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BIOL1025 - Fundamentals of cell biology and physiology > Endocrinology (4) - insulin and glucagon > Flashcards

Endocrinology (4) - insulin and glucagon Flashcards

1
Q

central regulated H regulates

A

anabolism - cell growth

catabolism - breakdown component for energy

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2
Q

in hunger - neurological changes

A

motor neurones - triggered - trembling

<40 = lethargy and <20 - permanent neurological damage

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3
Q

liver function

A

BG buffer system and ketone body formed - glycogen store, glycogenesis centre
largest store = muscle

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4
Q

2H work antagonistically e.g. insulin and glucagon

A

decrease BG = decrease insulin and increase glucagon

opposite when increase BG

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5
Q

fedstate

A

insulin dominate

glucose oxidised - stored as glycogen = fat and protein due to neurological trigger

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6
Q

fast state

A

glucagon dominate - increase glycogenolysis , gluconeogenesis

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7
Q

pathway - glycogen to glucose -

A

glycogen (glycogen phosphorylase) make 2 glucose
using ATP and going downstream
produce pyruvates which is modified by using CoA-SH and NAD+ -> NADH +CO2 to form acetyl CoA

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8
Q

citric acid cycle - TCA cycle - intermediates

A

burn out 2 C on acetyl CoA = Co2 and remove e- - energy

are induced and used for different functions as well

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9
Q

TCA cycle - from producing NADH

A

goes to e- transport chain = more ATP

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10
Q

TCA cycle - acetyl CoA from

A

breakdown of lipid as well

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11
Q

at low BG - triglyceride

A

broken down by adipocytes and FA - sent out to liver

oxidised = acetyl Co-A - transferred back into metabolism tissue

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12
Q

problem of acetyl Co-A

A

with CoA attached - liver cannot send out therefore broken down = acetoacetate - transferred
beta hydroxybutyrate is also produced and sent to tissues
take 2c in acetyl CoA put into acetoacetate and beta hydroxybutyrate

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13
Q

problem of acetone

A

cannot be used therefore excreted
so ketone bodies carried to metabolism tissues and reconvert acetoacetate and beta hydroxybutyrate back to acetyl-CoA put back to TCA

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14
Q

by product ketone body - not converted

A

acidic - COOH therefore dissociate = decrease pH

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15
Q

short term - very low BG - keto

A

lipid - converted to ketone bodies by liver - at normal ketosis
more energy with exception of acetone - excreted via urine/ breath
too much ketone - ketoacidosis - >7.1 - metabolic acidosis
forced by by keto diet - filter ketone out with water = osmotic diuresis

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16
Q

short term - too high BG

A

lose glucose in renal filtrate (reabsorbed) but too much (>180mg)
reabsorption overwhelmed and lost through urine = osmotic diuresis - denatured

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17
Q

long term - change in vascular cells

A

lining BV of endothelia - change ECM - it’s glycated (glucose + surface) = protein glycated
turnover> than normal - build up abnormal ECM - get cholesterol in deposited matrix = vascular disease

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18
Q

long term - increase in blood sugar - renal disease

A

different vascular disease - cardiac, renal fibrotic, retinal as retinal capillaries and peripheral vascular damage
all relates to same thing - abnormal , glycated ECM

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19
Q

how insulin in produced

A

as single preproprotein - cleaved C-peptide but A and B chains bind by disulphide bonds = mature insulin

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20
Q

beta cells for insulin secretion

consists of

A

has GLUT2 in membrane
high levels of ATP close it s gated K+ channels but Na - able to get in
effect membrane charge - more +ve

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21
Q

process of beta cells for insulin secretion as membrane charge becomes +ve

A

Ca2+ channel opens by cellular depolarisation - once charge becomes close to -30 millivolt (set point) - Ca+ allowed in cell and released from ER = insulin granule stored in vesicle - brought to cell surface and secreted

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22
Q

rapid insulin secretion - due to

GLUT2 use

A

monitoring amount of glucose in blood

need GLUT2 transporter for pathway to work and produce insulin

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23
Q

increase in insulin secretion caused by

A

increase BG, free FA and blood a.a.

gastrointestinal H - food ingested ( gastrin, cholecystokinin, secretin)

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24
Q

decrease in insulin secretion caused by

A

decrease BG - fasting

alpha-adrenergic activation - acute stress - low insulin save uptake for CNS

25
Q

insulin receptor

A 
class 2 RTKs - disulphide linked tetramer, remain together
class 1 RTKs - come together on ligand binds
26
Q

2alpha and 2beta subunits form ad function when insulin binds

A

heterotetramer
2 insulin bind to alpha subunits
2 beta subunits - brought together and kinase and auto phosphorylates each other - active autophosphorylation sites
kinase region and phosphorylates down stream molecules

27
Q

effect of insulin signalling (output)

