CoChat
Sign Up
Cited by 1,019Diabetes and associated disordersDiabetes, Cardiovascular Risks, and LipoproteinsDiabetes Management and Research

The DOI matches its Crossref record.

Emerging epidemic of type 2 diabetes in youth

Rosenbloom, A L, Joe, J R, Young, R S, Winter, W E·1999·Diabetes Care
DOI 10.2337/diacare.22.2.345
Open this paper in CoChat — free account

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.

Overview

Integrity signals

Registry

Crossref · 10.2337/diacare.22.2.345

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cited by

Sorted by citations

Items 601–700 of 999

Related

See all

Metadata

Authors
Rosenbloom, A. L., Joe, J. R., Young, R. S., & Winter, W. E.
Affiliations
University of Florida Health (US)
ORCID
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
DOI
10.2337/diacare.22.2.345
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.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review