Type 2 diabetes risk alleles in PAM impact insulin release from human pancreatic β-cells View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-08

AUTHORS

Soren K. Thomsen, Anne Raimondo, Benoit Hastoy, Shahana Sengupta, Xiao-Qing Dai, Austin Bautista, Jenny Censin, Anthony J. Payne, Mahesh M. Umapathysivam, Aliya F. Spigelman, Amy Barrett, Christopher J. Groves, Nicola L. Beer, Jocelyn E. Manning Fox, Mark I. McCarthy, Anne Clark, Anubha Mahajan, Patrik Rorsman, Patrick E. MacDonald, Anna L. Gloyn

ABSTRACT

The molecular mechanisms underpinning susceptibility loci for type 2 diabetes (T2D) remain poorly understood. Coding variants in peptidylglycine α-amidating monooxygenase (PAM) are associated with both T2D risk and insulinogenic index. Here, we demonstrate that the T2D risk alleles impact negatively on overall PAM activity via defects in expression and catalytic function. PAM deficiency results in reduced insulin content and altered dynamics of insulin secretion in a human β-cell model and primary islets from cadaveric donors. Thus, our results demonstrate a role for PAM in β-cell function, and establish molecular mechanisms for T2D risk alleles at this locus. More... »

PAGES

1122-1131

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41588-018-0173-1

DOI

http://dx.doi.org/10.1038/s41588-018-0173-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1105743457

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30054598


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