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      Relationship of Abdominal Visceral and Subcutaneous Adipose Tissue With Lipoprotein Particle Number and Size in Type 2 Diabetes


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          OBJECTIVE—Insulin resistance and type 2 diabetes are associated with an atherogenic lipoprotein profile. We examined the role of visceral and subcutaneous fat depots, independent of BMI, on the dyslipidemia associated with type 2 diabetes.

          RESEARCH DESIGN AND METHODS— A total of 382 subjects with type 2 diabetes underwent abdominal computed tomography to evaluate subcutaneous (SAT) and visceral adipose tissue (VAT) distribution and had anthropometric measurements to determine BMI and waist and hip circumference. Fasting blood was obtained for lipoprotein particle number and size using nuclear magnetic resonance spectroscopy. The relationship of lipoprotein particle number and size with BMI, SAT, and VAT was examined using multivariable regression models adjusted for age, sex, diabetes therapy, duration of diabetes, smoking, statin use, and A1C levels. The relation of VAT to lipoprotein particle number and size was further evaluated after the addition of BMI, BMI plus SAT, or BMI plus homeostatis is model assessment of insulin resistance (HOMA-IR) to the model.

          RESULTS—VAT was positively related to VLDL particle number ( P < 0.0001), LDL particle number ( P < 0.01), and VLDL size ( P < 0.0001) and negatively related to LDL size ( P < 0.0001) and HDL size ( P < 0.0001). These relationships remained unchanged after addition of BMI and SAT to the model. After addition of HOMA-IR, VAT remained positively related to VLDL particle number ( P < 0.0001) and size ( P < 0.01) and negatively related to LDL and HDL particle size ( P < 0.0001 for both comparisons). Neither BMI nor SAT was independently related to lipoprotein parameters.

          CONCLUSIONS—In patients with type 2 diabetes, higher VAT independent of BMI was associated with higher VLDL and LDL particle number, larger VLDL particles, and smaller LDL and HDL particles. This lipoprotein pattern has been associated with increased risk for atherosclerosis and cardiovascular disease.

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          Most cited references34

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            Obesity, metabolic syndrome, and cardiovascular disease.

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              Splanchnic lipolysis in human obesity.

              Elevated FFA concentrations have been shown to reproduce some of the metabolic abnormalities of obesity. It has been hypothesized that visceral adipose tissue lipolysis releases excess FFAs into the portal vein, exposing the liver to higher FFA concentrations. We used isotope dilution/hepatic vein catheterization techniques to examine whether intra-abdominal fat contributes a greater portion of hepatic FFA delivery in visceral obesity. Obese women (n = 24) and men (n = 20) with a range of obesity phenotypes, taken together with healthy, lean women (n = 12) and men (n = 12), were studied. Systemic, splanchnic, and leg FFA kinetics were measured. The results showed that plasma FFA concentrations were approximately 20% greater in obese men and obese women. The contribution of splanchnic lipolysis to hepatic FFA delivery ranged from less than 10% to almost 50% and increased as a function of visceral fat in women (r = 0.49, P = 0.002) and in men (r = 0.52, P = 0.002); the slope of the relationship was greater in women than in men (P < 0.05). Leg and splanchnic tissues contributed a greater portion of systemic FFA release in obese men and women than in lean men and women. We conclude that the contribution of visceral adipose tissue lipolysis to hepatic FFA delivery increases with increasing visceral fat in humans and that this effect is greater in women than in men.

                Author and article information

                American Diabetes Association
                August 2008
                : 57
                : 8
                : 2022-2027
                [1 ]Department of Medicine, Section of Endocrinology, Diabetes and Metabolism, Chicago, Illinois
                [2 ]Department of Medicine, University of Texas Health Science Center, San Antonio, Texas
                [3 ]Pritzker School of Medicine, The University of Chicago, Chicago, Illinois
                [4 ]Department of Mathematics, Statistics and Consulting Unit, Boston University, Boston, Massachusetts
                [5 ]Department of Medicine, Section of Cardiology, Rush University Medical Center, Chicago, Illinois
                [6 ]Department of Medicine, Section of Cardiology, University of Illinois College of Medicine, Chicago, Illinois
                [7 ]Takeda Global Research and Development, Deerfield, Illinois
                Author notes

                Corresponding author: Theodore Mazzone, tmazzone@ 123456uic.edu

                Copyright © 2008, 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.

                : 4 February 2008
                : 4 May 2008

                Endocrinology & Diabetes
                Endocrinology & Diabetes


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