Individuals with obesity require higher amounts of insulin to maintain normal blood glucose levels. Elevated insulin concentrations suppress lipolysis (fat breakdown) and further promote weight gain. As obesity progresses, many individuals develop insulin resistance.
When pancreatic insulin secretion is no longer sufficient to compensate for insulin resistance, carbohydrate metabolism becomes impaired, resulting in elevated fasting plasma glucose and glycated hemoglobin (HbA1c) levels. However, not all individuals with obesity develop type 2 diabetes mellitus. Some are able to maintain normal blood glucose concentrations through adequate compensatory insulin secretion.
The development of type 2 diabetes mellitus requires not only insulin resistance but also progressive pancreatic β-cell dysfunction. In addition, individuals with obesity commonly exhibit abnormalities in the incretin system, including impaired secretion and action of the incretin hormones GLP-1 and GIP, which further contribute to dysregulated glucose homeostasis.
Obesity is considerably more common among individuals with lower educational attainment and lower socioeconomic status. The prevalence of obesity also increases with age, reaching its highest levels among adults aged 45–64 years.
The exact proportion of patients with type 2 diabetes (T2DM) who are obese (BMI ≥30 kg/m²) varies by registry and study. However, several large epidemiological studies provide consistent estimates that are suitable for a review article.
Table. Prevalence of Obesity Among Patients with Type 2 Diabetes
Region | Patients with T2DM and Obesity (BMI ≥30 kg/m²) | Patients with T2DM and Normal Weight (BMI 18.5–24.9 kg/m²) | Comments |
Europe | 50–60% | 15–25% | Most European diabetes registries report that approximately one-half of patients with T2DM are obese. (NCBI) |
United States | 60–70% | 10–15% | Obesity is the predominant phenotype among adults with T2DM in the U.S. (International Diabetes Federation) |
India | 15–25% | 40–55% | T2DM frequently develops at lower BMI values (“lean diabetes” or “normal-weight diabetes”) owing to increased visceral adiposity and insulin resistance despite normal BMI. (Springer Nature Link) |
Key message
This comparison is commonly used in endocrinology textbooks to illustrate the ethnic differences in the relationship between BMI and type 2 diabetes. In South Asian populations, measures of central obesity (waist circumference or visceral fat) are generally more predictive of diabetes risk than BMI alone. (Springer Nature Link)
Obesity is therefore a major contributing factor to the development of type 2 diabetes mellitus in the majority of patients. However, in addition to obesity and insulin resistance, patients with type 2 diabetes mellitus also exhibit progressive impairment of insulin secretion due to pancreatic β-cell dysfunction. Consequently, type 2 diabetes mellitus can also develop in individuals with normal body weight, particularly when β-cell dysfunction predominates over insulin resistance. This phenotype is observed more frequently in South Asian populations and in some older adults, illustrating that obesity, while an important risk factor, is not a prerequisite for the development of type 2 diabetes mellitus.
Table. Normal-weight patients among people with type 2 diabetes
Region | Normal-weight patients with T2DM | Approximate share |
Europe | BMI 18.5–24.9 kg/m² | up to ~20% |
United States | BMI 18.5–24.9 kg/m² | ~9.5–15% |
India | BMI 18.5–24.9 kg/m² | ~25–40% |
Interpretation: Normal-weight type 2 diabetes is least common in the USA, somewhat more common in Europe, and considerably more common in India/South Asian populations, where type 2 diabetes often occurs at lower BMI because visceral fat and insulin resistance are higher at a given BMI. CDC/NHANES data reported 9.5% normal weight among U.S. adults with diabetes, while UK/European sources commonly describe up to ~20% as normal weight; Indian studies show a much larger normal-BMI subgroup