# African immigrants with type 2 diabetes present with three physiologic subtypes: implications for screening, diagnosis and treatment

**Authors:** Eliza A Huefner, Kauthrah Ntabadde, Grace G Smith, Simon Pierre Bigirimana, Christopher W DuBose, Arthur Sherman, Anne E Sumner

PMC · DOI: 10.1136/bmjdrc-2025-005504 · BMJ Open Diabetes Research & Care · 2026-03-18

## TL;DR

African immigrants with type 2 diabetes can be divided into three subtypes based on insulin resistance and secretion, which has implications for how the disease is managed and treated.

## Contribution

The study identifies three distinct physiologic subtypes of type 2 diabetes in African immigrants, offering new insights for targeted screening and treatment.

## Key findings

- Three T2D subtypes were identified: insulin-deficient, insulin-resistant, and a combination of both.
- Phenotypic differences were observed across the subtypes, including variations in BMI and central obesity.
- Weight gain was most significant in those who developed T2D, but not different between subtypes.

## Abstract

As type 2 diabetes (T2D) prevalence increases in the USA and Africa, factors from both regions affect African immigrants.

T2D in African immigrants was characterized by examining: (a) insulin deficiency and insulin resistance; (b) phenotypic presentation; (c) sociodemographic factors.

In 633 African immigrants (male: 62%, age 39±11, (mean±SD), range 20–70 years), body mass index (BMI): 27.8±4.6, range 18.8–46.2 kg/m2), weight gain information was collected, BMI and waist circumference (WC) measured and OGTT performed. Insulin resistance was defined by the lowest quartile of the Matsuda Index (≤2.80); insulin secretion by the Insulin Secretion Index (ISI). Insulin deficiency was defined as less than the maximum ISI in participants with T2D without IR (0.430). WC thresholds defined central obesity (men: WC ≥94 cm; women ≥80 cm).

Normal glucose tolerance, pre-diabetes and T2D occurred in 61%, 32% and 7%, respectively. Three subtypes of T2D were identified: insulin-deficient-T2D (ID-T2D) in 45%, insulin-resistant-T2D (IR-T2D) in 30%, insulin-deficient+insulin-resistant (ID+IR-T2D) in 25%. ID+IR-T2D had the highest glucose concentrations (all p<0.05), whereas insulins were highest in IR-T2D (all p<0.01). Phenotypic differences by T2D subtype were identified. In the ID-T2D group, 20% of participants had a healthy weight and central obesity occurred in 55%. In the IR-T2D and ID+IR-T2D groups, 100% had central obesity and a BMI in either the overweight or obese categories. Sociodemographic factors specifically, weight gain, sedentary lifestyle and percent married, increased across glucose tolerance category (p values <0.01) but did not differ by T2D subtype (p≥0.3).

Spanning the BMI spectrum from normal to obese, African immigrants have three subtypes of T2D. Weight gain was greatest in immigrants who developed T2D but did not differ by subtype. As life in America promotes weight gain, sharing information about the consequences of weight gain with all Americans, both native and foreign-born, is key to T2D prevention and treatment.

## Linked entities

- **Diseases:** type 2 diabetes (MONDO:0005148), pre-diabetes (MONDO:0006920)

## Full-text entities

- **Genes:** GAD2 (glutamate decarboxylase 2) [NCBI Gene 2572] {aka GAD65}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, KRT88P (keratin 88, pseudogene) [NCBI Gene 85348] {aka HBC, KRT122P, KRTHBP3}
- **Diseases:** insulin resistance (MESH:D007333), beta-cell dysfunction (MESH:D007340), T2D (MESH:D003924), Obesity (MESH:D009765), undernutrition (MESH:D044342), Hypothyroidism (MESH:D007037), LADA (MESH:D000071698), DI (MESH:C566784), hyperinsulinemia (MESH:D006946), HbA1c (MESH:D006445), Central obesity (MESH:D056128), anemia (MESH:D000740), insulin deficient diabetes (MESH:D003922), MARD (MESH:C565101), NGT (MESH:D018149), Diabetes (MESH:D003920), Weight gain (MESH:D015430), DM (MESH:D009223), IR (MESH:C537629), weight loss (MESH:D015431), sickle cell (MESH:D000755), OW (MESH:D050177), underweight (MESH:D013851), ID (MESH:C537985), hyperglycemia (MESH:D006943), infectious diseases (MESH:D003141), IFG (MESH:D007003), visceral adiposity (MESH:D007418), TB (MESH:D014390), glucose-6-phosphate dehydrogenase deficiency (MESH:D005955), pre (MESH:D058246)
- **Chemicals:** DI (-), TG (MESH:D013866), pyridoxal-5-phosphate (MESH:D011732), Alcohol (MESH:D000438), EDTA (MESH:D004492), creatinine (MESH:D003404), Glucose (MESH:D005947)
- **Species:** Human immunodeficiency virus 1 (no rank) [taxon 11676], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** A1C

## Full text

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## Figures

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## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC13007123/full.md

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Source: https://tomesphere.com/paper/PMC13007123