metabolism Flashcards
(201 cards)
1
Q
proteins digested into
A
amino acids
2
Q
polysaccharides digested into
A
monosaccharides
3
Q
TAG digested into
A
fatty acids
4
Q
what organ plays a central role in processing and distribution of nutrients, and supplies nutrients to tissues via bloodstream
A
liver
5
Q
Autotrophs
A
(“self-feeders”) make organic materials from inorganic materials in the environment
* The biosphere’s producers — Plants
6
Q
Heterotrophs
A
(“other-feeders”) use compounds produced by others
* The biosphere’s consumers — Animals
7
Q
What is Metabolism
A
Metabolism is the sum of the chemical reactions that convert nutrients
into energy and complex molecules within cells
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
9
Q
flows of metabolic pathways
A
inputs; outputs; passage along pathways
10
Q
pools of metabolic pathways
A
amounts of molecules
Filled (supplied) or emptied (by demand) by catabolic and anabolic pathways
11
Q
space and time of metabolic pathways
A
not all pathways necessarily occur at the same time, or in the same place
12
Q
3 main energy-containing nutrients
A
carbs, fats and proteins
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
14
Q
all metabolic pathways must have overall ____ free energy
A
negative
15
Q
can anabolic pathways simplu reverse catabolic pathway
A
NO
16
Q
glycolysis, substrate and product
A
1 glucose –> 2 molecules of pyruvate, makes 2ATP
17
Q
glycolysis takes place in
A
cytosol
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
19
Q
acetyl coA is a 2C acetyl croup esterified to
A
co-enzyme A
20
Q
aceytl coA has a central role in
A
metabolism
21
Q
acetyl coA is put into CAC and what energy do you get out
A
NADH
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
23
Q
where does CAC occur
A
mitochondria
24
Q
where does beta oxidation occur
A
mitochondria
25
3 main VFA
acetate
propionate
butyrate
26
enzymes from _____ and _____ digest dietary peptides and amino acids (protein)
stomach and pancreas
27
Protein breakdown (hydrolysis back to amino acids) occurs constantly in cells by two main pathways:
* Cytosolic pathway: involves ubiquitin and the proteasome
* Lysosomal pathway: proteins are taken up by lysosomes and hydrolysed by
proteases (cathepsins)
28
amino acids split into
amine group --> urea cycle --> urea
and
carbon skeleton --> multiple fates such as ketone bodies, acetyl coA, glucose, CO2
29
what is purpose of CAC etc making NADH
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
30
is pyruvate dehydrogenase reversible
NO its irreversible
31
can acetyl coA turn back into glucose
NO
32
gluconeogenesis
Plants: 3-phosphoglycerate
(Calvin cycle) → glucose
Animals: non-carbohydrate
precursors → glucose
– important in fasting
33
fats breakdown vs fatty acid synthesis
breakdown (beta oxidation)
location: mitochondria
coenzyme: NAD+/ FAD
enzymes: 4
synthesis
location: cytoplasm
coenzyme: NADPH
enzymes: 2
34
protein synthesis
Ribosomes translate mRNA and synthesize protein
35
enzymes lower
activation energy
36
mammalian genome has ~____ genes that code for proteins
30 000
37
in eukaryotes can one gene code for several proteins
yes
* post-translational modification
* alternate splicing of different exons in the mRNA transcript
38
To control the amount of a protein in a cell
– 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
39
Covalent modification alters protein _____ → regulates activity
conformation
40
what is a reversible way of regulated proteins
Common important modification: phosphorylation (addition of phosphate group) of serine, threonine or tyrosine side chains
41
protein kinases
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
42
what is an irreversible way to regulate proteins
activation of a precursor: ie inactive forms of proteins exist and then can be activated (irreversible)
43
protein kinase examples and what they are activated by
- 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
44
protein phosphatases
enzyme that cuts off phosphate groups from proteins (opposite of protein kinases)
45
protein control of activity by non-covalent binding of
effector; may enhance or inhibit activity (allosteric regulation like a built in regulatory network, feedback)
46
* Allosteric activation, inhibition
* Competitive inhibition
timescale:
less than 1 second
47
* Activation of preformed precursor proteins
* Activation/inactivation by reversible covalent
modification
time scale
seconds to minutes
48
* Synthesis of new protein in response to signals (e.g. hormones)
timescale
minutes to hours
49
* 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
days to weeks
50
Erythrocytes
carry O2 from lungs to tissues and CO2 from tissues to lungs
51
Plasma
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
52
blood delivers what nutrients to brain
glucose, ketone bodies
53
blood delivers what nutrients to cardiac muscle
