title: Elevation of fasting insulin and its association with cardiovascular disease risk in women with systemic lupus erythematosus.
abstract: Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis. We previously showed that SLE patients have a higher risk of insulin resistance (IR) and abnormal insulin secretion. The present study was to further investigate the relationship between fasting insulin levels and both classic and novel cardiovascular risk factors in patients with SLE. Body mass index (BMI), fasting glucose and insulin, lipid profile, oxidation markers, fibrinolytic factors, vascular function factors, and disease-specific variables were determined in a total of 87 female SLE patients. The homeostasis model assessment (HOMA) was used to evaluate the IR and secretion. SLE patients had significantly higher fasting insulin, HOMA IR, HOMA beta-cell, titers of autoantibodies against oxidized low density lipoprotein, systolic blood pressure, homocysteine, and brachial-ankle pulse wave velocity (baPWV) than age-matched healthy controls. There were no statistical differences in disease duration, anti-dsDNA, C3, C4, disease activity, and medication dosage between SLE patients stratified by fasting insulin levels. However, mean values for BMI, insulin, HOMA IR, HOMA beta-cell, triglyceride (TG), homocysteine, and baPWV were significantly higher in the SLE patients with hyperinsulinemia when compared with those SLE controls. In addition, fasting insulin levels were positively correlated with TG, homocysteine, blood pressure, plasminogen activator inhibitor 1, and baPWV in SLE patients. The elevation of fasting insulin levels in SLE patients is not only associated with IR, but is related to classic and novel cardiovascular risk factors. This study concludes that there is an insulin-related cardiovascular disease risk in SLE.
authors.affiliation: Department of Food Science, National Chiayi University, 300 University Road, Chia-Yi, 60004, Taiwan, ROC. timtso@mail.ncyu.edu.tw
authors.forename: Tim K
authors.initials: TK
authors.lastname: Tso
authors.forename: Wen-Nan
authors.initials: WN
authors.lastname: Huang
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D001786:Blood Glucose / Q000502:physiology; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000097:blood* / Q000209:etiology / Q000503:physiopathology*; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006710:Homocysteine / Q000097:blood; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011237:Predictive Value of Tests; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D015854:Up-Regulation / Q000502:physiology
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D008077:Lipoproteins, LDL; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D006710:Homocysteine