3 - Control of Metabolism and biochemistry (part 1) Flashcards

1
Q

what is teh energy balance equation

A

energy of body = energy intake - energy output

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2
Q

what is teh feedin centre

A

an area of the body that promoes feeling of hunger and the drive to eat

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3
Q

what is the satitey centre

A

area of body that promotes fullness and suppprese the feeding cenrue

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4
Q

waht is the satitery controled by

A

insulin

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5
Q

what is glucostatic theory

A

food intake is determined by the blood glucose, higher blood gluoce lower drive to eat

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6
Q

what is the lipo static theroy

A

Food intake is determined by fat stores

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7
Q

what is leptin

A

a peptide hromone released by fat stores which depresses feeding activity

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8
Q

what ar ethe energy outputs

A

celluarlar wrok
mechanical work
heat loss - about 50 % of energy output

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9
Q

what is metabolism

A

intergration of all the biocehmical processes within the body

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10
Q

3 elements of metabolims

A

utilising that energy for work
extracting energy from nutrients in food
storing erngyer

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11
Q

what is anabolic pathways

A

build up of food molcues

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12
Q

what is catolboic patheya

A

break down of food moclues

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13
Q

what is the absorbative state

A

ingested nutrietn supply the energy needs of the body and excess is stored

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14
Q

what is the post absobative state

A

fasted state where nutirein in plasma decrease

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15
Q

is post absoibatie catabolic or anabolic

A

catabolic

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16
Q

is a bsobvative anabolic or catabolic

A

anabolic

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17
Q

what is the meaning of an obligatory glucose utiliser

A

needs gluco9es to servive as it is it only source of energy

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18
Q

examples of obligator glucose utiliser

A

brain - can oly use glucose, apart from ketones in extreme circumstances

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19
Q

how is glucose maide

A

from glycogen
amio acids

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20
Q

normal range for blood clouse

A

4.2 - 6.3 mM
5 is normal

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21
Q

what range is hypoglycemai

A

bg<3mM

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22
Q

whihc ways can diabets effect insulin

A

loss of lipogensis - build up of fats
loss of metaboolism into thsiiedsu
loss of glycogeneisn, leading to loss of glycogen stores

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23
Q

what makes up fats

A

free fatty acids and glycerol

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24
Q

what ahppens to excess clgouse

A

turns to fats

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25
what is the prcoess of prote turning into clouse
break down to amiont acids then amion acids turned to gloucse though gluconegoensis
26
what thype of ells in teh pancreawse are endocrine
islets of langerhans
27
alpha cells
produced glucagon
28
beta cells
produced insulin
29
gamma cells
produced somatostatin
30
f cells
produced pancreatic polypeptide
31
what does insul cause at a celluallr level
uptake of suguars into cells, this cuase glucose oxidation, glycogen synthesis, fat synehtis, protein synethis
32
what is the reuslt of clucaogn
incrurea producito of glucose in the liver and then it enter the blood stream
33
what is the insulin precuares
proinsulin
34
what is proinsulin made up of
insulin ( 2 molecules) c peptide
35
when does pro insulin sectrieio occur
when b cells are activated
36
useuflnes of c peptides
it cna be used to show fucntio of pancrawse for those taking insulin suppleemets
37
what hormones lower bg
only insulin
38
how is exces glucose sotroend
glycoen in liver and mucles, and trigalycies in liver and adipose tissues
39
main energy source during absobative state
gloucse
40
how does abundenet glucose ente the cel
glut 2 transpoerter
41
effect of increase glcuose in cell
increase atp, leading to the potaium channel closing, this o;pens the ca channel , this then triggers the ca 2+ signally and realse insulin into the ciruclation
42
effect on beta cell of lower bg
atp low, so ka open, thius les effect on ca channels
43
what recepotr does insulin bind to
tyrosine kinase recepotors glut 4
44
how does the glut 4 trnapon work
when inuliin bindsm, it moves to the edge of the cell though exocytosis, this allows things glcuoses to go through into the cells
45
what is teh glut 1 and glut 3 cellfucntion
1 - basla glucose, uptake into the tissues, brain kideya and rbc
46
what is teh funcito fo glut 2 cell
b cell of prancrea dn liver
47
how does teh liver take up gloucse
though glut 2 transporters
48
effect of insulin on liver
binds to a tyrosine kinase inhibitor, reaction caues a hexocine molcues to lower glucose by causing glucose to turn into glucose 6 phosopahe and cuaing atp to turninto adp, this keep sinlusing lowe ing the cell driving more in
49
effect of low insulin on liver
glucose leavs the cell though glut 2 transporter due to lower glucose out side the cel
50
effect of insulin of glycogen phsopghase
inhibits it meaning that glygcogen is not broken down, hleping to lower bg levels
51
effect of insulin onf glycogen sysnthesi
increase it mucles and lvier, menaing glucose is turned to glycogen, through glycoen synthase
52
effect of inuslin on amino acids
increase uptake in muclce cauing protein syntehis
53
effect of insulin on protein synthiss proteeylssy
increase protein syntn and decrease protein brakinod (proeolysis)
54
effect of insulion on triglycolal synstehsi
increasea it in adipocyte and liver
55
effect of gluconueogies in liver
inhibits it
56
effect of insulin on growth homoen
if non existis it means growth hormeon is less effective
57
effect of insulin on na / ka aptapse
stimulats it cauing ka into cells
58
what inhibis insulin
low bg stomatostain a2/ sympathetic stress
59
what incues insulin
vagaus nerve amino acis bg glucaon gastrin, secreitn a, ckk, glp1 and gip due to them being rwlaed by ileum and jejumin in response to nutireants
60
why is iv gluocse less effectse than oral glouce atstiumalting insulin
due to iv glucose not activign vagal nerve
61
insulin half life
5 min
62