glucose, FA, ketone bodies
54
blood delivers what nutrients to skeletal muscle
glucose, FA, ketone bodies, amino acids
55
plasma proteins are involved in
blood coagulation and fibrinolysis
56
albumin (plasma protein)
carries fatty acids and many other molecules
57
lipoprotein (plasma protein)
carry TAGs and cholesterol esters
58
Most plasma proteins are synthesized in the
liver
59
After absorption from the gut, sugars (monogastrics; mainly glucose) and amino acids, VFAs, and some TAG, pass via the blood to the
liver
60
most TAG is stored in
adipose tissue via lymphatic system
(some in liver)
61
Hepatocytes transform nutrients into
fuels and precursors for other tissues
62
Kinds & amounts of nutrients supplied by the
liver vary with
diet and the time between feeds
63
liver: Demand by non-hepatic tissues depends on
the organ and on the activity of the animal
64
why does the liver have remarkable metabolic flexibility
* Builds up stores when fuel is plentiful; releases when needed
* Interacts with other organs via the blood, helped by hormones
65
GLUT2
glucose transporter ensures that hepatic glucose
concentration is the same as in blood
66
Glucose is phosphorylated by _____ to glucose-6-phosphate when it gets into liver
glucokinase (glucose-6-phosphate is negative and large and basically traps the glucose inside the liver cell)
then turned to glycogen
67
liver stores glucose as
glycogen
68
adipose tissue stores ____ and supplies ____
TAGS
fatty acids
69
adipose tissue is ___% of young mammals weight
15-25%
70
do all animals need blood glucose
YES; RBCs and brain rely on it!
71
cats and ruminants blood glucose
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
72
rumen microbes ferment
cellulose --> VFAs
73
horse digestion
digestible carbs --> stomach --> glucose
fat --> small instestine --> FAs
fermentable fiber --> large intestine --> VFAs
74
rumen microbes
Cellulytic bacteria, protozoa hydrolyze cellulose
75
rumen microbes turn cellulose
--> cellobiose --> glucose --> VFAs
76
fate of VFAs
bloodstream --> oxidized --> energy
also --> amino acids and vitamins
77
acetate
VFA, for energy and FA synthesis
78
propionate
VFA, forms glucose in gluconeogensis
79
butyrate
VFA, for energy and FA synthesis, some metabolized in rumen wall and liver then to tissues
80
VFA absorption
Passive diffusion
* 75% reticulo-rumen
* 20% omasum and abomasum
* 5% small intestine
81
bloat
lush pasture --> increase sugar --> increase gas
82
cats blood glucose comes from
glucogenic amino acids (amino acids from diet that have gone through gluconeogenesis)
83
horses and ruminants blood glucose come from
VFAs and glucogenic amino acids (amino acids that have undergone gluconeogenesis)
84
gluconeogenesis is active during
fasting
85
3 main substrates of gluconeogenesis
* Amino acids (from muscle protein breakdown)
* Glycerol (from fat breakdown)
* Lactate (from anaerobic glycolysis).
86
can fatty acids produce glucose
no!
87
what is the primary energy substrate
carbs -->
monogastrics: glucose,
ruminants; VFAs
88
what is primary substrate for fat synthesis
carbs -->
monogastrics; glucose
ruminants; acetate
89
extent of glucose absorption from gut
monogastrics; extensive
ruminants; little to none
90
cellular demand for glucose
non-ruminants= high
ruminants and cats= high
91
importance of gluconeogenesis
monogastrics= less importants
ruminants and cats= very important
92
intense exercise effects on cell
- cells need to generate lots of ATP
- means its taking glucose-6-phosphate and taking in through glycolysis to generate ATP
- J large
93
resting state (idling) effect on cells
- not much glycolysis is happening
- also not much gluconeogenesis happening
- these relatively balanced
- J is small and balanced
94
J= vf=vr
vf= glycolysis
vr= gluconeogenesis
95
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
futile cycle (constant unnecessary back and forth) making and burning ATP, no gain
96
how does substrate cycling (ie futile cycles) allow fine control of metabolism
* 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
in mitochondria ____ and ____ are tightly coupled
oxidation and phosphorylation
98
in mitochondria, NADH and FADH2 cannot be oxidized unless ____ is present
ADP
99
when would uncoupling of oxidation from phosphorylation occur
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
describe uncoupling of oxidation from phosphorylation in mitochondria
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
highest to lowest capacity for ATP production
OPPOSITE OF fastest to slowest ways to make ATP
* 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
fastest to slowest ways to make ATP
OPPOSITE OF highest to lowest capacity for ATP production
* 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
at rest muscles use ___% of O2
working they use up to ___%
50
90
104
contracting muscles
