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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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“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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“T ype 2 diabetes mellitus is becoming a major public health care problem in the world, originally affecting industrialized countries, but now extending to developing countries [1, 2].”
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“Such studies are important, but one could ask, “Why perform them in children?” Certainly type 2 diabetes and obesity are major and emerging problems in the young (5,6), and we are not yet certain that the pathogenesis of insulin resistance and type 2 diabetes are the same in children as in adults, especially those who…”
BackgroundDiabetes mellitus: Type 1 or type 2? The accelerator hypothesis
Wilkin, T. J. (2002) · The Journal of Pediatrics · doi:10.1067/mpd.2002.126010 · Cited by 9
The Impact of a Multi-disciplinary Management Approach on Diabetic Control in Young Saudi Patients
Udezue, E. O., Nashwan, R. H., Azim, A. A., et al. (2005) · Annals of Saudi Medicine · doi:10.5144/0256-4947.2005.85 · Cited by 9
Treatment of type 2 diabetes in youth: An argument for randomized controlled studies
Dean, H. (1999) · Paediatrics & Child Health · doi:10.1093/pch/4.4.265 · Cited by 9
Type 2 Diabetes in Youth: A New Epidemic
Dean, H. (2001) · Advances in experimental medicine and biology · doi:10.1007/978-1-4615-1321-6_1 · Cited by 9
“This is a devastating disease and it's only just begun ( 22 ).”
BackgroundDyck, R. F., Cascagnette, P., & Klomp, H. (2010) · Canadian Journal of Diabetes · doi:10.1016/s1499-2671(10)41009-6 · Cited by 8
Bariatric Surgery in Adolescents
Kane, T. D., Garcia, V. F., & Inge, T. H. (2007) · Springer eBooks · doi:10.1007/978-0-387-68062-0_49 · Cited by 9
Online diabetes education: design and evaluation with prospective diabetes camp counsellors
Heidgerken, A. D., Lewin, A. B., Geffken, G. R., et al. (2005) · Journal of Telemedicine and Telecare · doi:10.1258/1357633053499813 · Cited by 8
The metabolic syndrome: evolving evidence that thiazolidinediones provide rational therapy
Wyne, K. L. (2006) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2005.00522.x · Cited by 8
Mata‐Cases, M., Artola, S., Escalada, J., Loiola, P. E., Ferrer-García, J. C., Fornos, J. A., Girbés, J., & Rica, I. (2015) · Atención Primaria · doi:10.1016/j.aprim.2014.12.002 · Cited by 11
Mouraux, T., & Dorchy, H. (2005) · Archives de Pédiatrie · doi:10.1016/j.arcped.2005.03.041 · Cited by 8
Hong, S.-W., & Hamlin, M. J. (2005) · PubMed · Cited by 8
Nader, N. S., & Kumar, S. (2008) · Current Diabetes Reports · doi:10.1007/s11892-008-0066-2 · Cited by 8
In vitro and In vivo Studies of Drug-Drug Interaction between Metformin and Cefepime
Sultan, S. F. M. Z. (2015) · Pharmaceutica Analytica Acta · doi:10.4172/2153-2435.1000348 · Cited by 8
Egeland, G. M., Skjærven, R., & Irgens, L. M. (2002) · Paediatric and Perinatal Epidemiology · doi:10.1046/j.1365-3016.2002.00447.x · Cited by 8
Baskar, V., Kamalakannan, D., Holland, M. R., & Singh, B. M. (2004) · QJM · doi:10.1093/qjmed/hch123 · Cited by 8
“18–29 133 (35) 137 (46) 127 (24) 141 (24) 146 (34) 134 (14) 30–39 134 (44) 138 (54) 128 (33) 143 (28) 148 (36) 136 (19) 40–49 139 (43) 144 (40) 133 (45) 149 (28) 153 (26) 145 (30) 50–59 147 (45) 149 (44) 146 (47) 161 (21) 161 (21) 161 (22) 60–69 154 (40) 155 (33) 154 (46) 171 (17) 171 (9) 171 (25) >70 167 (27) 165 (19…”
Voss, L. D., Hosking, J., Metcalf, B. S., Jeffery, A., Frémeaux, A. E., & Wilkin, T. J. (2014) · Pediatric Diabetes · doi:10.1111/pedi.634 · Cited by 8
“Excess weight gain, leading to insulin resistance, appears to be a key factor, although the relationships may not be straightforward (2, 3).”
Background
Metadata
- 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
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