Comorbidities associated with morbid obesity and evolution with bariatric surgery: Alterations of lipid metabolism, hepatic steatosis, throm-bophilia and satiety factors

Background People who suffer from morbid obesity are at high risk for many diseases: atherogenic dyslipidemia, elevated blood pressure, type 2 diabetes, thromboembolism, hepatic steatosis, proinflammatory state, etc. Metabolic syndrome is characterized by the clustering of some, or all, of these metabolic abnormalities in the presence of underlying insulin resistance with a strong association with diabetes and cardiovascular disease morbidity and mortality. The pathophysiology is attributable to insulin resistance. Increased release of free fatty acids (FFAs) from adipocytes blocks the insulin signal transduction pathway, which induces endothelial dysfunction due to the generation of increased reactive oxygen species (ROS) and oxidative stress. Dyslipidemia, associated with high levels of triglycerides and low concentrations of high-density lipoproteins (HDLs), contributes to a proinflammatory state. These risk factors are strongly associated with an excess, and a particular bodily distribution, of adipose tissue. The Roux-en-Y gastric bypass (RYGBP) has become the gold standard of bariatric surgery. It represents a mixed technique, combining restriction derived from leaving a small stomach pouch near the esophagogastric junction by excluding the greater curvature, together with a small malabsorptive component derived from bypassing most of the stomach and duodenum. Surgical weight loss approaches are based on intestinal malabsorption and gastric reduction. "Success" has been defined as a maintained weight loss of ≥50% of excess body weight, which in turn is defined as the difference between body weight and ideal weight (for a given patient's gender and height). Aims Going deeply into the biochemical and molecular knowledge of co-morbidities associated with morbid obesity and the changes that they experience with the bariatric surgery: alterations of lipid metabolism, hepatic steatosis, satiety factors and thrombophilia. It is also noteworthy, as a possible ethiopathogenic mechanism, the study of the role that the lipoprotein- and the hepatic-lipase have in the hepatic steatosis. Likewise, the alterations of the lipid metabolism due to surgical stress would also be studied. Subjects 34 patients with an IMC>40 that enter in the hospital for elective operation of bariatric surgery. Instrumentalization Laparotomy and gastric by-pass type Foby-Capella will be carried out. Adipose tissue and hepatic biopsy samples will be taken (as carried out in a routine way). Samples of pre-operative blood 1, 3, 6, 9 and 12 months will also be collected (coinciding with usual analytic). Determinations Lipid profile, lipolitic activities, plasma lipoproteins and lipolitic activities, lipid composition and mRNA determination of different lipolitic enzymes in several tissues. Satiety factors (leptin, ghrelin and apoAIV). Thrombophilia (CRP and, PAI-1). Liver steatosis (histology, hepatic biochemistry and lipolitic enzymes (activities, mass and mRNA), that could be implied in steatosis). Nutritional factors will also be determined along the study as well as plasma stress factors (ACTH, cortisol, etc). © 2010 by Nova Science Publishers, Inc. All rights reserved.