Metabolic alterations in morbid obesity. Influence on the haemorheological profile
Article type: Research Article
Authors: Vayá, Amparo | Hernández-Mijares, Antonio | Suescun, Marta | Solá, Eva | Cámara, Rosa | Romagnoli, Marco | Bautista, Daniel | Laiz, Begoña
Affiliations: Hemorheology and Haemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Valencia, Spain | Endocrinology Service, Dr. Peset University Hospital, Valencia, Spain | Endocrinology Service, La Fe University Hospital, Valencia, Spain | Department of Physical Education and Sports, University of Valencia, Valencia, Spain | Epidemiology Service, Dr. Peset University Hospital, Valencia, Spain
Note: [] Corresponding author: Amparo Vayá, MD, PhD, Hemorheology and Hemostasis Unit, Service of Clinical Pathology, La Fe University Hospital, Avda. de Campanar, 21, 46009, Valencia, Spain. Tel.: and Fax: +34 963862714; E-mail: vaya_amp@gva.es
Abstract: There are few studies on haemorheological disturbances in morbidly obese patients. The role played by the metabolic syndrome on the rheological profile of morbidly obese subjects has not yet been established, and it is not clear whether morbidly obese, but “metabolically healthy”, show rheological alterations. We aimed to determine the whole rheological profile in 136 morbidly obese patients and 136 normo-weight volunteers, along with plasma lipids, inflammatory and insulin resistance parameters. Patients had statistically higher glucose, triglycerides, HbA1c, leptin, insulin, HOMA, CRP, leucocytes, fibrinogen, plasma viscosity (p < 0.001, respectively), erythrocyte aggregation at 3 s−1 (p = 0.011) and lower erythrocyte elongation index 60 Pa (p = 0.015). In the multivariate regression analysis, the anthropometric, lipidic, insulin resistance and inflammatory parameters predicted haemorheological variables (p < 0.001). No differences were observed for the rheological parameters when morbidly obese subjects with (n = 75) and without (n = 61) the metabolic syndrome were compared (p > 0.05), indicating that the altered rheological profile not only related to the metabolic syndrome, but to obesity itself. When further patients were classified as “metabolically healthy” obese (n = 23) and “metabolically unhealthy” obese (n = 113), the latter presented higher insulin resistance (insulin p < 0.01, HOMA p < 0.05, glucose p < 0.001, triglycerides p < 0.05 and HbA1c p < 0.01) than the former, but no differences in the rheological parameters (p > 0.05) were observed. When “metabolically healthy” obese (n = 23) were compared with “metabolically healthy” controls (n = 81), the former still showed higher HOMA (p < 0.001), triglycerides (p < 0.05), CRP (p < 0.001) and HbA1c (p < 0.05), higher fibrinogen (p < 0.001), plasma viscosity (p < 0.001), erythrocyte aggregation at 3 s−1 (p < 0.05), but a lower erythrocyte elongation index 60 Pa (p < 0.05). Morbidly obese subjects present a more pronounced altered rheological profile in those with metabolic alterations, although the “metabolically healthy” obese also displayed rheological alterations if compared with “metabolically healthy” non-obese controls. These rheological alterations relate to both insulin resistance and inflammation.
Keywords: Morbid obesity, metabolic syndrome, metabolic alterations, haemorheology
DOI: 10.3233/CH-2011-1417
Journal: Clinical Hemorheology and Microcirculation, vol. 48, no. 4, pp. 247-255, 2011