Accumulating data suggest that type 2 diabetes mellitus (T2DM) in younger people (aged <40 years), referred to as young-onset T2DM, has a more rapid deterioration of β-cell function than is seen in later-onset T2DM. Furthermore, individuals with young-onset T2DM seem to have a higher risk of complications than those with type 1 diabetes mellitus. As the number of younger adults with T2DM increases, young-onset T2DM is predicted to become a more frequent feature of the broader diabetes mellitus population in both developing and developed nations, particularly in certain ethnicities. However, the magnitude of excess risk of premature death and incident complications remains incompletely understood; likewise, the potential reasons for this excess risk are unclear. Here, we review the evidence pertaining to young-onset T2DM and its current and future burden of disease in terms of incidence and prevalence in both developed and developing nations. In addition, we highlight the associations of young-onset T2DM with premature mortality and morbidity.
β-cell decline is more rapid in young-onset (aged <40 years) versus late-onset type 2 diabetes mellitus (T2DM).
Young-onset T2DM has a greater risk of complications than type 1 diabetes mellitus.
The risk of complications in young-onset T2DM is high compared with late-onset T2DM, mainly due to a longer duration of disease.
Ethnicity and the intrauterine environment seem to be strong risk predictors for young-onset T2DM.
The prevalence of young-onset T2DM is higher in adolescent girls than in adolescent boys.
The incidence and prevalence of young-onset T2DM is strikingly high among Native American, Indigenous Australian, Pacific Islander and First Nation Canadian populations, highlighting the need for prevention initiatives in these populations.
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J.E.S. has received honoraria from Astra Zeneca, Sanofi, Novo Nordisk, MSD, Eli Lilly, Abbott, Mylan and Boehringer Ingelheim for giving seminars and for sitting on Advisory boards. All other authors declare no competing interests.
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A marker of kidney damage based on a moderate increase in urinary albumin excretion (for example, a urine albumin to creatinine ratio in the range of 30–300 mg/g).
A marker of kidney damage based on a severe increase in urinary albumin excretion (for example, a urine albumin to creatinine ratio of >300 mg/g).
- Estimated glomerular filtration rate
A marker of kidney function. Measured creatinine or cystatin C levels are inputted into formulae (also considering individual characteristics, for example, age, sex and race) to estimate the glomerular filtration rate.
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Magliano, D.J., Sacre, J.W., Harding, J.L. et al. Young-onset type 2 diabetes mellitus — implications for morbidity and mortality. Nat Rev Endocrinol 16, 321–331 (2020). https://doi.org/10.1038/s41574-020-0334-z
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