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Recently, I learned that one of the causes of Type II diabetes is that insulin receptors on cell surfaces lose their sensitivity due to long-term high exposure to insulin (which occurs as a result of high blood sugar).

How do receptors (like that for insulin) become more resistant to ligands? Is the receptor itself getting damaged? If so, how, and why don't other frequently activated proteins/receptors (like GPCR's) also get damaged? If not, then how does the cell become more "resistant" to insulin?

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  • $\begingroup$ There are different mechanisms for different receptors, so this is a very broad question. It's usually a negative feedback from within the cells. For insulin resistance, you can check Figure 1 in this article. $\endgroup$ – Jan Jun 22 at 17:11
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    $\begingroup$ The field of insulin resistance is a very active research area and hundreds of research papers on the topic are published every year. There appear to be many mechanisms involved in the development of insulin resistance and to give a full answer might not be possible at this time. $\endgroup$ – Jeppe Nielsen Jun 27 at 0:40

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