Background Bariatric surgery reverses obesity-related comorbidities, including type 2 diabetes mellitus. Several studies have already described differences in anthropometrics and body composition between Roux-en-Y gastric bypass and laparoscopic adjustable gastric banding patients, but the role of adipokines in the outcomes after the different types of surgery is not known. Hypothesis Differences in weight loss and reversal of insulin resistance exist between the two groups and correlate with changes in adipokines. Methods Fifteen severely obese women (mean BMI: 46.7 kg/m2) underwent two types of laparoscopic weight loss surgery (Roux-en-Y gastric bypass = 10, adjustable gastric banding = 5). Weight, waist and hip circumference, body composition, plasma metabolic markers, and lipids were measured at set intervals during a 24-month period after surgery. Results At 24 months, Roux-en-Y patients were overweight (BMI 29.7 kg/m2) while gastric banding patients remained obese (BMI 36.3 kg/m2). Roux-en-Y patients lost significantly more fat mass than gastric banding patients (mean difference 16.8 kg, p < 0.05). Likewise, leptin levels were lower in the Roux-en-Y patients (p = 0.003) and levels correlated with weight loss, loss of fat mass, insulin levels, and Homeostasis Model of Assessment 2 (HOMA-IR). Adiponectin correlated with insulin levels and HOMA-IR (r = −0.653, p = 0.04 and r = −0.674, p = 0.032, respectively) in the Roux-en-Y patients at 24 months. Conclusions After two years weight loss and normalization of metabolic parameters were less pronounced in patients who underwent gastric banding compared to patients who underwent Roux-en-Y gastric bypass. Our findings require confirmation in a prospective randomized trial.

Objective-To define muscle metabolic and cardiovascular changes following surgical intervention in clinically severe obese patients.Background-Obesity is a state of metabolic dysregulation which may lead to maladaptive changes in heart and skeletal muscle, including insulin resistance and heart failure. In a prospective longitudinal study 43 consecutive patients were subjected to metabolic profiling, skeletal muscle biopsies and resting echocardiograms at baseline as well as three and nine months after bariatric surgery.

Background Obesity is a systemic disorder associated with an increase in left ventricular mass and premature death and disability from cardiovascular disease. Although bariatric surgery reverses many of the hormonal and hemodynamic derangements, the long-term collective effects on body composition and left ventricular mass have not been considered before. Hypothesis The decline in fat mass and lean mass after weight loss surgery is associated with a decline in left ventricular mass. Methods Fifteen severely obese women (mean body mass index or BMI: 46.7 ± 1.7 kg/m2) with medically controlled hypertension underwent bariatric surgery. Left ventricular mass and plasma markers of systemic metabolism, together with BMI, waist and hip circumferences, body composition (fat mass and lean mass), and resting energy expenditure (REE) were measured at 0, 3, 9, 12 and 24 months. Results Left ventricular mass continued to decline linearly over the entire period of observation, while rates of weight-loss, loss of lean mass, loss of fat mass, and REE all plateaued at 9 months (p<0.001 for all). Parameters of systemic metabolism normalized by 9 months, and showed no further change at 24 months after surgery. Conclusions Even though parameters of obesity, including BMI and body composition, plateau, the benefits of bariatric surgery on systemic metabolism and left ventricular mass are sustained. We propose that the progressive decline of left ventricular mass after weight loss surgery is regulated by neurohumoral factors, and may contribute to improved long-term survival.

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Obesity is an independent risk factor for cardiovascular disease. Data from the Framingham Study have reported a higher incidence of heart failure in obese individuals compared with a normal cohort. The body initially copes with the abundance of fuel present in an obese milieu by storing it in adipose tissue. However, when the storage capacity is exceeded, the excess energy is taken up and stored ectopically as fat in vital organs such as the heart. Indeed, intramyocardial lipid overload is present in hearts of obese patients, as well as in hearts of animal models of obesity, and is associated with a distinct gene expression profile and cardiac dysfunction. By imposing a metabolic stress on the heart, obesity causes it to hypertrophy and ultimately to fail. Conventional measures to treat obesity include diet, exercise, and drugs. More recently, weight loss surgery (WLS) has achieved increasing prominence because of its ability to reduce the neurohumoral load, normalize metabolic dysregulation, and improve overall survival. The effects of WLS on systemic metabolic, neurohumoral, and hemodynamic parameters are well described and include an early normalization of serum glucose and insulin levels as well as reduction in blood pressure. WLS is also associated with reverse cardiac remodeling, regression of left ventricular hypertrophy, and improved left ventricular and right ventricular function. By targeting the source of the excess energy, we hypothesize that WLS improves contractile function by limiting exogenous substrate availability to the metabolically overloaded heart. These changes have also been found to be associated with increased levels of adiponectin and improved insulin sensitivity. Taken together, the sustained beneficial effects of WLS on left ventricular mass and function highlight the need to better understand the mechanism by which obesity regulates cardiovascular physiology.