Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

in hunger - neurological changes

A

motor neurones - triggered - trembling

<40 = lethargy and <20 - permanent neurological damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

liver function

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2H work antagonistically e.g. insulin and glucagon

A

decrease BG = decrease insulin and increase glucagon

opposite when increase BG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

fedstate

A

insulin dominate

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

fast state

A

glucagon dominate - increase glycogenolysis , gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TCA cycle - from producing NADH

A

goes to e- transport chain = more ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

TCA cycle - acetyl CoA from

A

breakdown of lipid as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

by product ketone body - not converted

A

acidic - COOH therefore dissociate = decrease pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how insulin in produced

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

increase in insulin secretion caused by

A

increase BG, free FA and blood a.a.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

decrease in insulin secretion caused by

A

decrease BG - fasting

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

25
insulin receptor
``` class 2 RTKs - disulphide linked tetramer, remain together class 1 RTKs - come together on ligand binds ```
26
2alpha and 2beta subunits form ad function when insulin binds
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
effect of insulin signalling (output)
- v. rapid fusion of intracellular vacuoles with cell surface carry GLUT4 and a.a. transport in membrane - activate intracellular E - increase gene expression
28
fast transfer of glucose of a.a. transporters to membrane | modifying vesicles
``` 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
some signalling cascade goes down to PkB - phosphorylation of GSK3
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
IRS-1
insulin receptor S1
31
PI-3K
phospho-Inositol - 3-kinase
32
PkB
phosphokinase beta
33
increasing gene expression - slowest
kinase amplification chain - ERK | MAPK goes into nucleus and turns on transcription factor
34
results for carbohydrate from effects of insulin signalling
glucose used/stored, excess glycogen converted to FA | inhibits gluconeogenesis but glucose used as energy source/ store
35
results for protein from effects of insulin signalling
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
results for lipid from effects of insulin signalling
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
glucagon - glucose agonist - alpha cells - glycaemia - increase blood sugar level
due to decrease in BG - its secretion | has BLUT1 - allow glucose in cell and broken down in TCA cycle = ATP
38
decrease in BG in glucagon-glucose agonist
decrease ATP:ADP ratio
39
K+ channel activated by ATP means | in terms of Ca2+ etc
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
glucagon function - amplification of making glucose
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
glucagon causes
glycogenolysis and gluconeogenesis = increase BG - opposing insulin increase a.a. uptake for energy
42
regulation of glucagon expression and release | decrease blood sugar
induce glucagon (ATP gated) - before meal
43
regulation of glucagon expression and release | increase blood sugar
inhibit glucagon expression - after meal
44
paradoxically - v. high serum a.a.
increase glucagon release = glucose
45
diabetes
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
type 1 diabetes
lack insulin secretion due to AI destruction of beta cell | combo of genetic and environmental factor
47
type 2 diabetes
body cannot respond to insulin (non-insulin dependent)
48
osmotic diuresis
in adrenal diabetes and insulin failure | cause cushing's disease or gestation diabetes
49
signs - high BG - >180mg/100ml
urine contains glucose - osmotic diuresis - polyuria - dehydration - increase thirst
50
use protein and lipids as metabolic fuels
increase appetite and wasting and metabolic acidosis
51
metabolic acidosis
lipid convert to ketone bodies | therefore more osmotic diuresis, acetone breath
52
fibrosis
long term hyperglycaemia - change in endothelial cell ECM caused by glycation = damage to peripheral nerve due to insufficient blood supply
53
signs of diseases
vascular damage, hypertension and cardiovascular disease
54
abnormal (glycation) matrix shown
laid down and cholesterol being placed in this | getting glycated protein cross linked ECM - break down - BV start packing up
55
eye - diabetic retinopathy
BV close up
56
BV pack and ulcer - in what tissue
peripheral tissue | if v. bad - lose limb
57
incidence / prevalence - type 1
1-30 new case | highest - Scandinavia
58
incidence / prevalence - type 2
3800000 in UK

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions