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GM&H II (24/10) (Glucagon (Raise blood Glu
Works via cAMP-mediated…
GM&H II (24/10)
Glucagon
Raise blood Glu
- Works via cAMP-mediated cascades
~ Liver: activate GP, inactivate GS
~ Liver: reduce [F2,6BP] so
stimulate GNG, inhibit Glycolysis
~ Inhibit Pyruvate Kinase
(prevents Phosphoenolpyruvate from
being converted to A-CoA)
- Amass Phosphoenolpyruvate favours GNG
~ Stimulate PEPCK
:pencil2: works via Tyr Kinase Rec via cAMP
- GP: gly→ glu
- Pyruvate Kinase: first steps in Glycolysis
~ "transfer of Phosphate*
Affects Adipose T to spare glu 4 brain
- also via cAMP cascades
- @ adipose T: activate TAG hydrolysis
~ Phosphorylate perilipin -
to expose the lipid droplet to Lipases
(perilipin - essential in mobilising fats)
~ Activates hm-sensitive Lipase
- Result in FA transport to other Ts
~ glu is spared for brain
-
Increase blood Glu
- Glucagon stimulate liver cells to bd gly,
~ release glu into blood
- Stress hm Epinephrine
:pencil2: hm gly stores - 4 itself, selfish
~ 4 FOF response
Adrenaline:
- Stimulate same cAMP cascades
as Glucagon in fat & liver, but...
~ also stimulate Glucagon, inhibit Ins secretions
~ bd musc & liver gly
~ stimulate Glycolysis, thus Lactate 🐝
(via Anaerobic respiration)
Stage One
(fasting)
Typical post meal, low Glu
- ↑ GLUCAGON, ↓ INS
- Liver: ↑ Gly degradation & GNG
(x have much Gly stored in liver so fast deplete)
- Musc: ↓ Glu use
- Liver & Adipose T:
~ ↑ TAG degradation
~ ↑ 𝛃-oxidation
~ ↓ FA synth
- [Glu] maintained
"but then Gly is depleted, so what abt the br?"
- alt fuels can be used by other cells in bod
Stage Three
- Fat reserves depleted
- Pros: pri é source - real trouble
~ x stored - loss of func
- Muscs deplete fast
- Non-ess pros used up 1st
Metabolic Problems
- Kidneys take over GNG from Liver
~ bc issa problem?
- After non-ess, ess pros used
(eg heart musc)
- Eventually stop cell func
~ organs shut down
Overall Effect
- Pancreas: ↓ Ins secretions
- ↓ Metabolic rate
- Organs shrink
~ Villi in gut - less capacity
to absorb nutrition
- Total body shut down & DEATH
Fuel Use
Over 4 hrs of Normal H Metm:
- After meal: ↑glu,
~ Ins stimulate Glycolysis & Gly synth
- 2+ hrs after: blood glu starts to drop
~ Secrete gly via pancreas
~ liver gly release glu
- 4 hrs: (more bd of liver gly)
~ more glucagon
~ more TAG hydrolysis,
~ FA - fuel 4 musc & liver
(so glu → brain)
:pencil2: Ins stimulate:
- Glu uptake & FA synth
- "post prandial" = after eating
Effects of
Prolonged Fast
Musc beings to be used 4 fuel
- Liver (trans)deaminates aas
~ convert amino grs → urea
~ C skeletons of glucogenic aa
converted to pyruvate,
then to glu via GNG
(to maintain glu level)
~ provides glu 4 br
- FA oxidised to A-CoA but
OAA depleted to make glu,
(during GNG) so forms KBs
~ exported to other Ts
:pencil2: A-CoA x go thru TCAc,
(bc OAA depleted to make glu)
- amass A-CoA ; KBs 4 br / other Ts
- FFAs x cross barrier so x for br
-
GNG
- Liver, some in kidneys (when starve)
- Some steps reverse of Glycolysis
~ several differences
- Starts in mta - OAA 🐝
- Pyruvate → OAA → Glu
- FA x used bc can't convert A-CoA to pyruvate :red_flag:
Precursors:
- Lactate - from RBC
- Glycerol - from TAG, only lil amt available :red_flag:
- AAs - remove amine gr, can enter as
pyruvate or OAA
- NB: all TCA intermediates can be converted to OAA
-
Early Starvation
18-48h since last meal
- Fast muscular wasting - 80g/day
~ due to max GNG activity - 4 br
~ thus max urea production
- NB: as prolong starve, KBs meet br é needs,
~ less need 4 glu, less musc degraded
- Then 20g/day - imp 4 survival!
~ High early bc bod thinks will be fed soon
Stage Two
From 24 hrs since last meal
- Lasts 24 days
- Fat: pri é source
- Liver bd FAs → KBs
- After 1 week, br use Glu + Ketones
Plasma Levels of FAs, Glu, KBs
during a 6-week Fast
-