drswapna05
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may be silly q.
in glycolysis conversion of fructose 6 p to fruc2,6 bis p is controlled by insulun and glucagon,it means if glucagon iis present no formation of fruc 2,6 bis p so how glycolysis take place in rbc during this.
or is it that if insulin is there PFK 1 activated indirectly,i.e insulin activates pfk1 indirectly and if glucagon is there fruc 6 p is converted to fruc1,6 bp without conversion of fruc 6p to fruc 2,6 bis
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| drswapna05
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In wet beri beri decreased ATP leads to inc ketoacids in cardiac muscle why?
is it because since dec atp ,more oxdn of fatty acids to produce energy and ketones produce energy.so is it that both fatty acids r also increased in blood or only ketoacids
some one explain
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| drswapna05
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for 1 st q is it that in brain and rbs PFK is not effected by insulin or glucagon.
correct me if wrong
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| me007
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Wet beriberi is the term used for the cardiovascular involvement of thiamine deficiency. The chronic form of wet beriberi consists of 3 stages. In the first stage, peripheral vasodilation occurs, leading to a high cardiac output state. This leads to salt and water retention mediated through the renin-angiotensin-aldosterone system in the kidneys. As the vasodilation progresses, the kidneys detect a relative loss of volume and respond by conserving salt. With the salt retention, fluid is also absorbed into the circulatory system. The resulting fluid overload leads to edema of the dependent extremities.
By the time significant edema occurs, the heart has been exposed to a severely high workload to pump the required cardiac output needed to satisfy end organ requirements. Parts of the heart muscle undergo overuse injury, which results in the physical symptoms of tachycardia, edema, and high arterial and venous pressures. These changes can lead to myocardial injury, expressed as chest pain.
A more rapid form of wet beriberi is termed acute fulminant cardiovascular beriberi or Shoshin beriberi. The predominant injury is to the heart, and the rapid deterioration follows the inability of the heart muscle to satisfy the body's demands because of its own injury.
where did you get that info about ketoacids in cardiac muscle?
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| anandortho
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TPP is required for p.dehydrogenase to convert pyruvate which is an alfa ketoacid to acetyl co a....now 2 things happend...ketoacid accumulate ...and ATP is depleted as no acetyl co a to go to tca cycle...hope that explains
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| drswapna05
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thank you anandortho and me007 for taking time and explaining.
actually meoo7 what i was asking was why ketoacids accumulate in wetberiberi.
it is in kaplan notes in glycolysis chapter .i understood idid not consider that pyruvate is alpha keto acid.
now i llearnt that alpha keto acid is pyruvic acid
beta is acetoacetic acid
gamma is levulinic acid
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