Increase in Plasma Endotoxin Concentrations and the Expression of Toll-Like Receptors and Suppressor of Cytokine Signaling-3 in Mononuclear Cells After a High-Fat, High-Carbohydrate Meal
Implications for insulin resistance
- Husam Ghanim, PHD1,
- Sanaa Abuaysheh, BS1,
- Ching Ling Sia, BS1,
- Kelly Korzeniewski, BS1,
- Ajay Chaudhuri, MD2,
- Jose Manuel Fernandez-Real, MD1 and
- Paresh Dandona, MD1
- 1Division of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo, and Kaleida Health, Buffalo, New York;
- 2Biomedical Research Institute of Girona, Hospital of Girona, CIBERobn Fisiopatologica de la Obesidad y Nutricion, Ministry of Science, Girona, Spain.
- Corresponding author: Paresh Dandona, pdandona{at}kaleidahealth.org.
Abstract
OBJECTIVE To compare the effect of a high-fat, high-carbohydrate meal (HFHC) with that of a high-fiber and fruit meal on the concentrations of endotoxin (lipopolysaccharide [LPS]), LPS-binding protein (LBP), the expression of toll-like receptors (TLRs), and the suppressor of cytokine signaling-3 (SOCS-3) in mononuclear cells.
RESEARCH DESIGN AND METHODS Healthy lean subjects were given 910 calories of either an HFHC meal (n = 10) or an American Heart Association (AHA)-recommended meal rich in fiber and fruit (n = 10) after an overnight fast. Blood was collected before and at 1, 2, and 3 h after the meal. Cellular indexes of oxidative and inflammatory stress; the expression of SOCS-3, TLR2, and TLR4 in mononuclear cells; and plasma concentrations of LPS and LBP were measured.
RESULTS HFHC meal intake induced an increase in plasma LPS concentration and the expression of SOCS-3, TLR2, and TLR4 protein, reactive oxygen species generation, and nuclear factor-κB binding activity (P < 0.05 for all). These increases were totally absent after the AHA meal rich in fiber and fruit.
CONCLUSIONS The novel changes described after the HFHC meal elucidate further the mechanisms underlying postprandial inflammation and also provide the first evidence explaining the pathogenesis of insulin and leptin resistance mediated by SOCS-3 after such meals. In contrast, an AHA meal does not induce these effects.
Footnotes
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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.
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- Received May 28, 2009.
- Accepted August 15, 2009.
- © 2009 by the American Diabetes Association.














