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Background: Obesity is a debilitating disease and is becoming more prevalent in the United States. Roux-en Y gastric bypass surgery (RYGB) has been successful in inducing long-term weight loss in the severely obese. Research in mice suggests that leptin, a hormone produced by the gut and adipose tissue, is associated with satiety, appetite and energy expenditure. Methods: Twenty-one patients will be assessed at baseline (before surgery), at 1 mo., and at 6 mo. following RYGB. Changes in plasma leptin and leptin receptor (OB-R) concentrations will be determined by enzyme-linked immunoassay (ELISA). Changes in the clinical outcomes resting energy expenditure (REE) and appetite scores, will be measured by indirect calorimetry and visual analog scales, respectively. Student t-tests were used to determine significant changes from baseline, p<0.05. Results: Following RYGB, leptin concentrations decreased from 139.35 at baseline to 82.74 and 47.85 ng/ml at 1 mo. and 6 mo. respectively. Baseline scores in appetite (4.81) decreased to 2.19, at 1 mo. and to 3.33 at 6 mo. There was an increase in OB-R concentrations from baseline to 1 mo. but values were decreased to basal levels at 6 mo. (28.02, 31.90, 30.53 ng/ml, respectively). REE was no different from baseline at 1 mo. but was decreased at 6 mo. post surgery (2129,2056, and 1885 kcal/day, respectively). Conclusions: Our findings suggest that acute decreases in plasma leptin and increases in OB-R observed at 1 mo. and 6 mo. post surgery did not correspond with the changes in appetite (which decreased and then increased) and changes in REE (which only decreased at 6 mo. post surgery). This shows reduced leptin concentrations do not adversely affect REE and appetite following RYGB.
Obesity can cause high blood pressure, cardiovascular disease, type II diabetes, and high cholesterol. Caloric restriction via dieting reduces energy expenditure and increases appetite which may lead to weight regain. Roux-en Y gastric bypass (RYGB) is the most effective form of bariatric surgery and induces dramatic weight loss. Leptin and its receptors (OB-R) function in promoting satiety and increasing energy expenditure. Several studies have shown that following bariatric surgery leptin levels decrease. Our objective was to determine whether a decrease in leptin and leptin receptor relates to changes in energy expenditure and appetite in severely obese women following RYGB surgery.
Plasma concentrations of leptin and OB-R concentrations were determined using enzyme-linked immunoassay (ELISA, R&D Systems, Minneapolis, USA). Energy expenditure will be measured following an overnight fast using indirect calorimetry. Body fat composition was determined by air displacement plethysmography. Appetite was assessed by asking patients to fill out a visual-analogue scale before consuming breakfast.
Leptin concentrations decreased significantly from an average of 139.4±10.05 (baseline) to 82.7±9.00 ng/ml (1 months). Leptin concentration continued to decrease to 47.9±4.64 ng/ml at 6 months. From baseline to 1 mo., appetite significantly decreased from 4.8 ±0.52 to 2.2¬±0.42 and was still decreased compared to baseline at 6 months (3.3¬±0.49). There was a significant increase in leptin receptor concentrations (OB-R) from baseline 28.0±1.74 to 31.9±1.74 ng/ml at 1 month (n=21) but levels were restored to baseline (30.5±1.55 ng/ml) at 6 months. Total fat decreased from 72.4±2.46 (baseline) to 63.6±1.66 kg (1month) and continued to significantly decrease to 42.3±1.77kg after 6 months (n=20). Lean mass was also decreased significantly from baseline (54.3±1.41) to 1 month (51.1±0.92) then further at 6 months (50.4± 1.00 kg). Resting energy expenditure decreased significantly from baseline (2129.0±86.63) to 6 months (1884.7¬±46.92 kcal/day). At 1 month changes from baseline were insignificant (2056.1¬±69.42kcal/day).
• We chronicled the changes in leptin, appetite, and REE over 6 months following RYGB.
• In contrast to animal data, in humans a decrease in leptin is not correlated to a decrease in REE following weight loss.
• OB-R levels were up-regulated in response to a decrease in leptin at 1 mo. post surgery.
• In spite of the reduction in satiety hormone activity and lowered REE over 6 mo., weight loss continued in patients who had RYGB.
• This suggests other mechanisms contribute to weight loss and appetite suppression in these patients.
I would like to acknowledge Brittni Pitts, Dr. Nana Gletsu, Dr. Edward Lin, Dr. Thomas R. Ziegler, Dr. Ih-Ping Huang, Dr. C. Daniel Smith, and Dr. Li Gu. This material is based upon work supported by the Howard Hughes Medical Institute under Grant No.52003727, by the National Science Foundation Award # 0450303 (Sub-award # I-66-606-63 to Emory University), by the NIH/NIDDK Award #1 R03 DK067167-01A1, and the NIH/NCRR General Research Center Grant #M01 RR00039.
My research consisted of examining morbidly obese patients before and after a Roux-en Y gastric bypass surgery, which is a surgery where the stomach is stapled off to form a pouch which serves as the new stomach. The new stomach is the width of a thumb and the volume of a tennis ball. Also the small intestine is reconstructed so that the digestive tract is shortened. I focused on a hormone called leptin that is produced in fat tissue and the gut that signals to the brain that you are "full." My research consisted of measuring and studying the effects of the surgery on the leptin and its receptor, energy expenditure (metabolism), and appetite.
RT-PCR, GLucose tolerance test and performing ELISA kits
nutrition, Roux-en Y gastric bypass, obesity, satiety hormones, and metabolism
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