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Feedback inhibition works when the product of the process is an inhibitor of one or more steps in the process producing the product. An example is the release of insulin upon consumption of food. Eating releases raises blood sugar and high blood sugar releases insulin, which reduces blood sugar levels.
No, it is not true. PEP, or phosphoenolpyruvate, is actually a substrate for phosphofructokinase (PFK), a key enzyme in glycolysis. PEP is converted to fructose-1,6-bisphosphate by PFK, which is an important step in the glycolytic pathway.
metabolic inhibition
feedback inhibition
Feedback inhibition
There are two main types of feedback inhibition: competitive inhibition, where an inhibitor competes with the substrate for the active site of an enzyme; and non-competitive inhibition, where an inhibitor binds to a site on the enzyme other than the active site, altering the enzyme's shape and reducing its activity.
Feedback inhibition works when the product of the process is an inhibitor of one or more steps in the process producing the product. An example is the release of insulin upon consumption of food. Eating releases raises blood sugar and high blood sugar releases insulin, which reduces blood sugar levels.
The feeling of fullness and hunger are examples of the negative feedback inhibition.
Feedback inhibition works when the product of the process is an inhibitor of one or more steps in the process producing the product. An example is the release of insulin upon consumption of food. Eating releases raises blood sugar and high blood sugar releases insulin, which reduces blood sugar levels.
feedback inhibition
No, it is not true. PEP, or phosphoenolpyruvate, is actually a substrate for phosphofructokinase (PFK), a key enzyme in glycolysis. PEP is converted to fructose-1,6-bisphosphate by PFK, which is an important step in the glycolytic pathway.
feedback inhibition
feedback inhibition
feedback inhibition
The steroid hormones produced by the adrenal cortex exhibit feedback inhibition on ACTH production, therefore a low concentration of corticosteroids (as seen in Addisons disease) will not exhibit this feedback inhibition. Without this inhibition, ACTH levels are not regulated and therefore rise.
metabolic inhibition
an accumulation of effectors slows the pathway.