Joshua G. Leichman

Body Weight, Insulin Resistance, and Serum Adipokine Levels 2 Years after 2 Types of Bariatric Surgery

OBJECTIVE Bariatric surgery reverses obesity-related comorbidities, including type 2 diabetes mellitus. Several studies have already described differences in anthropometrics and body composition in patients undergoing Roux-en-Y gastric bypass compared with laparoscopic adjustable gastric banding, but the role of adipokines in the outcomes after the different types of surgery is not known. Differences in weight loss and reversal of insulin resistance exist between the 2 groups and correlate with changes in adipokines. METHODS Fifteen severely obese women (mean body mass index [BMI]: 46.7 kg/m(2)) underwent 2 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, patients who underwent Roux-en-Y were overweight (BMI 29.7 kg/m(2)), whereas patients who underwent gastric banding remained obese (BMI 36.3 kg/m(2)). Patients who underwent Roux-en-Y lost significantly more fat mass than patients who underwent gastric banding (mean difference 16.8 kg, P<.05). Likewise, leptin levels were lower in the patients who underwent Roux-en-Y (P=.003), and levels correlated with weight loss, loss of fat mass, insulin levels, and Homeostasis Model of Assessment 2. Adiponectin correlated with insulin levels and Homeostasis Model of Assessment 2 (r=-0.653, P=.04 and r=-0.674, P=.032, respectively) in the patients who underwent Roux-en-Y at 24 months. CONCLUSION After 2 years, weight loss and normalization of metabolic parameters were less pronounced in patients who underwent gastric banding compared with patients who underwent Roux-en-Y gastric bypass. Our findings require confirmation in a prospective randomized trial.

Dramatic Reversal of Derangements in Muscle Metabolism and Left Ventricular Function After Bariatric Surgery

OBJECTIVE The study objective was to define muscle metabolic and cardiovascular changes after surgical intervention in clinically severe obese patients. METHODS Obesity is a state of metabolic dysregulation that can lead to maladaptive changes in heart and skeletal muscle, including insulin resistance and heart failure. In a prospective longitudinal study, 43 consecutive patients underwent metabolic profiling, skeletal muscle biopsies, and resting echocardiograms at baseline and 3 and 9 months after bariatric surgery. RESULTS Body mass index decreased (mean changes, 95% confidence interval [CI]): 7.7 kg/m(2) (95% CI, 6.70-8.89) at 3 months and 5.6 kg/m(2) (95% CI, 4.45-6.80; P<.0001) at 9 months after surgery, with restoration of insulin sensitivity and decreases in plasma leptin at the same time points. Concurrent with these changes were dramatic decreases in skeletal muscle transcript levels of stearoyl coenzyme-A desaturase and pyruvate dehydrogenase kinase-4 at 3 and 9 months (P<.0001, for both) and a significant decrease in peroxisome proliferation activated receptor-alpha-regulated genes at 9 months. Left ventricular relaxation impairment, assessed by tissue Doppler imaging, normalized 9 months after surgery. CONCLUSION Weight loss results in the reversal of systemic and muscle metabolic derangements and is accompanied by a normalization of left ventricular diastolic function.

Association of plasma free fatty acids and left ventricular diastolic function in patients with clinically severe obesity

BACKGROUND Obesity is an important contributor to many cardiovascular risk factors and has been associated with abnormalities in cardiac contractile function. Causes of impaired contractile function are not fully understood and may include an oversupply of substrates. OBJECTIVE We tested the hypothesis that metabolic dysregulation may adversely influence cardiac function. Specifically, we examined the effects of plasma free fatty acids and insulin sensitivity on left ventricular function in patients with clinically severe obesity. DESIGN We measured metabolic and cardiac variables in 64 obese patients [body mass index (BMI; in kg/m(2)) > 35], including 2-D complete echocardiogram with M-mode and tissue Doppler imaging, anthropometric measurements, and analysis of blood chemistries. RESULTS The median (25th and 75th percentile) age and BMI were 46 y (36, 53 y) and 51.5 (42.5, 56.5), respectively. The prevalence of diabetes, hypertension, and insulin resistance were 38%, 53%, and 90%, respectively. Plasma free fatty acid (FFA) concentrations were elevated in the cohort. No association was observed between insulin sensitivity or anthropometric measurements and left ventricular contractile function. However, FFA concentration was independently associated with diastolic function (r = -0.33, P = 0.01), and 40% of the cohort showed age-adjusted diastolic impairment as measured by tissue Doppler imaging. CONCLUSION The negative association between FFA and diastolic function, in the setting of insulin resistance, suggests that excess FFA may exert a lipotoxic effect on the heart.

