Journal
BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 19, Issue 3, Pages 405-419Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.beem.2005.04.009
Keywords
impaired glucose tolerance (IGT); type 2 diabetes (T2DM); visceral fat; intramyocellular fat (IMCL); insulin resistance; non-alcoholic fatty liver disease (NAFLD); metabolic syndrome; adiponectin; C-reactive protein (CRP)
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Funding
- NCRR NIH HHS [M01 RR 06022, M01 RR 00125] Funding Source: Medline
- NICHD NIH HHS [R01 HD 40787, R01 HD 28016, K24 HD 01464] Funding Source: Medline
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The prevalence of childhood obesity is increasing worldwide, is is the prevalence of obesity-related co-morbidity. Altered glucose metabolism, manifested as impaired glucose tolerance (IGT), appears early in obese children and adolescents. Obese young people with IGT are characterized by marked peripheral insulin resistance and a relative P-cell failure. Lipid deposition in muscle and the visceral compartment, and not only adiposity per se, is related to increased peripheral insulin resistance, the 'driving force' of the metabolic syndrome. Other elements of the metabolic syndrome, such as dyslipidemia and hypertension, are already present in obese youngsters and worsen with the degree of obesity. Similarly, markers of systemic 'low-grade inflammation' worsen with increasing adiposity. The long-term impact on cardiovascular and liver morbidity of obesity-related insulin resistance in young people is expected to emerge as these youngsters become young adults.
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