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Glu Metm & Ho
(24/10) (Blood Glu Ho (5 PHASES OF GLU HO :pencil2:…
Glu Metm & Ho
(24/10)
Blood Glu Ho
A balancing act
- between Fuel Availability & T Needs
- eq: 5 mmol
- balance - harder when involve diseases
After a carb-rich meal:
- Change [glu],
~ and the hms [Ins] & [glucagon]
:pencil2: Ins - track glu level, proportional
- Glucagon: opp to glu & Ins
~ opposing effects to Ins
-
Normal
- Fasting levels - 3.5-5.5 mM
- Fed levels - 5.5-7 mM
- 45% all glu → brain
- mM x 18 = mg/dL
Brain
- Consumes 20% total body O2 @ rest
~ (Br - 2% total bod weight)
- Metm uses 130g glu/day
- Generated ATP used by Na+/K+ ATPases (ion chs)
to maintain memb potential 4 NI conduction
- Preferred guel: glu
~ starve: KBs (𝛃-hydroxybutyrate)
No gly stores :pencil2:
- liver & musc do
- for every 1g gly stored, carry 3g water
~ x physiologically feasible
Dpds on blood glu
- Lower bloogd [glu] (<2.5 mM) cause:
~ br dysfunction, coma
- Extended period (hypoglycemia):
~ irreversible br damage / death
Low Blood Glu
Physiological effects in Hs
-
Glucose
:pencil2: glycogenolysis: bd gly
- some: only use glu 4 fuels
~ eg RBCs
When eat:
- Intestines → blood: increase
- High blood glu:
~ Pancreas → blood - INSULIN
- pancreas - endocrine organ, 𝛃 cells
INSULIN -
high glu, "fast"
Stimulate conversion of excess Glu to Gly
- Musc & fat: stimulate glu uptake
(via Glu transporters)
~ Glu (phosphorylated) → G-6-P
- :red_flag: Liver: stimulate Gly Synthase,
inactivates Gly Phosphorylase
~ G-6-P (polymerised) → Gly
:pencil2: glu stored as...
- ...gly in liver, musc
- ...fat in adipose T
~ GS; gly - activate by dephosphorylation
~ GP: bd gly - inactivate by dephosphorylation
Stimulate conversion of excess Glu to Fat
- Liver: stimulate Glycolysis
~ G-6-P → (pyruvate →) A-CoA
- Liver: stimulate TAG synthesis
~ A-CoA → TAG, exported by VLDL
- Fat: stimulate TAG synth
Table: Effects of Ins on Blood Glu
- ↑ Glu uptake = ↑ Glu transporters (in target molcs)
- Liver: activate Glucokinase (phosphorylate Glu)
~ so high transporters capacity
~ so stimulate Glu uptake
- PFK: phosphofructokinase
- 3 main effects: glu uptake, gly production,
storage of FAs & TAG
Glycogen Storage
Ins affects Liver
- in/activation of metabolic enzs
- 4 Gly synthesis & bd
- Glu transport in liver is high capacity,
(on all the time - unlike musc, adipose T)
~ insensitive to Ins
Ins affects Musc - & adipose T
- Also affects Glu transport
~ stimulate Glu transporters to cell surface
to increase glu uptake
- In/activation of metabolic enzs
~ 4 Gly synth & bd
- activate GS: UDP-Glu → Gly
:pencil2: signal transduction
- ; 2nd messengers like cAMP,
~ stimulate GS: UDP-Glu → Gly
- @ same time, Ins signalling molc turns off GP
- when Ins + rec, change enz activity win secs-mins
LO:
- Describe main funcs of Ins to maintain blood glu levels
- Und: glycogen levels regulated via Ins
& actions of metabolic enzs
- Und: must balance btn glycogen & Ins
- Und what type of rec Ins signals thru
- Und the stages of starvation
- Describe the 3 stages, what fuels used in each
- Describe overall effect of starvation on body
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