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• W2103405338 abstract "Purpose of review This review focuses on recent literature on insulin resistance in youth with type 2 diabetes mellitus (T2DM). Insulin resistance is associated with a variety of cardiometabolic problems leading to increased morbidity and mortality across the lifespan. Recent findings Functional pancreatic β-cell changes play a role in the transition from obesity to impaired glucose tolerance (IGT). Insulin resistance drives islet cell upregulation, manifested by elevated glucagon and c-peptide levels, early in the transition to IGT. Surrogate measurements of insulin resistance and insulin secretion exist but their accuracy compared to clamp data is imperfect. Recent large longitudinal studies provide detailed information on the progression from normoglycemia to T2DM and on the phenotype of T2DM youth. Defining prediabetes and T2DM remains a challenge in youth. Lifestyle interventions do not appear as effective in children as in adults. Metformin remains the only oral hypoglycemic agent approved for T2DM in youth. Summary New insights exist regarding the conversion from insulin resistance to T2DM, measurement of insulin resistance and phenotypes of insulin resistance youth, but more information is needed. Surrogate measurements of insulin resistance, additional treatment options for insulin resistance and individualization of treatment options for T2DM adolescents in particular require further investigation." @default.
• W2103405338 created "2016-06-24" @default.
• W2103405338 creator A5005491526 @default.
• W2103405338 creator A5077027324 @default.
• W2103405338 creator A5077829479 @default.
• W2103405338 date "2012-08-01" @default.
• W2103405338 modified "2023-09-26" @default.
• W2103405338 title "Insulin resistance in type 2 diabetic youth" @default.
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• W2103405338 doi "https://doi.org/10.1097/med.0b013e3283557cd5" @default.
• W2103405338 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4296021" @default.
• W2103405338 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22732484" @default.
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