{"id":109914,"date":"2026-03-30T16:03:32","date_gmt":"2026-03-30T14:03:32","guid":{"rendered":"https:\/\/www.pcb.ub.edu\/a-study-by-ibec-has-created-a-mutational-map-of-the-hormone-amylin-that-reveals-its-role-in-type-2-diabetes\/"},"modified":"2026-03-30T16:48:57","modified_gmt":"2026-03-30T14:48:57","slug":"a-study-by-ibec-has-created-a-mutational-map-of-the-hormone-amylin-that-reveals-its-role-in-type-2-diabetes","status":"publish","type":"post","link":"https:\/\/www.pcb.ub.edu\/en\/a-study-by-ibec-has-created-a-mutational-map-of-the-hormone-amylin-that-reveals-its-role-in-type-2-diabetes\/","title":{"rendered":"A study by IBEC has created a mutational map of the hormone amylin that reveals its role in type 2 diabetes"},"content":{"rendered":"

A study by the Institute for Bioengineering of Catalonia (IBEC<\/a>), based in the University of Barcelona Science Park (PCB-UB) has created a mutational map of the hormone amylin, the aggregation of which can damage pancreatic cells and lead to type 2 diabetes. The team analysed 1,916 variants of the protein and compared the results of this mutational map with genetic and clinical data from 500,000 individuals. The study, published in Nature Communications<\/em>, sheds new light on the role of genetics in diabetes and could lead to the development of safer and more effective drugs.
\n<\/strong><\/p>\n

While it was already known that certain mutations could alter this aggregation capacity, understanding of this process was fragmented and based on isolated studies. \u201cFor the first time, we can systematically map how thousands of mutations modulate amylin aggregation, bringing human genetics closer to molecular mechanisms,\u201d says Benedetta Bolognesi<\/strong>, the principal investigator of the Protein Phase Transitions in Health and Disease<\/a> group at IBEC, who is also the lead author of the study.<\/p>\n

\u2018We have created a map that allows us to anticipate the potential impact of these mutations in the population,\u2019 adds Marta Badia<\/strong>, a researcher in the same group and first author of the study. \u2018We are not assessing toxicity, but rather the protein\u2019s intrinsic propensity to form fibres. This is a first step, but an extremely necessary one.\u201d<\/p>\n

Amyloid aggregates are small clusters of proteins that clump together abnormally, damaging organs and tissues in the process. The first amyloids to be described in human tissue, over a century ago, were amylin aggregates, also known as IAPP. These deposits are now known to damage the beta cells of the pancreas and contribute to the development of type 2 diabetes, a disease that affects more than 100 million people.<\/p>\n

Although amylin is very similar across mammals, small differences in its sequence mean that species such as mice or bears do not form amyloids or develop diabetes. In fact, introducing the human version of the protein into a mouse generates pancreatic amyloids and eventually causes the disease to develop.<\/p>\n

In order to gain a comprehensive understanding of how the amylin sequence influences its aggregation, the IBEC team analysed 1,916 variants of the protein using a technique known as deep mutational scanning. This methodology involves generating and measuring the behaviour of thousands of slightly different versions of the same protein all at once. This kind of \u2018mass screening\u2019 allows researchers to observe with great precision which mutations promote or hinder amyloid formation. The group had previously used this strategy to map the entire mutational landscape of the A\u03b242 peptide, which is implicated in Alzheimer\u2019s disease, as well as other proteins involved in neurodegeneration. Using the same approach, the team has now created a comprehensive atlas of amylin mutations.<\/p>\n

\u201cMost people are familiar with amyloids because of their link to Alzheimer\u2019s disease and other neurodegenerative conditions, but they actually occur in many other diseases too. Our strategy here is very similar to the one we used with A\u03b242: studying how mutations affect amyloid formation. Only this time, we\u2019re applying it to diabetes,\u201d explains Badia<\/strong>.<\/p>\n

When certain mutations accelerate a process that is difficult to predict<\/strong><\/h3>\n

The study\u2019s findings reveal that there is a particularly sensitive region in the amylin sequence where most mutations prevent the formation of fibrils. However, the analysis also identified mutations that accelerate aggregation, a phenomenon which is difficult to predict using conventional methods and that could have clinical relevance, as a faster rate of aggregation might contribute to the early onset of pancreatic damage.<\/p>\n

To evaluate this in the context of human health, the team compared their mutational map results with genetic and clinical data from 500,000 individuals collected by the UK Biobank. Although the sample size remains small, they found that variants that reduce aggregation are more prevalent in individuals without diabetes. Badia<\/strong> adds: \u2018Even so, it is important to make it clear that diabetes is multifactorial and these mutations are just one piece of the puzzle.\u2019<\/p>\n

The study also incorporates evolutionary information by comparing human amylin with that of different species. The sequences of animals such as mice and polar bears, which do not develop diabetes despite their extreme diets or prolonged periods of hibernation, are inherently less amyloidogenic. This is a well-known fact, and the new atlas reproduces it with great precision. \u2018These animals have exactly the changes needed to prevent the protein from forming fibres. Knowing which switches to flip is key to designing new drugs,\u2019 explains Bolognesi<\/strong>.<\/p>\n

As well as improving our understanding of aggregation mechanisms, the mutational atlas opens up new therapeutic opportunities. It enables the identification of mutations that reduce aggregation, provides a rational basis for designing new amylin analogues and helps anticipate the impact of genetic variants that may emerge in the population as genetic sequencing becomes more widespread.<\/p>\n

\u201cOur aim is for this map to serve as a tool for the scientific and clinical communities,\u201d Bolognesi<\/strong> concludes.<\/p>\n

\u00bb Article of reference: <\/strong>Marta Badia, Cristina Batlle, Benedetta Bolognesi. Massively parallel quantification of mutational impact on IAPP amyloid formation. Nature Communications (2026). DOI:\u00a0https:\/\/doi.org\/10.1038\/s41467-026-70611-z<\/a><\/p>\n

\u00bb Link to the news: <\/strong>IBEC website [+]<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"

A study by the Institute for Bioengineering of Catalonia (IBEC), based in the University of Barcelona Science Park (PCB-UB) has created a mutational map of the hormone amylin, the aggregation…<\/p>\n","protected":false},"author":14,"featured_media":109909,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"footnotes":""},"categories":[36],"tags":[231],"class_list":["post-109914","post","type-post","status-publish","format-standard","has-post-thumbnail","category-science","tag-ibec-en"],"acf":[],"yoast_head":"\nA study by IBEC has created a mutational map of the hormone amylin that reveals its role in type 2 diabetes - Parc Cient\u00edfic de Barcelona<\/title>\n<meta name=\"description\" content=\"The study, published in Nature Communications, sheds new light on the role of genetics in diabetes and could lead to the development of more effective drugs.\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.pcb.ub.edu\/en\/a-study-by-ibec-has-created-a-mutational-map-of-the-hormone-amylin-that-reveals-its-role-in-type-2-diabetes\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"A study by IBEC has created a mutational map of the hormone amylin that reveals its role in type 2 diabetes - 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