A
  • v. rapid fusion of intracellular vacuoles with cell surface carry GLUT4 and a.a. transport in membrane
  • activate intracellular E
  • increase gene expression
28
Q

fast transfer of glucose of a.a. transporters to membrane

modifying vesicles

A 
insulin receptor activated - look for IRS-1 phosphorylase - binds to kinase in membrane - PI-3K 
take Pi(4,5)P2 and add phosphate - increase charge
- kinase attachment (PDK-1) bind to PkB = vesicle modification
has lots of intermediate step - can be amplified
29
Q

some signalling cascade goes down to PkB - phosphorylation of GSK3

A

active - remain glycogen synthase alpha in active state - inactivating the activator
increase activity of glycogen synthase - store glycogen - muscle and liver cell
decrease activity of glycogen phosphorylation - decrease glycogen use
increase glucokinase, PFK-1, pyruvate dehydrogenase - use glucose - breakdown

30
Q

IRS-1

A

insulin receptor S1

31
Q

PI-3K

A

phospho-Inositol - 3-kinase

32
Q

PkB

A

phosphokinase beta

33
Q

increasing gene expression - slowest

A

kinase amplification chain - ERK

MAPK goes into nucleus and turns on transcription factor

34
Q

results for carbohydrate from effects of insulin signalling

A

glucose used/stored, excess glycogen converted to FA

inhibits gluconeogenesis but glucose used as energy source/ store

35
Q

results for protein from effects of insulin signalling

A

insulin works with growth H
increase protein formation and storage and uptake of a.a.
decrease breakdown
increase gene transcription/ translation - inhibiting protein catabolism - gluconeogenesis

36
Q

results for lipid from effects of insulin signalling

A

excess glucose - convert to acetyl CoA to FA in liver

stops lipid breakdown - FA released as VLDL absorbed by adipocytes - inhibits H sensitive lipase - increase storage

37
Q

glucagon - glucose agonist - alpha cells - glycaemia - increase blood sugar level

A

due to decrease in BG - its secretion

has BLUT1 - allow glucose in cell and broken down in TCA cycle = ATP

38
Q

decrease in BG in glucagon-glucose agonist

A

decrease ATP:ADP ratio

39
Q

K+ channel activated by ATP means

in terms of Ca2+ etc

A

decrease ATP - close channel but Na+ channel open due to depolarisation = increase polarity in membrane
voltage gated Ca2+ channel opens - Ca2+ enter = vesicles and H fuses with membrane - release glucagon into EC space into blood

40
Q

glucagon function - amplification of making glucose

A

bind to G protein-linked receptor - splits and activated
alpha unit bind to adenyl cyclase - activated
=ATP convert to CAMP binds to Pka - activated
phosphorylase - cleaves glycogen = glucose-1 phosphate = glucose
highly amplified - 5-10 ug of glucagon = x2 BG in mins

41
Q

glucagon causes

A

glycogenolysis and gluconeogenesis = increase BG - opposing insulin
increase a.a. uptake for energy

42
Q

regulation of glucagon expression and release

decrease blood sugar

A

induce glucagon (ATP gated) - before meal

43
Q

regulation of glucagon expression and release

increase blood sugar

A

inhibit glucagon expression - after meal

44
Q

paradoxically - v. high serum a.a.

A

increase glucagon release = glucose

45
Q

diabetes

A

failure of water reabsorption of kidney collecting duct
2 flavour - insipidus(no taste) and Meletus(sweet) - increase glucose and ketone body
2 forms - type 1 and 2 - both lack utilisation of glucose - mobilise of lipid and protein = energy

46
Q

type 1 diabetes

A

lack insulin secretion due to AI destruction of beta cell

combo of genetic and environmental factor

47
Q

type 2 diabetes

A

body cannot respond to insulin (non-insulin dependent)

48
Q

osmotic diuresis

A

in adrenal diabetes and insulin failure

cause cushing’s disease or gestation diabetes

49
Q

signs - high BG - >180mg/100ml

A

urine contains glucose - osmotic diuresis - polyuria - dehydration - increase thirst

50
Q

use protein and lipids as metabolic fuels

A

increase appetite and wasting and metabolic acidosis

51
Q

metabolic acidosis

A

lipid convert to ketone bodies

therefore more osmotic diuresis, acetone breath

52
Q

fibrosis

A

long term hyperglycaemia - change in endothelial cell
ECM caused by glycation
= damage to peripheral nerve due to insufficient blood supply

53
Q

signs of diseases

A

vascular damage, hypertension and cardiovascular disease

54
Q

abnormal (glycation) matrix shown

A

laid down and cholesterol being placed in this

getting glycated protein cross linked ECM - break down - BV start packing up

55
Q

eye - diabetic retinopathy

A

BV close up

56
Q

BV pack and ulcer - in what tissue

A

peripheral tissue

if v. bad - lose limb

57
Q

incidence / prevalence - type 1

A

1-30 new case

highest - Scandinavia

58
Q

incidence / prevalence - type 2

A

3800000 in UK

BIOL1025 - Fundamentals of cell biology and physiology (21 decks)

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