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Serum Insulin and Inflammatory Markers in Overweight Individuals with and without Dyslipidemia

The Heart Research Institute (P.B.), Sydney, New South Wales 2050, Australia; University of Ottawa Heart Institute (Y.R.M.), Ottawa, Ontario, Canada K1Y 4W7; Genetics Research (K.S., V.M., D.W.), GlaxoSmithKline, Collegeville, Pennsylvania 19406; Department of Internal Medicine and Biocenter Oulu (Y.A.K.), University of Oulu, FIN-90014 Oulu, Finland; Gladstone Institute of Cardiovascular Disease (R.M., T.B.), University of California, San Francisco, San Francisco, California 94158; Department of Medicine (G.W.), Lausanne University Hospital, 1011 Lausanne, Switzerland; and Center for Human Nutrition (S.M.G.), University of Texas Southwestern Medical Center, Dallas, Texas 75235

Address all correspondence and requests for reprints to: Prof. Philip Barter, The Heart Research Institute, 114 Pyrmont Bridge Road, Camperdown, New South Wales 2050, Australia. E-mail: barterp{at}hri.org.au.

Context: The worldwide epidemic of overweight and obesity is setting the scene for a new wave of premature cardiovascular disease.

Objective: The objective of this study was to define relationships between dyslipidemia and other metabolic abnormalities in overweight subjects.

Design: This study included comparison of overweight subjects with and without dyslipidemia.

Setting: The setting was an institutional practice.

Patients: Dyslipidemic subjects (n = 715) had plasma triglyceride greater than or equal to the 75th percentile in combination with high-density lipoprotein cholesterol (HDL-C) less than or equal to the 25th percentile. Unrelated, normolipidemic controls (n = 1073) had HDL-C higher than the median and triglyceride lower than the median. It was a requirement for the control subjects to have a body mass index (BMI) greater than 25 kg/m².

Main Outcome Measures: The main outcome measures included BMI, inflammatory markers, adipokines, blood pressure, and fasting plasma glucose and insulin.

Results: The mean BMI in the subjects and controls was 28.7 and 28.2 kg/m², respectively. Subjects had higher levels of plasma high-sensitivity C-reactive protein (3.0 vs. 2.0 mg/liter; P < 0.001), lower levels of adiponectin (4.7 vs. 6.6 mg/liter; P < 0.001), and, after adjustment for age, BMI, gender, smoking, statin, and ß-blocker use, higher systolic (P = 0.001) and diastolic (P = 0.05) blood pressures. Fasting plasma glucose, insulin, and homeostasis model of assessment-insulin resistance were all significantly higher in subjects than controls (P < 0.0001).

Conclusions: Identification of people solely on the basis of an elevated plasma triglyceride and a low HDL-C uncovers an overweight group of people who have a generalized metabolic disorder. In contrast, overweight people with normal plasma lipids have normal glucose and insulin metabolism, low levels of inflammatory markers, and normal blood pressure. Such people may thus be at relatively low risk of developing diabetes and cardiovascular disease despite being overweight.