35-38 Flashcards
1
Q
what is stored instead of ATP?
A
fuels to maintain a supply of glucose between meals to provide immediate feul for increased activity, and for long periods when food intake may be adequate
2
Q
what does fat storage consist of?
A
TAG
3
Q
how is TAG stored in adipose tissues?
A
in droplets
4
Q
what is the limit to fat storage?
A
there is no limit, its un limited
5
Q
what is the structure of TAG?
A
3 fatty acids and 1 glyclerol
6
Q
where does the fatty acids and the glycerol for TAG come from?
A
chylomicrons for fatty acids
the backbone of glucose is for the glycerol
7
Q
what does the activation of fatty acids go to?
A
acetyl-CoA
8
Q
what does the esterfication of acyl groups of TAG go to?
A
glycerol 3-phosphates
9
Q
what stimulates the reaction of turning the acyl groups into glycerol 3-phosphate?
A
insulin
10
Q
what stimulates the lipoprotein lipase in the capillaries of adipose tissues?
A
insulin
11
Q
what is the process for the formation of glycerol?
A
glycolysis
when DHAP is converted to glycerol-P by the glycerol-3-phosphate dehydrogenase enzyme
glycerol-3-phosphate acyltransferase and phosphatidate phosphatase followed by diacylglycerol acyltransferase
12
Q
what catalyses the hydrolysis of TAG?
A
hormone-sensitive lipase
this is stimulated by adrenaline and glucagon hormones
this releases FFA and glycerol
13
Q
what is the structure of glycogen?
A
a branched polysaccaride with (a) 1-4 and (a) 1-6 glycosidic bonds
14
Q
where is glycogen stored?
A
in the liver and mucsles and has granules in cytoplasm
15
Q
where does glycogen synthesis occur?
A
mainly in liver and muscle immediatly after a meal
16
Q
what does glycogen synthesis require?
A
energy inputs (ATP and UTP)
has help from glycogen synthase and branching enzymes
17
Q
what stimulates the glycogen synthesis?
A
insulin
18
Q
what does hexokinase use ATP for?
A
to turn glucose to glucose 6-P
19
Q
what doe glucose 6-P do?
A
traps glucose in the cell
20
Q
what does mutase do?
A
doesnt require ATP
turns glucose 6-P to glucose 1-P and is reversible
21
Q
how does glucose 1-P go to UDP-glucose?
A
using UTP which goes to PPi
22
Q
what is UDP-glucose reactive with?
A
glycogen (n) which will form glucogen (n+1) and release UDP
glycogen (n+1) is the new glycosidic bond
23
Q
waht is excess glucose converted into?
A
acetyl-CoA and then into fatty acids by the FA synthase complex in liver cytosol
24
Q
what is liver glucogen released to?
A
as glucose into the blood for the brain
25
what does muscle glycogen do?
releases feul for glycolysis within muscle cells
26
what is excess glucose carbon converted into and where?
fatty acids and occurs mainly in the liver
27
what is the process for glucose carbon converted into fatty acids?
it is an energy-requiring process
its exported as TAGs in VLDL
it is stimulated by insulin
28
what feuls can the brain use?
glucose and not fatty acids
29
what feul does RBCs use?
glucose
30
what feul does the liver use?
mainly fatty acids
31
what feul does the heart use?
mainly fatty acids
32
how much glucose do we need to supply the brain with each day?
120g
33
why do we need to conserve as miuch protein as possible?
to maintain structure and functions, so we dont wanna start breaking down our muscles
34
what is glycogen?
is a polypeptide hormone that is produced by pancreatic (a) cells when the blood glucose drops
35
how much fat does the average person have?
15 kilos
36
how long can 15 kilos of fat produce energy for in a person?
around 40 days
37
what does glycogen stimulate?
lipolysis
38
what does fatty acids feul?
all aerobic tissues except the brain
39
how much energy does fat produce?
38kJ/g
40
what is the highest source of energy?
fat
41
how much kJ a day does the average person expends?
10000 for someone that weights 10kg
42
how much glucose does the liver give the brain each day?
around 20g
43
what is the bodies reserve glucose?
liver glycogen that we use first when we are starving
44
what does glycogen do to the liver?
stimulates the breakdown of glucogen in the liver and mobilizes it back to glucose which can provide enough glucose to the brain for one day
45
what is the structure og glycogen phosphorylase?
a debranching enzyme
46
what regulates the glycogenesis?
glycogen
47
what is the glycogenesis in the liver?
the liver takes a phosphate off the glucose 6-phosphate which makes the glucose be able to cross into the blood and can reach our required amount of glucose in the brain for one day
48
what is glucneogenesis?
the formation of glucose that occurs mainly in the liver and also the kidney cortex
49
what does the synthesis of glucose come from?
lactate from muscle glycogen, alanine from muscle protein and glycerol from adipose tissue (TAG)
50
what is alanine?
amino acids which can be used to stop the breakdown of proteins within the body
51
what stimulates alanine?
glycogen
52
what does fatty acid oxidation require?
energy
53
what does fatty acids do when it comes to gluconeogenesis?
cannot be used to make glucose but the B-oxidation provides ATP and NADH which can be used in gluconeogenesis
54
where does alanine come from?
muscle tissue
55
where does lactate come from?