Progressive regression of left ventricular hypertrophy two years 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. We hypothesized that the decrease in fat mass and lean mass after weight loss surgery is associated with a decrease in left ventricular mass. METHODS Fifteen severely obese women (mean body mass index [BMI]: 46.7+/-1.7 kg/m(2)) with medically controlled hypertension underwent bariatric surgery. Left ventricular mass and plasma markers of systemic metabolism, together with body mass index (BMI), waist and hip circumferences, body composition (fat mass and lean mass), and resting energy expenditure were measured at 0, 3, 9, 12, and 24 months. RESULTS Left ventricular mass continued to decrease linearly over the entire period of observation, while rates of weight loss, loss of lean mass, loss of fat mass, and resting energy expenditure all plateaued at 9 [corrected] months (P <.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 decrease of left ventricular mass after weight loss surgery is regulated by neurohumoral factors, and may contribute to improved long-term survival.

The metabolic syndrome and the heart--a considered opinion.

ZusammenfassungStörungen des Allgemeinstoffwechsels, wie sie sich im Metabolic Syndrome manifestieren, führen zu einer Reihe von kardiovaskulären Komplikationen. Wir berichten hier über die Konsequenzen der Insulinresistenz für den Herzmuskel. Die Überlastung des Myokards mit Fettsäuren und Glukose führt zu weitreichenden funktionellen und morphologischen Veränderungen, die Virchow schon vor 150 Jahren als „fettige Atrophie“ beschrieben hat.SummaryThe metabolic syndrome (MS) is a multifactorial, heterogeneous group of risk factors for the development of cardiovascular disease. Here we review the evidence in support of the hypothesis that metabolic dysregulation of the body as a whole leads to contractile dysfunction of the heart due to an imbalance of substrate uptake (increased) and substrate oxidation (decreased). The consequences of this imbalance were already recognized 150 years ago by Virchow when he described “fatty atrophy” of the heart as a “true metamorphosis of the heart muscle cell.”

The metabolic syndrome and the heart

ZusammenfassungStörungen des Allgemeinstoffwechsels, wie sie sich im Metabolic Syndrome manifestieren, führen zu einer Reihe von kardiovaskulären Komplikationen. Wir berichten hier über die Konsequenzen der Insulinresistenz für den Herzmuskel. Die Überlastung des Myokards mit Fettsäuren und Glukose führt zu weitreichenden funktionellen und morphologischen Veränderungen, die Virchow schon vor 150 Jahren als „fettige Atrophie“ beschrieben hat.SummaryThe metabolic syndrome (MS) is a multifactorial, heterogeneous group of risk factors for the development of cardiovascular disease. Here we review the evidence in support of the hypothesis that metabolic dysregulation of the body as a whole leads to contractile dysfunction of the heart due to an imbalance of substrate uptake (increased) and substrate oxidation (decreased). The consequences of this imbalance were already recognized 150 years ago by Virchow when he described “fatty atrophy” of the heart as a “true metamorphosis of the heart muscle cell.”

Early Benefits From Weight-Loss Surgery

The carefully conducted study by the Oxford group ([1][1]) reports beneficial effects of weight loss after 2 nonpharmacological interventions, diet or bariatric surgery. In case of the latter, we have made similar observations except at a much earlier time point ([2][2]). Three months after

The metabolic syndrome and the heart—@@@Insulinresistenz des Herzens: a considered opinion

ZusammenfassungStörungen des Allgemeinstoffwechsels, wie sie sich im Metabolic Syndrome manifestieren, führen zu einer Reihe von kardiovaskulären Komplikationen. Wir berichten hier über die Konsequenzen der Insulinresistenz für den Herzmuskel. Die Überlastung des Myokards mit Fettsäuren und Glukose führt zu weitreichenden funktionellen und morphologischen Veränderungen, die Virchow schon vor 150 Jahren als „fettige Atrophie“ beschrieben hat.SummaryThe metabolic syndrome (MS) is a multifactorial, heterogeneous group of risk factors for the development of cardiovascular disease. Here we review the evidence in support of the hypothesis that metabolic dysregulation of the body as a whole leads to contractile dysfunction of the heart due to an imbalance of substrate uptake (increased) and substrate oxidation (decreased). The consequences of this imbalance were already recognized 150 years ago by Virchow when he described “fatty atrophy” of the heart as a “true metamorphosis of the heart muscle cell.”