ATP splits, → energy → fibre contracts
Transfers high-energy Pi → contracting element
ATP → ADP + Pi
** need to be able to regenerate ATP
105
3 sources of ATP for muscle contraction
* Phosphocreatine (PC)
* Glycolysis
* Oxidative phosphorylation
106
Phosphocreatine (PC) positives and negatives as a source for ATP for muscle contraction
positives
* Very quick: 4–5s > aerobic
* One step → energy
Negatives
* Little PC stored, used up quickly
107
rest to exercise oxygen transition
*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
very quick exercise (couple of seconds)
phosphocreatine as source of ATP
109
short burst of exercise (couple of mins) source of ATP
anaerobic metabolism (ie glycolysis)
110
long exercise (hours) source of ATP
aerobic metabolism
111
carb sources during exercises
- blood glucose
- muscle glycogen
112
fat sources during exercise
- plasma FA (from adipose tissue lipolysis)
- intramuscular triglycerides
113
protein sources during exercise
small contribution to total energy
114
blood lactate sources during exercise
gluconeogenesis via cori cycle
115
cori cycle
muscle --> lactate --> liver gluconeogenesis --> glucose --> muscle
116
metabolic cooperation between liver and skeletal muscle
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
what is primary fuel in low-intensity exercise
fats (needs aerobic conditions ie needs oxygen)
118
what is primary fuel in hgih-intensity exercise
carbs
119
crossover concept: Fat → carb as exercise ↑↑, why
* Recruit fast muscle fibers
* ↑ blood epinephrine
120
in prolonged exercise; CHO
--> fat metabolism
121
advantages of TAG for storing energy (4)
* Highly reduced: More energy
* Nonpolar: Anhydrous fat droplets: compact
* More space: Larger total energy store
* Insulation
122
disadvantages of TAG as energy store
- 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
advantages of polysaccharides (glycogen and starch) for energy storage
- most flexible energy source
- very polar, soluble
- hydrolysis --> glucose
- glucose stored as glycogen can be very branched and compact
124
disadvantages of polysaccharides (glycogen, starch) for energy storage
- 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
glycogen is a polymer of
glucose
126
glycogen: a chain of
glucose
can be branched; lots of end points so many places glucose can be added or removed
pretty bulky
127
glycogen synthesis
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
glucose homeostasis during exercise is mediated by hormones like
- noradrenalin (NE), epinephrine (E)
- insulin, glucagon
- thyroxine, cortisol (growth hormone)
129
hormones
small molecules of intercellular communication
130
3 modes of action of hormones
- autocrine; act upon themselves
- paracrine; acts locally
- endocrine; everywhere else, ie acts far away via bloodstream
131
hormone classes based on chemical structure
- steroid hormones
- peptides
- amino acid derivatives
132
hormones alter metabolism in ____ cells
target
133
in presence of high blood glucose (lots of glucose in blood) _____ is released by pancreas
insulin
134
what does insulin do
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
what does liver do when stimulates by insulin
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
what does skeletal muscle do when stimulated by insulin
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
what does adipose tissue do when stimulated by insulin
takes up glucose from the blood, it is turned into fatty acids and glycerol, and stored as TAG (fat)
138
when there is low blood glucose, ____ is released from pancreas
glucagon
139
what does glucagon do when released from pancreas
- 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
what does liver do when stimulates by glycogen
- 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
what does adipose tissue do when stimulates by glycogen
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
Blood glucose concentration is tightly controlled To prevent
hyperglycaemia and hypoglycaemia
143
Blood glucose ____ after meals
increases
144
Blood glucose ____ as cells take it up and metabolise it
decerases
145
insulin and glucagon are synthesized in
islets of langerhans; small cell clusters in pancreas
146
insulin _____ glucose storage
increases (ie stimulates the take up of glucose from the blood and therefore decreases blood glucose)
147
glucagon _____ blood glucose
increases
148
type 1 diabetes
auto-immune disease; pancreas does not produce enough insulin
149
type 2 diabetes
pancreas produce insulin normally but it is ineffective
150
insulin increases
glucagon increases
glucose storage
blood glucose
151
glucose is ____ so it needs help to cross cell membrane; this is done by:
polar
glucose transporters: GLUT proteins
152
GLUT 1
widespread glucose transporter protein
153
GLUT 2,3,4,5,7
tissue-specific glucose transporter proteins
154
