Type 2 diabetes is often described as a disease closely linked to excess body weight.
But new research suggests that this familiar picture does not fit millions of people in Africa who develop the condition while remaining lean.
Researchers from Amsterdam UMC and the University of Ghana found that type 2 diabetes may develop through very different biological routes depending on a person’s body mass index, or BMI.
Their findings suggest that some lean patients may need a different approach to treatment.
Diabetes develops when the body can no longer keep blood sugar within a healthy range. Insulin, a hormone made by the pancreas, normally helps move sugar from the blood into cells, where it can be used for energy.
In the form of type 2 diabetes commonly seen in people with overweight or obesity, the body often becomes less responsive to insulin. The pancreas initially tries to compensate by making more insulin, but over time it may no longer be able to keep blood sugar under control.
The new study suggests that the problem can look quite different in lean African adults. Instead of mainly struggling to respond to insulin, many appear to have a pancreas that does not produce enough insulin in the first place.
This distinction matters because most international treatment advice has been developed from research in populations where type 2 diabetes is strongly associated with excess weight. In wealthy countries, about nine in 10 people with the disease are overweight, according to the researchers.
In Africa, however, the pattern is very different. Almost four in 10 African adults with type 2 diabetes are lean, and in some rural areas, including parts of Ghana, the figure may reach six in 10.
First author Sabrina Esmail estimated that roughly 10 million lean people with diabetes in Africa may not fit the standard picture of the disease. For this group, a shortage of insulin may be more important than resistance to insulin.
The researchers studied data from more than 3,300 African adults with type 2 diabetes from Ghana, Nigeria and Kenya, as well as African participants living in Europe. They compared differences in body size, insulin-related biology and complications linked to diabetes.
The results showed that lean and heavier patients did not simply have the same disease at different body weights. Their patterns of complications also differed, supporting the idea that different biological processes may be involved.
Lean patients were more likely to develop damage to the small blood vessels in the eye, known as diabetic retinopathy, and they experienced more strokes. People with higher body weight were more likely to have high blood pressure and a greater risk of cardiovascular disease.
Chronic kidney disease, however, appeared at similar rates in both groups. The researchers found that differences in body fat explained many of the other contrasts between lean and heavier patients.
The reasons people develop the two forms may also be different. Excess body fat is a major contributor to insulin resistance, while some lean patients may have experienced poor nutrition early in life or had a low birth weight.
Poor nutrition during pregnancy or childhood can affect how organs grow and develop. If the pancreas does not develop fully, it may have less ability to produce insulin later in life, especially when the body faces greater demands with age.
This creates an important question about treatment. In many African health systems, lean and heavier patients are treated using the same general guidelines and often receive medicines such as metformin or sulfonylureas.
Those medicines can be useful in type 2 diabetes, but treatment designed mainly around the usual insulin-resistant form of the disease may not always be the best match for someone whose main problem is inadequate insulin production. The researchers are therefore calling for clinical trials specifically involving lean African patients.
The issue may extend beyond Africa. Previous research using the UK Biobank found that people of African ancestry can develop diabetes at a lower BMI than people of European ancestry, while studies of African migrants have reported earlier diabetes and poorer blood sugar control.
Project leader Charles Agyemang said there is no reason to assume that the treatment problem disappears when African patients move to Europe. This raises questions about whether BMI cutoffs and treatment guidelines developed mainly from European populations work equally well for everyone.
The research was published in Diabetologia and was conducted by Amsterdam UMC, the University of Ghana and collaborating institutions. It adds to growing evidence that the label “type 2 diabetes” may include several forms of disease that reach the same result—high blood sugar—through different pathways.
The findings are important, but they do not yet prove that current medicines are ineffective or harmful for lean African patients. The study identifies biological differences and patterns of complications, but targeted treatment trials are still needed to show whether changing therapy improves health outcomes.
That is also the study’s most important practical message. Rather than assuming every person with type 2 diabetes has the same underlying problem, future care may need to consider body composition, insulin production, ancestry, early-life nutrition and other factors before choosing treatment.
If those trials confirm the researchers’ conclusions, diabetes care could become more personalized for millions of people who have been poorly represented in past research.
For now, patients should continue prescribed treatment and discuss any concerns with their healthcare team rather than changing diabetes medicines on their own.
