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

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
Q

what is the prcoess of prote turning into clouse

A

break down to amiont acids then amion acids turned to gloucse though gluconegoensis

26
Q

what thype of ells in teh pancreawse are endocrine

A

islets of langerhans

27
Q

alpha cells

A

produced glucagon

28
Q

beta cells

A

produced insulin

29
Q

gamma cells

A

produced somatostatin

30
Q

f cells

A

produced pancreatic polypeptide

31
Q

what does insul cause at a celluallr level

A

uptake of suguars into cells, this cuase glucose oxidation, glycogen synthesis, fat synehtis, protein synethis

32
Q

what is the reuslt of clucaogn

A

incrurea producito of glucose in the liver and then it enter the blood stream

33
Q

what is the insulin precuares

A

proinsulin

34
Q

what is proinsulin made up of

A

insulin ( 2 molecules)
c peptide

35
Q

when does pro insulin sectrieio occur

A

when b cells are activated

36
Q

useuflnes of c peptides

A

it cna be used to show fucntio of pancrawse for those taking insulin suppleemets

37
Q

what hormones lower bg

A

only insulin

38
Q

how is exces glucose sotroend

A

glycoen in liver and mucles, and trigalycies in liver and adipose tissues

39
Q

main energy source during absobative state

A

gloucse

40
Q

how does abundenet glucose ente the cel

A

glut 2 transpoerter

41
Q

effect of increase glcuose in cell

A

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
Q

effect on beta cell of lower bg

A

atp low, so ka open, thius les effect on ca channels

43
Q

what recepotr does insulin bind to

A

tyrosine kinase recepotors
glut 4

44
Q

how does the glut 4 trnapon work

A

when inuliin bindsm, it moves to the edge of the cell though exocytosis, this allows things glcuoses to go through into the cells

45
Q

what is teh glut 1 and glut 3 cellfucntion

A

1 - basla glucose, uptake into the tissues, brain kideya and rbc

46
Q

what is teh funcito fo glut 2 cell

A

b cell of prancrea dn liver

47
Q

how does teh liver take up gloucse

A

though glut 2 transporters

48
Q

effect of insulin on liver

A

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
Q

effect of low insulin on liver

A

glucose leavs the cell though glut 2 transporter due to lower glucose out side the cel

50
Q

effect of insulin of glycogen phsopghase

A

inhibits it meaning that glygcogen is not broken down, hleping to lower bg levels

51
Q

effect of insulin onf glycogen sysnthesi

A

increase it mucles and lvier, menaing glucose is turned to glycogen, through glycoen synthase

52
Q

effect of inuslin on amino acids

A

increase uptake in muclce cauing protein syntehis

53
Q

effect of insulin on protein synthiss proteeylssy

A

increase protein syntn and decrease protein brakinod (proeolysis)

54
Q

effect of insulion on triglycolal synstehsi

A

increasea it in adipocyte and liver

55
Q

effect of gluconueogies in liver

A

inhibits it

56
Q

effect of insulin on growth homoen

A

if non existis it means growth hormeon is less effective

57
Q

effect of insulin on na / ka aptapse

A

stimulats it cauing ka into cells

58
Q

what inhibis insulin

A

low bg
stomatostain
a2/ sympathetic
stress

59
Q

what incues insulin

A

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
Q

why is iv gluocse less effectse than oral glouce atstiumalting insulin

A

due to iv glucose not activign vagal nerve

61
Q

insulin half life

A

5 min

62
Q
A

Endocrine (20 decks)

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