Increased Fasting Triglyceride Levels Are Associated With Hepatic Insulin Resistance in Caucasian but Not African-American Adolescents

  1. Robert P. Hoffman, MD
  1. From the Division of Pediatric Endocrinology, The Clinical Research Center of The Ohio State University College of Medicine and Public Health, Columbus, Ohio
  1. Address correspondence and reprint requests to Robert P. Hoffman, MD, Children’s Hospital ED541, 700 Children’s Dr., Columbus, OH 43205. E-mail: hoffmanr{at}pediatrics.ohio-state.edu

Increased lipid levels are related to insulin resistance in children and adults (1–3). Insulin resistance occurs due to an inability to suppress hepatic glucose production (HGP) or to stimulate peripheral glucose uptake. It is not clear whether hyperlipidemia primarily affects hepatic or peripheral insulin sensitivity. In this study, the stable-labeled, frequently sampled intravenous glucose tolerance test (4–7) was used to measure total-body insulin sensitivity (Si), peripheral insulin sensitivity (Si*) (5), and hepatic insulin resistance (HIR) (8) in African-American and Caucasian adolescents.

RESEARCH DESIGN AND METHODS

Healthy, Tanner stage 1–5, Caucasian (n = 18, age 14.0 ± 2.6 years, BMI 23.0 ± 3.2 kg/m2) and African-American (n = 10, age 14.1 ± 2.3, BMI 25.6 ± 5.1) subjects were studied. Informed written consent and assent were obtained. The protocol was approved by The Ohio State University Office of Responsible Research.

Studies were performed in the Clinical Research Center of The Ohio State University after overnight fasting. Intravenous catheters were placed in the antecubital fossa of each arm. A bolus of 25% dextrose in water with ∼13% [6-6]D2 glucose (Cambridge Isotopes, Cambridge, MA) was given over 1 min (4,7,9). The total dose was 250 mg/kg. Blood samples were taken at −10, 0, 2, 4, 6, 8, 12, 14, 16, 19, 22, 27, 32, 42, 52, 62, 72, 82, 92, 102, 122, 142, 162, and …

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