RBCs
56
where does glycerol come from?
adipose tissue
57
what does the liver need to make glucose?
alanine, lactate, glycerol and glycogen which turns it into glucose
58
what happens to some proteins when amino acids are needed?
they are degraded to amino acids to make glucose
59
where are ketone bodies synthesised?
in the liver
60
what are ketone bodies used for?
they can be used as an energy source for the brain
61
what is the structure of the ketone bodies?
short molecules that are made into acetyl-CoA which works in conjuction with the glucose to produce energy for the brain to function
62
when does the brain use ketone bodies?
when it is starving
63
what happens if we dont reach the required glucose for the day?
then we start using alanine from muscles which over time the breakdown can lead to death
64
what are the metabolic adaptations to starvation?
fatty acids are used by all aerobic tissues except the brain, ketone bodies can be used by the brain to slow down the rate at which we need to breakdown our proteins so the body can last longer
65
how much ATP is enough for 1 second of muscle contractions?
5umol/g
66
what is anaerobic exercise?
high intensity, rapid generation of force, short periods
67
what is aerobic exercise?
steady supply of ATP at low intensity, prolonged, sustained exercise
68
what type of exercise do most activities require?
a bit of both
69
what type of exercise is used the longer you exercise?
the more aerobic is used but there is still some anaerobic exercise
70
how does anaerobic exercise generate ATP?
it doesnt use oxygen so it generates it through phosphocreatine and glycogen
71
how does aerobic exercise generate ATP?
requires oxygen and uses the process oxidation of glucose and fatty acids to produce ATP
72
what is phosphocreatine?
an on-site, fast fuel
it has about 20 umol/g muscle which allows us to go for about 10 seconds
its a high energy phosphate compound
73
how does phosphocreatine work?
the phosphate can be transferred to ADP to make ATP
its an energy buffering system
74
what phosphorylizes the creatine?
creatine kinase
75
what happens if we have too much creatine?
the body the turns it into creatinine which is then excreted through the urinary system
76
what does creatine do for the body?
gives us the ability to do more work in the muscles
77
what is glycogen in muscles?
an on-site store of glucose in the muscle
78
what does glycogen do in the body?
mobilzed to glucose 1-phosphate by glycogen phosphorylase wich cleaves off and gives us glucose 1-phosphate
this is then converted into glucose 6-phosphate which is the feul for anaerobic glycolysis to go into pyruvate
79
what can the making of alot of glucose 1-phosphate lead to?
a build up of lactic acid
80
what is anaerobic glycolysis?
the muscle glycogen source of feul and oxygen is not required
ATP is generated by substrate-level-phosphorylation
81
what is pyruvate reduced to?
lactate to regenerate NAD+ which allows us to keep glycolysis going
82
what can lactic acid lead to?
muscle pH drops thus fatigue
83
what are some factors that regulate glycolysis in exercising muscles?
glycogen mobilisation is stimulated by Ca+ and adrenaline
phosphofructokinase activity
84
what does Ca+ do in glycolysis?
it binds to phosphorylase kinase to help glycogen mobilisation and can help with muscle contractions
85
what is phosphofructokinase activity in glycolysis regulation?
its increased by allosteric regulators (+AMP, +Pi)
86
what can adrenaline kinase turn ADP+ADP into?
ATP+AMP
87
what is aerobic generation of ATP?
oxidation of glucose and fatty acids
this involves an active CAC, ETC of oxidative phosphorylation
88
what does carnitine help with?
moving fatty acids across the mitochondrial membrane for metabolization
89
what is aerobic?
type I fiber property, slow speed of contraction, high endurance, high capillary density, high mitochondrial density and an oxidative metabilc character
90
what is anaerobic?
type II fiber property, fast speed of contractions, low endurance, low mitochoindrial density, high glycogenolytic enzyme activity, high glycolytic enzyme activity and a glycolytic metabolic character
91
what are muscle adaptations to enduarance training?
selective hypertrophy of type I fibers
increased number of blood capillaries per muscle fiber
increased myoglobin content per unit of tissue
increased size and number of mitochondria
increased cristae
increased capacity of mitochondria to generate ATP by oxidative phosphorylation
increased capacity to oxidise lipids to make more ATP and carbohydrates
92
what is EPO doping?
a performance enhancing drugs
it increases RBC count and gives you more oxygen
93
what is EPO?
erthropoeitin
94
what does anaerobic steriods give us?
more muscle
95
what do growth factors give us?
more muscle
96
what does myostatin do?
tells the body to stop making muscle
97
what happens if we turn the myostatin off?
then our bodies will make more muscle
98
what are some symptoms of diabetes?
fatigue, weight loss, intense thirst, frequent urination, hyperglycaemia, glucosuria and ketones
99
how many types of diabetes are there?
