
  • smaller increase in blood glucose after meals
  • helps animals lose weight
  • increases insulin sensitivity
  • increases diabetes control
  • feel full longer
  • increase physical endurance
184
Q

high glycaemic index increases

A

carbs after work

185
Q

what happens in adipose when low blood glucose

A

lipolysis:
TAG –> FA+ glycerol
FA can be used in liver, skeletal muscle and cardiac muscle via beta oxidation

186
Q

during starvation

A
  • no glucose stores, no glycogen
  • liver makes glucose via gluconeogenesis from amino acids
  • means skeletal muscle is doing proteolysis; protein –> amino acids (this only happens when fat stores run out!!!!! last resort)
  • adipose is undergoing lipolysis: TAG –> FA + glycerol
  • glycerol is used for gluconeogenesis in liver
  • FA can be used as energy in skeletal muscle via beta oxidation
  • liver turns FA into ketone bodies via beta oxidation and ketogenesis
  • cardiac muscle and brain uses ketone bodies as energy source (FA can be turned to ketone bodies in liver)
187
Q

ketone bodies are produced in

A

liver during fasting

188
Q

in tissues other than liver, ketone bodies can be converted into

A

acetyl coA and fed into CAC and oxidative phosphorylation

189
Q

2 main ketone bodies

A

acetoacetate
beta-hydroxybutyrate

190
Q

leptin is greek for

A

thin

191
Q

during starvation describe what happens in CAC

A

since malate, one of the substrates of CAC can be used for gluconeogenesis, this will occur and then malate will not turn into oxolacetate and acetyl coA will start to accumulate and turn into ketone bodies

192
Q

how was leptin found

A
  • in lab mice
  • 2 mutant copies of gene (ob/ob) that encodes for a peptide hormone called leptin → eat as if starving even when they are fat
  • without leptin; can’t link adipose stores to hunger
  • if inject leptin into these mice, they would be normal and lose weight
  • db/db mice were obese bc they had an issue with leptin receptor
  • inject leptin into these mice and wouldn’t help them
193
Q

leptin system

A
  • leptin produced in adipose tissue
  • leptin receptor in brain
  • more leptin in blood; signals brain that fat stores are full
194
Q

leptin and starvation

A
  • adipose tissue shrinks
  • less secretion of leptin
  • leptin levels decreased
  • lower thyroid hormone (lower BMR)
  • lower sex hormone
  • increase glucocorticoid; mobilizes energy stores
195
Q

some obesity relate disease in dogs

A
  • Arthritis
  • Hip dysplasia
  • Ruptured cruciate
  • Congestive heart failure
  • Dyspnea
  • Dermatitis
  • Anal Sac disease
  • Hyperlipidaemia
  • Hypertension
  • Hypothyroidism
  • Diabetes
  • Cushing’s disease
  • Cancer
196
Q

milk carbohydrate

A

disaccharide lactose
- one molecule glactose- one molecules glucose

197
Q

milk fats

A

mostly TAG globules

198
Q

milk proteins

A

caseins, serum or whey proteins

199
Q

lactation increases metabolism, what hormone is important

A

growth hormone

200
Q

ketosis

A

high levels of ketone bodies in blood

201
Q

ketosis in dairy cattle

A
  • ketones increased because so much FA in lactating cow
  • body thinks its full
  • increases acidity in blood
  • weight loss, loss appetite, less milk yield

VETS1003 (23 decks)

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