Stefanie R van Mil1, Guy H E J Vijgen2, Astrid van Huisstede3, Boudewijn Klop4, Gert-Jan M van de Geijn5, Erwin Birnie6,7, Gert-Jan Braunstahl3, Guido H H Mannaerts2, L Ulas Biter2, Manuel Castro Cabezas4. 1. Department of Surgery, Franciscus Gasthuis, PO Box 10900, 3004 BA, Rotterdam, The Netherlands. stefanievanmil@caiway.net. 2. Department of Surgery, Franciscus Gasthuis, PO Box 10900, 3004 BA, Rotterdam, The Netherlands. 3. Department of Pulmonology, Franciscus Gasthuis, PO Box 10900, 3004 BA, Rotterdam, The Netherlands. 4. Department of Internal Medicine, Franciscus Gasthuis, PO Box 10900, 3004 BA, Rotterdam, The Netherlands. 5. Department of Clinical Chemistry, Franciscus Gasthuis, PO Box 10900, 3004 BA, Rotterdam, The Netherlands. 6. Department of Statistics and Education, Franciscus Gasthuis, PO Box 10900, 3004 BA, Rotterdam, The Netherlands. 7. Division Women and Baby, Department of Obstetrics and Gynecology, University Medical Center Utrecht, PO Box 85500, 3508 GA, Utrecht, The Netherlands.
Abstract
BACKGROUND: Obesity is related to increased cardiovascular risk. It is unknown whether increasing levels of obesity also increase levels of cardiovascular risk factors and systemic inflammation. This study describes the relationship between classic cardiovascular risk factors and inflammatory markers with BMI in a group of obese and non-obese subjects. MATERIALS AND METHODS: Obese subjects (BMI ≥ 30 kg/m2; n = 576; mean ± SD BMI 43.8 ± 7.58 kg/m2) scheduled for bariatric surgery were included. The reference population consisted of non-obese volunteers (BMI < 30 kg/m2; n = 377, BMI 25.0 ± 2.81 kg/m2). The relationship between BMI quintiles and the levels of cardiovascular risk factors was analyzed. Adipose tissue volumetry was performed in 42 obese subjects using abdominal CT scans. RESULTS: The obese group included more women and subjects with type 2 diabetes mellitus, hypertension, and current smoking behavior. In obese subjects, HDL-C and triglycerides decreased with increasing BMI. Systolic and diastolic blood pressure, total cholesterol, LDL-C, and apoB were not related to BMI in the obese group, in contrast to the non-obese group. Inflammatory markers CRP, leukocyte count, and serum complement C3 increased with increasing BMI in the obese group, while these relations were less clear in the non-obese group. The subcutaneous adipose tissue surface was positively correlated to BMI, while no correlation was observed between BMI and visceral adipose tissue. CONCLUSIONS: Markers of inflammation are strongest related to BMI in obese subjects, most likely due to increased adipose tissue mass, while cardiovascular risk factors do not seem to deteriorate above a certain BMI level. Limited expansion capacity of visceral adipose tissue may explain these findings.
BACKGROUND:Obesity is related to increased cardiovascular risk. It is unknown whether increasing levels of obesity also increase levels of cardiovascular risk factors and systemic inflammation. This study describes the relationship between classic cardiovascular risk factors and inflammatory markers with BMI in a group of obese and non-obese subjects. MATERIALS AND METHODS:Obese subjects (BMI ≥ 30 kg/m2; n = 576; mean ± SD BMI 43.8 ± 7.58 kg/m2) scheduled for bariatric surgery were included. The reference population consisted of non-obese volunteers (BMI < 30 kg/m2; n = 377, BMI 25.0 ± 2.81 kg/m2). The relationship between BMI quintiles and the levels of cardiovascular risk factors was analyzed. Adipose tissue volumetry was performed in 42 obese subjects using abdominal CT scans. RESULTS: The obese group included more women and subjects with type 2 diabetes mellitus, hypertension, and current smoking behavior. In obese subjects, HDL-C and triglycerides decreased with increasing BMI. Systolic and diastolic blood pressure, total cholesterol, LDL-C, and apoB were not related to BMI in the obese group, in contrast to the non-obese group. Inflammatory markers CRP, leukocyte count, and serum complement C3 increased with increasing BMI in the obese group, while these relations were less clear in the non-obese group. The subcutaneous adipose tissue surface was positively correlated to BMI, while no correlation was observed between BMI and visceral adipose tissue. CONCLUSIONS: Markers of inflammation are strongest related to BMI in obese subjects, most likely due to increased adipose tissue mass, while cardiovascular risk factors do not seem to deteriorate above a certain BMI level. Limited expansion capacity of visceral adipose tissue may explain these findings.
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