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      Plasma Ceramides Are Elevated in Obese Subjects With Type 2 Diabetes and Correlate With the Severity of Insulin Resistance

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          Abstract

          OBJECTIVE—To quantitate plasma ceramide subspecies concentrations in obese subjects with type 2 diabetes and relate these plasma levels to the severity of insulin resistance. Ceramides are a putative mediator of insulin resistance and lipotoxicity, and accumulation of ceramides within tissues in obese and diabetic subjects has been well described.

          RESEARCH DESIGN AND METHODS—We analyzed fasting plasma ceramide subspecies by quantitative tandem mass spectrometry in 13 obese type 2 diabetic patients and 14 lean healthy control subjects. Results were related to insulin sensitivity measured with the hyperinsulinemic-euglycemic clamp technique and with plasma tumor necrosis factor-α (TNF-α) levels, a marker of inflammation. Ceramide species (C18:1, 18:0, 20:0, 24:1, and 24:0) were quantified using electrospray ionization tandem mass spectrometry after separation with high-performance liquid chromatography.

          RESULTS—Insulin sensitivity (mg · kg −1 · min −1) was lower in type 2 diabetic patients (4.90 ± 0.3) versus control subjects (9.6 ± 0.4) ( P < 0.0001). Type 2 diabetic subjects had higher ( P < 0.05) concentrations of C18:0, C20:0, C24:1, and total ceramide. Insulin sensitivity was inversely correlated with C18:0, C20:0, C24:1, C24:0, and total ceramide (all P < 0.01). Plasma TNF-α concentration was increased ( P < 0.05) in type 2 diabetic subjects and correlated with increased C18:1 and C18:0 ceramide subspecies.

          CONCLUSIONS—Plasma ceramide levels are elevated in type 2 diabetic subjects and may contribute to insulin resistance through activation of inflammatory mediators, such as TNF-α.

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          Most cited references 45

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          A rapid method of total lipid extraction and purification.

           E G BLIGH,  W. Dyer (1959)
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            Inflammation, stress, and diabetes.

            Over the last decade, an abundance of evidence has emerged demonstrating a close link between metabolism and immunity. It is now clear that obesity is associated with a state of chronic low-level inflammation. In this article, we discuss the molecular and cellular underpinnings of obesity-induced inflammation and the signaling pathways at the intersection of metabolism and inflammation that contribute to diabetes. We also consider mechanisms through which the inflammatory response may be initiated and discuss the reasons for the inflammatory response in obesity. We put forth for consideration some hypotheses regarding important unanswered questions in the field and suggest a model for the integration of inflammatory and metabolic pathways in metabolic disease.
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              Diabetes

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                Author and article information

                Journal
                Diabetes
                diabetes
                Diabetes
                American Diabetes Association
                0012-1797
                1939-327X
                February 2009
                : 58
                : 2
                : 337-343
                Affiliations
                [1 ]Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio
                [2 ]Department of Physiology, Case Western Reserve University School of Medicine, Cleveland, Ohio
                [3 ]Department of Endocrinology, Diabetes, and Metabolism, Cleveland Clinic, Cleveland, Ohio
                [4 ]Department of Gastroenterology/Hepatology, Cleveland Clinic, Cleveland, Ohio
                [5 ]Department of Cardiovascular Medicine and Center for Cardiovascular Diagnostics and Prevention, Cleveland Clinic, Cleveland, Ohio
                [6 ]Department of Nutrition, Case Western Reserve University School of Medicine, Cleveland, Ohio
                [7 ]Division of Diabetes, University of Texas Health Science Center, San Antonio, Texas
                Author notes

                Corresponding author: John P. Kirwan, kirwanj@ 123456ccf.org

                Article
                582337
                10.2337/db08-1228
                2628606
                19008343
                Copyright © 2009, American Diabetes Association

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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                Categories
                Metabolism

                Endocrinology & Diabetes

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