sing
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extreme and prolonged fasting can cause:
A. Blood glucose of less than 40 mg/dL
B. The brain uses glucose exclusively for energy demands
C. Decreased hepatic glycerol utilization.
D. Lower than expected hepatic gluconeogenesis
E. Low ketone bodies in serum due to muscle utilization
A&Y
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| MLF
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D) Lower than expected hepatic gluconeogenesis
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| sing
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why? i thought during fasting, intake was low. so blood glucose level was low. so body needed to increase blood glucose by increase gluconeogenesis. why it is the opposite? could anyone explain?
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| MLF
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Yes but this is EXTREME fasting in which there is more ketones being made, not glucose.
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| mjl1717
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A-as far as i know the body is still trying to maintain a normal glucose maybe slightly subnormal but not 40(thats probably an unconscious ER visit)!
B-false -brain can use ketones!
C-false-I think the liver uses this for energy
D-**TRUE AFTER 2-3 weeks WE USE PRIMARILY KETONES!
E-false just the opposite!
Can anyone comment on answer C??
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| sing
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thanks a lot. i am clear now.
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| vrach
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The increased glycerol production due to elevated lipolysis is used in the gluconeogenesis pathway to give glucose.
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| luckiest
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I've read further information from some textbook , 
a)when blood glucose less than 80 insulin will decrease and follow by increase glucagon, epinephrine ,cortisol when BG level 65-70 .SO by this step by step process if the blood glucose reach 40 there're defect in the mechanism such as insulin and glucagon intolerance due to DM I and the aptient has no symptom(adrenergic) of lowering blood glucose so call hypoglycemic unawareness and may be plus the iatrogenic insulin bam!
b)At short trerm fasting ,the brain and RBC are main consumer of glucose
others use glycerol or ketone bodies
But in this Q say long term so I guess the brain will use ketone too
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| luckiest
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c) in short term it's insulin glucagon that act
in long term it's epinephrine,cortisol
and its increase hepatic glycogenolysis&gluconeogenesis and the latter need glycerol ,amino acid ,lactate >so it must increase hepatic glycerol utilization
d) in short term fasting glucose is from glycogenolysis 75%(use what in the stock first) and gluconeogenesis 25%
In LONG TERM :when the stored glycogen are out THE GLUCONEOGENESIS IS PROMINENT
E) high ketone bodies from lipolysis
SO I find the less opponent fact to answer B
FEEL FREE TO CORRECT OR ADD ANYTHING
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| adeelmd
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it is d. Gluconeogensis starts after 12 hours of fasting and drops down gradually in one week. The brain uses ketones after one week... (to preserve protein it starts breaking down fat).. this entire process is initiated with hypoglycemia- increase b-oxidation- increased acetyl coa- increased ketones. This is converted back to acetyl coa in the brain- which inh pyruvate dehydrogenase and glycolysis (no uptake, no glucogenesis needed cuz plasma levels don't go down) (hence no hypoglycemia). I would think that eventually (near death) the glucose level would have to fall.. (glucose to fat to ketones) but i cant find any mention of this, so i'd have to go with d.
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