NS FL 10 BB Q8

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Joined: Tue Jun 25, 2019 11:23 am

NS FL 10 BB Q8

Post by mgarc805 » Mon Aug 12, 2019 2:35 pm

Evidence in the passage suggests that IGFs bind to a variety of receptors
Insulin-like growth factor (IGF) is a hormone secreted by the liver upon stimulation by growth hormone. It is highly similar to insulin. It binds to a variety of receptors in order to mediate human growth
so if the insulin receptors in the cells are damaged that statement would suggest that there are other receptors that are stimulated by IGF that may or may not produce stunt growth yet there is no evidence in either direction. On the other hand, the receptor mutation leads to the inability to bind to insulin so although insulin is not being produced in more quantity the one produced is not being used which can be thought as being in excess. I have an example for my point:

let's say that we are in the combustion of methane in my back yard. earth is not producing more oxygen than normal just because I am burning methane instead the one that has been hanging out is enough to react as much methane so is thought to be in excess. just like insulin an its receptor if the mutation really lowers the amount of insulin that binds to the receptor no more insulin is being created but the once present is in excess now.

with that being said if IGFs could bind to insulin receptors then conversely insulin could bind to other IGFs receptors. I know there isn't much evidence for that beyond consequential assumptions but given that IGF would still exert their effects because of the presence of other receptors I believe answer choice B sounds plausible.

answer choice A is too general in the sense that insulin receptors would prevent SOME types of cell from getting glucose but not all.
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Re: NS FL 10 BB Q8

Post by NS_Tutor_Mathias » Wed Aug 14, 2019 4:55 pm

No need to overthink excess/lack of. These terms simply mean in comparison to physiological concentrations, which are fixed values that we have observed in the organism being discussed.

For now, discard this question entirely. After some review of the literature, I can safely say that this question has major flaws. The best possible answer is indeed the one that states decreased cellular uptake of glucose would be the primary driver of developmental stunting. That probably not entirely right either, but it is a reasonable inference of the kind you would be expected to make on the MCAT.

Real Donohue patients rarely live beyond one year, probably in large part for this very reason, as heavily impaired glucose regulation simply makes a mess of everything.

The IGF and Insulin receptor interaction is not the pathway by which IGF mediates growth regulation. This is done through separate IGF receptors. The insulin receptor actually has a relatively low affinity for IGF, and there is no reason to assume that transient formation of insulin receptor/IGF complexes would inhibit normal IGF signaling through the IGF receptor.
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