Nikhil Prasad Fact checked by:Thailand Medical News Team Oct 10, 2026 1 hour, 15 minutes ago
Scientists have uncovered a troubling mechanism through which SARS-CoV-2, the virus responsible for COVID-19, may damage insulin-producing pancreatic cells and contribute to diabetes, particularly among older individuals.
New research reveals how SARS-CoV-2 proteins may trigger harmful pancreatic amyloid deposits,
disrupting insulin secretion and potentially increasing diabetes risk after COVID-19.
Researchers from the Chinese Academy of Medical Sciences, Peking Union Medical College, Institute of Laboratory Animal Science, Institute of Aging and Health, Institute of Pathogen Biology, and Plastic Surgery Hospital conducted the investigation.
Viral Proteins Trigger Harmful Deposits
The study discovered that SARS-CoV-2 spike and nucleocapsid proteins interact directly with islet amyloid polypeptide (IAPP), also called amylin, a hormone normally released alongside insulin.
These interactions accelerate the formation of abnormal amyloid fibers, creating dense deposits that disrupt pancreatic beta cells responsible for producing and releasing insulin.
Older Pancreatic Cells Face Greater Damage
Experiments involving rhesus macaques revealed striking age-related differences.
Among older infected animals, approximately 89% of examined pancreatic islets contained IAPP deposits, compared with minimal deposits in uninfected older animals and virtually none in infected adults.
Microscopic examinations also revealed extensive cellular damage, including disrupted internal membranes, inflammatory activity, and activation of necroptosis, a destructive form of programmed cell death.
Importantly, mature insulin granules declined by more than 80%, while immature or empty vesicles increased nearly threefold.
Insulin Production and Release Become Disrupted
Laboratory experiments demonstrated that viral proteins dramatically accelerated IAPP aggregation.
When pancreatic beta cells encountered both IAPP and viral proteins, intracellular insulin content fell to approximately 51%–58% of control levels.
Glucose-stimulated insulin secretion also declined substantially, while potassium-stimulated secretion showed even greater impairment, suggesting damage to the machinery responsible for releasing insulin.
Experiments using pancreatic islets engineered to produce human IAPP confirmed similar abnormalities.
Further analysis identified impaired insulin processing, disrupted vesicle transportation, endoplasmic reticulum stress, and complement-related inflammatory responses.
Potential Implications for Post-COVID Diabetes
The findings suggest that viral proteins may initiate a chain reaction involving amyloid accumulation, defective insulin storage, inflammation, and eventual beta-cell failure.
As highlighted in this
Thailand Medical News report, th
e discovery provides a possible biological explanation for increased diabetes risk following COVID-19.
However, the research primarily involved animal models and laboratory experiments. Human studies are necessary to establish how frequently this mechanism occurs and whether treatments targeting IAPP aggregation can prevent diabetes.
The study findings were published in the peer reviewed journal: Signal Transduction and Targeted Therapy.
https://www.nature.com/articles/s41392-026-02914-y
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https://www.thailandmedical.news/articles/coronavirus
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