are both insulin and glucagon always present in circulation
yes, at different concentrations; always some futile cycle happening
155
GLUT2; where and rate
liver, endocrine pancreas
rate of glucose uptake proportional to glucose concentration
156
GLUT 3 where
brain, nerves; high glucose demand
157
GLUT4 where
insulin-sensitive transporter; only in muscle and adipose tissue
158
insulin ____ liver glycolysis
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
what does insulin do to the enzymes in glycolysis to promote glycolysis
dephosphorylates them (removes a phosphate group) which activates them
160
glucagon ___ liver glycolysis
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
what does glucagon do to the enzymes involved in glycolysis to slow the process
phosphorylates the key enzymes (addition of a phosphate group) in order to deactivate them
162
glycogen synthase and glycogen phosphorylase
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
insulin effect on glycogen synthase and glycogen phosphorylase
increase glycogen synthase; ie adds glucose to glycogen and increases glucagon storage
164
insulin _____ glucagon secretion
suppresses
165
mechanism of insulin action
* 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
insulin release is triggered by
glucose metabolism; ie high blood glucose
167
insulin _____ glycogen synthase and _____ glycogen phosphorylase
increases
decreases
glycogen stores glucose; insulin when blood glucose is high; activates glycogen synthase to store more glucose to decrease blood glucose
168
second messengers
small molecules that transmit signals
169
G protein coupled receptors produces
IP3
170
normal blood glucose in
monogastrics
ruminants
birds
monogastrics: 5mM
ruminants; 3mM
birds; 14mM
171
cats and horses blood blucose
- little to no glucose from feed
- rely on gluconeogenesis for blood glucose
172
in ruminants describe glucagon and insulin after a feed
- 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
IP3 and DAG are both
second messengers
174
is IP3 polar
yes very, therefore in cytosol
175
is DAG polar
no, therefore in membranes
176
second messenger vs intracellular signalling
- 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
epinephrine (adrenaline)
- 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
cortisol
- liver: increase gluconeogenesis
- muscle: proteolysis: stimulates release of amino acids
- adipose: stimulates hydrolysis of TAG into fatty acids
- counterbalances insulin
179
T3 controls
basal metabolic rate (BMR)
180
T3 binds to
transcription factor RXR/THR --> promoter of some genes
stimulates expression in some genes; alters transcription
181
mammalian fuel reserves
glycogen (liver and muscle)
TAG (adipose)
protein (muscle)
182
glycaemic index of food
rate at which glucose concentration in blood increases after eating that food
183
low glycaemic index diets
- smaller increase in blood glucose after meals
- helps animals lose weight
- increases insulin sensitivity
- increases diabetes control
- feel full longer
- increase physical endurance
184
high glycaemic index increases
carbs after work
185
what happens in adipose when low blood glucose
lipolysis:
TAG --> FA+ glycerol
FA can be used in liver, skeletal muscle and cardiac muscle via beta oxidation
186
during starvation
- 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
ketone bodies are produced in
liver during fasting
188
in tissues other than liver, ketone bodies can be converted into
acetyl coA and fed into CAC and oxidative phosphorylation
189
2 main ketone bodies
acetoacetate
beta-hydroxybutyrate
190
leptin is greek for
thin
191
during starvation describe what happens in CAC
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
how was leptin found
- 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
leptin system
- leptin produced in adipose tissue
- leptin receptor in brain
- more leptin in blood; signals brain that fat stores are full
194
leptin and starvation
- adipose tissue shrinks
- less secretion of leptin
- leptin levels decreased
- lower thyroid hormone (lower BMR)
- lower sex hormone
- increase glucocorticoid; mobilizes energy stores
195
some obesity relate disease in dogs
* Arthritis
* Hip dysplasia
* Ruptured cruciate
* Congestive heart failure
* Dyspnea
* Dermatitis
* Anal Sac disease
* Hyperlipidaemia
* Hypertension
* Hypothyroidism
* Diabetes
* Cushing’s disease
* Cancer
196
milk carbohydrate
disaccharide lactose
- one molecule glactose- one molecules glucose
197
milk fats
mostly TAG globules
198
milk proteins
caseins, serum or whey proteins
199
lactation increases metabolism, what hormone is important
growth hormone
200
ketosis
high levels of ketone bodies in blood
201
ketosis in dairy cattle
- ketones increased because so much FA in lactating cow
- body thinks its full
- increases acidity in blood
- weight loss, loss appetite, less milk yield
