Type 2 diabetes can also affect people who are not overweight.
Interview: Santina RussoThe number of cases of type 2 diabetes is increasing, even in children. What do we know about its causes, and how can people protect themselves against it? Eleonora Seelig, a specialist in diabetes, shares her expertise.
Eleonora Seelig, diabetes is seen as a disease of affluence. Do you share that view?
Not entirely. Obesity and a lack of exercise are indeed strong risk factors for type 2 diabetes. Unfortunately, we’re also increasingly seeing this disease in children, where it’s generally connected with severe obesity. There are, however, other risk factors such as age or genetic predisposition. In contrast, type 1 diabetes is not caused by lifestyle factors.
Remind us of the difference between type 1 and type 2 diabetes.
Type 1 is an autoimmune disease in which the immune system destroys specific cells of the pancreas, known as beta cells. This means that hardly any insulin is produced. Insulin is the hormone responsible for ensuring that the sugar we take up with food is absorbed from the bloodstream into locations including the muscles and fatty tissue, where it is then metabolized. If the hormone is lacking, blood sugar levels rise uncontrollably. Patients therefore have to receive insulin from outside the body.
That sounds challenging.
It is. The pancreas continuously monitors how much sugar is in the blood and how much insulin it needs to release. Patients with type 1 diabetes need to do this work themselves. They learn to estimate the amount of carbohydrates in different foods and how much insulin is therefore required. At the same time, the patients need to know what their blood sugar level was before the meal — which depends on whether they’ve been exercising, for example. Today, there are modern pump systems that connect to a glucose sensor and can automatically handle some of the insulin administration. Nevertheless, it’s challenging for people with the disease to keep their blood sugar under control.
Is research underway into new treatment approaches?
Yes. One idea is to produce and transplant new insulin-producing cells from stem cells. These cells can be modified so that the immune system does not attack them, but cellular therapies of this kind are not yet advanced enough for use in patients.
And what’s the situation with type 2 diabetes?
In type 2 diabetes, the pancreas produces insulin, but tissues in the body are increasingly resistant to it. Relative to type 1, blood sugar levels rise more slowly. That’s why, in type 2, the symptoms — such as increased thirst, needing to urinate more often, weight loss and fatigue — are more insidious than in type 1. The disease can therefore go unnoticed for a long time, allowing complications to develop over the space of many years. Examples include impaired kidney function, hardening of the blood vessels or a loss of sensation in the feet. Among other objectives, treatment seeks to reduce blood sugar levels and the insulin resistance of tissues.
How can this be achieved?
Lifestyle changes are an effective tool, when overweight patients lose weight and take more exercise. Medicines also help. Patients are often prescribed metformin, which slows down sugar production in the liver and improves the insulin sensitivity of tissues. Other key medications include GLP-1 receptor agonists such as semaglutide. These reduce blood sugar, increase the sensation of fullness and often lead to weight loss.
Do we know how this insulin resistance develops?
There are various hypotheses. One convincing explanation in my view is “lipotoxicity”: Normally, surplus energy is stored in fatty tissue. Once this “healthy” storage is exhausted, it’s stored in the muscular system and in organs such as the liver. As part of this process, metabolites are produced that can interfere with the effect of insulin in cells. Other mechanisms also come into play, such as the distribution of body fat, free fatty acids and inflammatory mediators. The dominant factors presumably differ from person to person. This could also explain why type 2 diabetes can occur in individuals who are not overweight, as it depends not only on body weight but also on where the fat is stored and how effectively fatty tissues can absorb surplus energy.
As well as obesity, simply being older is also a risk factor. How can people protect themselves?
Here, too, the key issue is weight. People can reduce their risk of type 2 diabetes by watching their diet and doing plenty of exercise. It’s also sensible for people over the age of 35 to have their blood sugar measured every three years or so in order to detect diabetes early and respond in good time.
You carry out your own research into steroid-induced diabetes, the form that can develop after people take steroids such as cortisone.
Correct. We know that cortisone increases sugar production in the liver and simultaneously hampers the effect of insulin in tissues. In medicine, however, cortisone is widely used to inhibit inflammatory responses, such as asthma, skin diseases or joint pain. It’s therefore all the more important to compensate for its side effects. We have evidence to suggest that metformin, the diabetes drug I mentioned earlier, also reduces the risk of steroid-induced diabetes. Next, we want to conduct a clinical trial to explore what happens if patients who take cortisone also take metformin preventively alongside it. The medication is well tolerated, and my hope is that this will allow us to prevent steroid-induced diabetes.
How did you end up working on diabetes?
I had already worked with patients with type 1 diabetes as part of my doctoral dissertation. Back then, I also monitored the patients overnight as part of a clinical trial and could quiz them on all kinds of things. I learned so much from them — it was fascinating. Even now, I still learn from my patients every day.
More articles in this issue of UNI NOVA (November 2026).