Hyperproinsulinemia: clinical manifestations similar to those seen in DM type 2?

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Knicks

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In hyperproinsulinemia, a peptidase does not cleave proinsulin into insulin and C-peptide..... which means that insulin levels are gonna be low.

In the kaplan clinical correlate side margin, it says that the clinical manifestations similar to those seen in DM type 2.

Why type 2, and not type 1?

Can someone give the actual reason? (not what you think the reason is, but the ACTUAL reason).


Thanks.

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In hyperproinsulinemia, a peptidase does not cleave proinsulin into insulin and C-peptide..... which means that insulin levels are gonna be low.

In the kaplan clinical correlate side margin, it says that the clinical manifestations similar to those seen in DM type 2.

Why type 2, and not type 1?

Can someone give the actual reason? (not what you think the reason is, but the ACTUAL reason).


Thanks.

Hyperproinsulinemia has been "proposed" to be more frequent in type 2 diabetes due to its mechanism of pathogenesis. It has been attributed to either a direct β-cells defect or an indirect effect of cell dysregulation under sustained elevated blood glucose (hyperglycemia). Sustained elevated levels of blood Glucose easily paint the picture of the Pt who doesnt take care of their diabetes/overweight/ didnt even know they have it...etc. The main proposed Mechanism of pathogensis of DM2 is Post receptor defects (i.e tyrosine kinase defects, GLUT 4 abnormalities, etc) d/t the elevated Glucose. Whereas DM1 is AutoAb to Beta cells.
Also some alleles of insulin can also cause hyperproinsulinemia. A DM 2 person results in all these defective insulin mechanisms d/t elevated Glucose levels...thats not the case with DM 1. Thats why they say it presents most like DM2. Thats all I got for you. You can read more below

http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176730
 
^^ Wonderful. Thanks a lot! :)


This article actually prob says it better and easier to glance over...Hope that helps a little :)

"These findings indicate that elevated proinsulin and proinsulin/insulin ratios are secondary to increased demands on ß-cell secretion induced by hyperglycemia and insulin resistance with no discernible influence of family history of diabetes"
http://aje.oxfordjournals.org/cgi/content/full/155/9/834
 
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