In morbidly obese patients undergoing bariatric surgery, the decrease in left ventricular mass at 1 year correlated only with the decrease in leptin levels (P<0.01).
Observational (n=61)
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Does weight loss induced by laparoscopic adjustable gastric banding reduce left ventricular mass and leptin levels in morbidly obese patients?
Weight loss induced by bariatric surgery reduces left ventricular mass in morbidly obese patients, and this reduction correlates with decreases in leptin levels, suggesting leptin may mediate human left ventricular hypertrophy.
valor p: p=<0.01
CONTEXT: Obesity is frequently associated with left ventricular hypertrophy, even when uncomplicated by hypertension or diabetes mellitus. Left ventricular hypertrophy is an important risk factor for congestive heart failure. OBJECTIVE: The objective of this study was to evaluate the relationship between leptin and left ventricular mass in uncomplicated, morbid (grade 3) obesity and the existence of leptin receptors and intracellular signaling proteins in the human heart. DESIGN: Left ventricular mass (LVM) was calculated through electrocardiogram reading in normotensive grade III obese patients (World Health Organization classification) undergoing bariatric surgery laparoscopic adjustable gastric banding (LAGB) at baseline and 1 yr later. The control group was composed of healthy lean normotensive subjects. Leptin receptors were detected by PCR and immunocytochemistry in human heart biopsies. SETTING: This study was performed at university hospitals. PATIENTS: Thirty-one grade 3 obese patients and 30 healthy nonobese normotensive, age- and sex-matched control subjects were studied. INTERVENTION: Obese subjects underwent LAGB to induce weight loss and were evaluated at baseline and after 1 yr. RESULTS: LVM, plasma leptin, glucose, insulin levels, and homeostasis model assessment index were higher in obese than in lean controls (P < 0.01); at univariate regression analysis, LVM correlated with body mass index, leptin, and homeostasis model assessment index; at multiple regression analysis, LVM only correlated with leptin levels (P = 0.001). Obese subjects were reevaluated 1 yr after LAGB, when their body mass index changed from 46.2 +/- 1.24 to 36.6 +/- 1.05 kg/m(2) (P < 0.01); the decrease in LVM correlated only with the decrease in leptin levels (P < 0.01). We demonstrated that long and short isoforms of the leptin receptor and intracellular proteins mediating leptin signaling were expressed in human heart by RT-PCR, immunocytochemistry, or both methods. CONCLUSIONS: These data suggest that leptin could contribute to the left ventricular hypertrophy in humans.
Perego et al. (Fri,) conducted a observational in Morbid (grade III) obesity (n=61). Laparoscopic adjustable gastric banding (LAGB) vs. Healthy lean normotensive subjects was evaluated on Correlation between decrease in left ventricular mass and decrease in leptin levels (p=<0.01). In morbidly obese patients undergoing bariatric surgery, the decrease in left ventricular mass at 1 year correlated only with the decrease in leptin levels (P<0.01).