Racial Disparity in Glucagon-Like Peptide 1 and Inflammation Markers Among Severely Obese Adolescents

  1. Pedro A. Velásquez-Mieyer, MD1,
  2. Patricia A. Cowan, PHD2,
  3. Sylvia Pérez-Faustinelli, MD1,
  4. Ramfis Nieto-Martínez, MD, MSC3,
  5. Cesar Villegas-Barreto, MD1,
  6. Elizabeth A. Tolley, PHD4,
  7. Robert H. Lustig, MD5 and
  8. Bruce S. Alpert, MD1
  1. 1Department of Pediatrics, University of Tennessee Health Science Center, Memphis, Tennessee
  2. 2Department of Nursing, University of Tennessee Health Science Center, Memphis, Tennessee
  3. 3Department of Physiology, Universidad Centro-Occidental “Lisandro Alvarado,” Barquisimeto, Venezuela
  4. 4Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee
  5. 5Department of Pediatrics, University of San Francisco, San Francisco, California
  1. Address correspondence and reprint requests to Pedro Velásquez-Mieyer, MD, Pediatrics, Le Bonheur Children’s Medical Center, 50 North Dunlap, Memphis, TN 38103. E-mail: pvelasquez{at}utmem.edu

Abstract

OBJECTIVE—Compared with Caucasians, obese African-American adolescents have a higher risk for type 2 diabetes. Subclinical inflammation and reduced glucagon-like peptide 1 (GLP-1) concentration are linked to the pathogenesis of the disease. We determined the relationship between insulin resistance, β-cell activity, and subclinical inflammation with GLP-1 concentrations and whether racial disparities in GLP-1 response were present in 49 obese adolescents (14 ± 3 years; 76% African American; 71% female).

RESEARCH DESIGN AND METHODS—Subjects underwent physical examination and an oral glucose tolerance test. We measured levels of high-sensitivity CRP (CRPhs), fibrinogen, glucose, GLP-1total, GLP-1active, and insulin. Insulin and glucose area under the curve (AUC), insulinogenic index (ΔI30/ΔG30), and composite insulin sensitivity index (CISI) were computed. Subjects were categorized by race and as inflammation positive (INF+) if CRPhs or fibrinogen were elevated.

RESULTS—No racial differences were seen in mean or relative BMI. Thirty-five percent of subjects had altered fasting or 2-h glucose levels (African American vs. Caucasian, NS), and 75% were INF+ (African American vs. Caucasian, P = 0.046). Glucose and insulin, CISI, and ΔI30/ΔG30 values were similar; African Americans had lower GLP-1total AUC (P = 0.01), GLP-1active at 15 min (P = 0.03), and GLP-1active AUC (P = 0.06) and higher fibrinogen (P = 0.01) and CRPhs (NS) compared with Caucasians.

CONCLUSIONS—African Americans exhibited lower GLP-1 concentrations and increased inflammatory response. Both mechanisms may act synergistically to enhance the predisposition of obese African Americans to type 2 diabetes. Our findings might be relevant to effective deployment of emerging GLP-1–based treatments across ethnicities.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 9 January 2008. DOI: 10.2337/dc07-1525.

    The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of the National Center for Research Resources, National Institute of Nursing Research, National Institutes of Health, or Children’s Foundation Research Center.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.

    • Accepted December 23, 2007.
    • Received August 3, 2007.
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  1. Published online before print January 9, 2008, doi: 10.2337/dc07-1525 Diabetes Care April 2008 vol. 31 no. 4 770-775
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