2
100
what is type 1 diabetes?
an auto immune destruction of B-cells
its onset between ages 1-25 years
its due to genetic and enviromental factors
101
what is the treatment for type 1 diabetes?
insulin injections
102
what is type 2 diabetes?
resistance to action of insulin
onsets from 45 and onwards years
people are obese
its due to genetivc and enviromental factors
103
what is the treatment for type 2 diabetes?
dieting, exercise and drugs
104
what happens if our blood glucose levels get too low?
sweating, heartbeat increases and sympathetic nervous system may induce vomiting
105
what happens if the blood glucose levels get too high?
we start the non-enzymatic glycation of protein which gets modified proteins that can become compromised and can lead to implications of the capillaries and other areas of the body
can also lead to constriction of blood vessels that leads to gangrene and limb amputation
106
where is insulin secreted from?
B-cells in the pancreas
107
what is insulin?
a peptide hormone secreted in response to high glucose (after a meal) which can drive the uptake of glucose into the tissues
108
what does insulin work on?
liver, muscle and adipose tissue
109
what pathways are effected in type 1 diabetes?
all pathways
110
what pathways are effected in type 2 diabetes?
only some
these could include metabolism, DNA/RNA/protein synthesis, glycogen synthesis
111
what is anti catabolic?
inhibition
112
what is anabolic?
activation that leads to uptake of feuls
113
what ar ethe metabolic consequences of a lack of insulin?
impaired glucose uptake and storage by muscles and liver, increased mobilisation of glycogen for more glucose in the blood, increased glucose synthesis, increased lipolysis, increased ketone body synthesis, reduced removal of TAG from the blood, increased breakdown of tissue protein which leads to weight loss
114
what happens if the body thinks its getting less glucose?
then it starts breaking down proteins and we have weight loss
this is like a starving reaction
115
what can the build up of ketone bodies in the blood lead to?
they can be very acidic and can lead to acidosis
116
what goes up as B-oxidation increases?
the amount of ketone bodies
117
what is the insulin injections?
from recombinant human insulin to mimic the normal rise in insulin caused by a meal
118
what causes hypoglycaemia?
too much insulin and can lead to a coma if the glucose levels in the blood gets too low
119
what is BMI?
the body mass index
120
how is BMI calculated?
weight (kg)
(over)
height (squared) (m)
121
what if someones BMI is greater than 30?
the person is obese
122
what if someones BMI is between 30-25?
then they are overweight
123
what if someones BMI is between 25-20?
then the person is a healthy weight
124
what if someones BMI is less than 20?
then the person is underweight
125
what can an increase in BMI lead to?
high increase in type 2 diabetes and coronary heart disease?
126
what is CHD?
coronary heart disease
127
what does uncoupled mitochondria generate?
heat not ATP
128
what is brown fat?
special thermogenic tissue found in hibernating animals
more common in babies instead of adults
129
what does brown fat consist of?
many mitochondria and fat droplets
130
what is UCP?
uncoupling protein
131
what is uncoupling protein?
originally found in brown fat
its present in the inner mitochondrial membrane
they are regulated proton channels in the membrane
132
what is uncouple ATP synthesis?
from fatty acid oxidation
an electrochemical potential gradient dissipates which results in releasing heat thus increasing metabolic rate and burns excess feuls
133
what are metabolic adaptatiions to cold in penguins?
avian uncoupling protein which is highly expressed in mitochondria and pectoral muscles
this oxidises fatty acids to generate heat
134
what is avUCP?
avian uncoupling protein
135
what do FDG-PET scans show?
areas of high glucose use and high metabolic rate
136
what are BAT-oriented strategies?
to combat obesity to burn off excess feuls as heat
137
what is switching on brown fat diffentation?
might be a potential thermapatic approach for humans obesity treatment
138
how much is obseity related to genes?
30-80%
139
what does the obese gene code?
for leptin
140
what do obese people not produce?
leptin
141
what is leptin?
a hormone that is secreted by fat cells
it signals the brain to decrease food intake an increase energy expenditure
it maintains a normal animal energy balance
142
where is the leptin receptor?
in the hypothalymus of the brain and several other tissues
