Why COVID Can Raise Diabetes Risk — A Plain-Language Summary of New Research
A newly published review paper looks at why some people develop diabetes after COVID, particularly as part of Long COVID. It’s not claiming a single cause, and it’s not saying this happens to everyone. Instead, it explains how several biological disruptions can stack together in vulnerable people.
Here’s the short version in everyday terms.
COVID isn’t just a lung infection. The virus can affect many organs involved in blood sugar control, including the pancreas, muscles, fat tissue, blood vessels, and even the gut.
First: the pancreas.
The pancreas makes insulin. The review summarises evidence that SARS-CoV-2 can enter pancreatic cells, and that viral RNA or protein fragments can linger there after the acute infection. This can stress or damage insulin-producing cells, reduce insulin output, or interfere with how insulin is processed.
Second: inflammation and the immune system.
Long COVID is often marked by ongoing low-grade inflammation. Inflammation makes the body less responsive to insulin (insulin resistance). In some people, immune disruption may also interfere with the normal “brakes” that prevent autoimmunity, nudging the system toward diabetes-like patterns.
Third: it’s not just insulin — it’s insulin response.
Blood sugar control depends on how muscles, fat, and the liver respond to insulin. The paper explains how COVID-related inflammation, vascular injury, and mitochondrial stress can make these tissues ignore insulin’s signal, even if insulin levels are normal.
Fourth: the virus disrupts a key hormonal balance system.
SARS-CoV-2 interferes with the ACE2 / renin–angiotensin system — a network that normally helps regulate inflammation, blood flow, and metabolism. When this system is knocked out of balance, it can push the body toward inflammation, insulin resistance, and metabolic stress.
Fifth: the gut plays a role.
COVID can alter the gut lining and the gut microbiome. These changes can promote inflammation and affect how nutrients and metabolites are processed, which again feeds into insulin resistance.
What this paper does not say:
• COVID does not automatically cause diabetes
• Most people recover without developing metabolic disease
• This is about risk, not inevitability
• Genetics, age, body composition, illness severity, and prior health all matter
The takeaway:
In some people, COVID sets off a chain reaction — lingering viral material, immune dysregulation, inflammation, vascular stress, and metabolic disruption. Over time, that combination can tip the system into new-onset diabetes, sometimes months after the initial infection.
This review helps explain why that risk exists biologically, rather than treating post-COVID diabetes as a mystery or coincidence.
⸻
Credits & acknowledgements
Thanks to Dave and Vipin for highlighting and discussing this work.
Paper authors: Shitaye et al., Frontiers in Endocrinology (2025) — “Molecular analysis of long COVID and new-onset diabetes mellitus”
A newly published review paper looks at why some people develop diabetes after COVID, particularly as part of Long COVID. It’s not claiming a single cause, and it’s not saying this happens to everyone. Instead, it explains how several biological disruptions can stack together in vulnerable people.
Here’s the short version in everyday terms.
COVID isn’t just a lung infection. The virus can affect many organs involved in blood sugar control, including the pancreas, muscles, fat tissue, blood vessels, and even the gut.
First: the pancreas.
The pancreas makes insulin. The review summarises evidence that SARS-CoV-2 can enter pancreatic cells, and that viral RNA or protein fragments can linger there after the acute infection. This can stress or damage insulin-producing cells, reduce insulin output, or interfere with how insulin is processed.
Second: inflammation and the immune system.
Long COVID is often marked by ongoing low-grade inflammation. Inflammation makes the body less responsive to insulin (insulin resistance). In some people, immune disruption may also interfere with the normal “brakes” that prevent autoimmunity, nudging the system toward diabetes-like patterns.
Third: it’s not just insulin — it’s insulin response.
Blood sugar control depends on how muscles, fat, and the liver respond to insulin. The paper explains how COVID-related inflammation, vascular injury, and mitochondrial stress can make these tissues ignore insulin’s signal, even if insulin levels are normal.
Fourth: the virus disrupts a key hormonal balance system.
SARS-CoV-2 interferes with the ACE2 / renin–angiotensin system — a network that normally helps regulate inflammation, blood flow, and metabolism. When this system is knocked out of balance, it can push the body toward inflammation, insulin resistance, and metabolic stress.
Fifth: the gut plays a role.
COVID can alter the gut lining and the gut microbiome. These changes can promote inflammation and affect how nutrients and metabolites are processed, which again feeds into insulin resistance.
What this paper does not say:
• COVID does not automatically cause diabetes
• Most people recover without developing metabolic disease
• This is about risk, not inevitability
• Genetics, age, body composition, illness severity, and prior health all matter
The takeaway:
In some people, COVID sets off a chain reaction — lingering viral material, immune dysregulation, inflammation, vascular stress, and metabolic disruption. Over time, that combination can tip the system into new-onset diabetes, sometimes months after the initial infection.
This review helps explain why that risk exists biologically, rather than treating post-COVID diabetes as a mystery or coincidence.
⸻
Credits & acknowledgements
Thanks to Dave and Vipin for highlighting and discussing this work.
Paper authors: Shitaye et al., Frontiers in Endocrinology (2025) — “Molecular analysis of long COVID and new-onset diabetes mellitus”
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