Emerging epidemic of type 2 diabetes in youth
Abstract
This review considers the epidemiologic evidence of an increasing incidence of type 2 diabetes in youth, the classification and diagnostic issues related to diabetes in young populations, pathophysiologic mechanisms relevant to the increasing incidence, the role of genetics and environment, and the community challenge for prevention and treatment. Type 2 diabetes in youth has been recognized to be frequent in populations of native North Americans and to comprise some 30 percent of new cases of diabetes in the 2nd decade of life, largely accounted for by minority populations and associated with obesity. Among Japanese schoolchildren, type 2 diabetes is seven times more common than type 1, and its incidence has increased more than 30-fold over the past 20 years, concomitant with changing food patterns and increasing obesity rates. The forms of diabetes seen in children and youth include typical type 1, occurring in all races; type 2, seen predominantly in minority youth; atypical diabetes, seen as an autosomal dominantly transmitted disorder in African-American populations; and maturity-onset diabetes of the young (MODY), seen rarely and only in Caucasians. Of the nonautoimmune forms of diabetes seen in youth, only type 2 diabetes is increasing in incidence. Proper classification requires consideration of onset (acute/severe versus insidious), ethnicity, family history, presence of obesity, and if necessary, studies of diabetes related autoimmunity. Insulin resistance predicts the development of diabetes in Pima Indians, in offspring of parents with type 2 diabetes, and in other high-risk populations. African-American children and youth have greater insulin responses during glucose tolerance testing and during hyperglycemic clamp study than do whites. There is also evidence of altered beta-cell function preceding the development of hyperglycemia. Of particular interest is the evidence that abnormal fetal and infantile nutrition is associated with the development of type 2 diabetes in adulthood. The thrifty phenotype hypothesis states that poor nutrition in fetal and infant life is detrimental to the development and function of the beta-cells and insulin sensitive tissues, leading to insulin resistance under the stress of obesity. The thrifty genotype hypothesis proposes that defective insulin action in utero results in decreased fetal growth as a conservation mechanism, but at the cost of obesity-induced diabetes in later childhood or adulthood. The vast majority of type 2 diabetes in adults is polygenic and associated with obesity. Monogenic forms (MODY, maternally transmitted mitochondrial mutations) are rare, but are more likely to appear in childhood. Linkage studies of the common polygenic type 2 diabetes have emphasized the heterogeneity of the disorder. The prevention and treatment of type 2 diabetes in children and youth is a daunting challenge because of the enormous behavioral influence, difficulty in reversing obesity, and typical nonadherence in this age-group. The emerging epidemic of type 2 diabetes in the pediatric population, especially among minorities whose proportion in the U.S. population is increasing, presents a serious public health problem. The full effect of this epidemic will be felt as these children become adults and develop the long-term complications of diabetes.
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Type 2 diabetes is becoming more frequent among adolescents and young adults in parallel with the obesity epidemic.
“In parallel with the obesity epidemic, type 2 diabetes is becoming more frequent among adolescents and young adults (12,13)”
From Diabetes and Cancer (2010) · cites this paper as [12]
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Preventing Type 2 diabetes and the dysmetabolic syndrome in the real world: a realistic view
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“An alarming increase in type 2 diabetes mellitus among children and adolescents has emerged (1, 2) at the same time that national surveys have shown a trend towards an increasing prevalence of overweight and obesity in the US population (3).”
BackgroundType 2 Diabetes in Children: Clinical Aspects and Risk Factors
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Tölle, T. R., Xu, X., & Sadosky, A. (2005) · Journal of Diabetes and its Complications · doi:10.1016/j.jdiacomp.2005.09.007 · Cited by 199 · see citing works
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Type 2 diabetes in the child and adolescent
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Air pollution and risk of type 2 diabetes mellitus: A systematic review and meta-analysis
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Obesity, overweight and ethnicity.
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Influence of Maternal Obesity on Insulin Sensitivity and Secretion in Offspring
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“However, the limited -cell capacity is regarded as being of “little significance” (2) in the absence of obesity.”
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“The incidence of type 2 diabetes has increased among children worldwide (49, 132, 140, 154), and this is thought to be a consequence of the pediatric obesity epidemic (87, 135).”
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Methodological considerations and future insights for 24-hour dietary recall assessment in children
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β-Cell Function Across the Spectrum of Glucose Tolerance in Obese Youth
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“The unabated rise in the prevalence of childhood obesity (1) has been accompanied by the emergence of impaired glucose tolerance (IGT) as well as type 2 diabetes (2) in childhood.”
Risk factors that may modify the innate and adaptive immune responses in periodontal diseases
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“Although patients with type 2 diabetes are typically older than 40 years of age (11), earlier onset of type 2 diabetes (20–30 years of age) is becoming increasingly more common, particularly in Pacific Island and southern Asian populations (327, 428).”
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Measuring the Prevalence of Overweight in Texas Schoolchildren
Hoelscher, D. M., Day, R. S., Lee, E. S., Frankowski, R. F., Kelder, S. H., Ward, J. L., & Scheurer, M. E. (2004) · American Journal of Public Health · doi:10.2105/ajph.94.6.1002 · Cited by 159 · see citing works
- Authors
- Rosenbloom, A. L., Joe, J. R., Young, R. S., & Winter, W. E.
- Affiliations
- University of Florida Health (US)
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 1999-02-01
- Volume
- 22
- Issue
- 2
- Pages
- 345-354
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W2152591650
- Cited by
- 1,019
- References
- 0
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 6 · 2023: 5 · 2022: 10 · 2021: 13 · 2020: 8 · 2019: 22 · 2018: 20 · 2017: 16 · 2016: 17 · 2015: 32 · 2014: 36 · 2013: 39 · 2012: 38
- FWCI
- 29.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes Care (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- type 2 diabetes, youth, diabetes incidence, obesity, insulin resistance, beta-cell dysfunction, thrifty phenotype, thrifty genotype hypothesis, maturity-onset diabetes of the young, atypical diabetes, African American children, Pima Indians, genetic susceptibility, diabetes prevention, diabetes treatment, minority groups, diabetes classification
- MeSH terms
- Adolescent, Adult, Age Factors, Arizona, Canada, Child, Child, Preschool, Chromosome Mapping, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, DNA, Mitochondrial, Female, Humans, Indians, North American, Male, NADH Dehydrogenase, RNA, Ribosomal, RNA, Transfer, Amino Acid-Specific, Point Mutation, White People
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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