The Impact of Bariatric Surgery on Nitrogen Balance at Six months Post-surgery.

PURPOSE: Obesity, defined as abnormal or excessive fat accumulation that presents a risk to health, rose from 8.6 to 10.5% in Singapore's residents. Bariatric surgery, the primary treatment for severe obesity, induces fat and muscle loss. Adequate protein intake is vital for preventing muscle loss. This study examines nitrogen balance in individuals with obesity pre- and post-surgery. MATERIALS AND METHODS: Sixteen participants with severe obesity (BMI ≥ 32.5 kg/m2) undergoing bariatric surgery (14 sleeve gastrectomy, 2 Roux-en-Y gastric bypass) and 20 normal-weight controls (BMI < 25 kg/m2) were recruited. Nitrogen balance, calculated from dietary protein intake and urine nitrogen excretion, was assessed. Participants with obesity were re-evaluated 6 months post-surgery. Data were analyzed using parametric methods. RESULTS: At baseline, controls had a BMI of 20.8 ± 2.1 kg/m2; those with obesity had 40.9 ± 7.3. Daily calorie and protein intake for participants with obesity were not statistically significantly different from controls (calorie intake at 1467 ± 430 vs. 1462 ± 391 kcal, p = 0.9701, protein intake 74.2 ± 28.7 vs. 64.6 ± 18.3 g, p = 0.2289). Post-surgery, BMI, fat-free mass, fat mass, total energy intake, carbohydrate, and protein intake decreased significantly (p < 0.01). Protein oxidation and urine nitrogen excretion did not change after bariatric surgery. However, nitrogen balance significantly reduced from 2.62 ± 5.07 to - 1.69 ± 5.07 g/day (p = 0.025). CONCLUSION: Dietary protein intake is inadequate in individuals with obesity at 6 months post-bariatric surgery and contributes to a state of negative nitrogen balance.

De Novo Glycine Synthesis Is Reduced in Adults With Morbid Obesity and Increases Following Bariatric Surgery.

Background: Glycine is a dietary non-essential amino acid that is low in obesity and increases following bariatric surgery. However, the exact mechanism responsible remains unclear and it is unknown whether hypoglycinemia is a cause or consequence of insulin resistance. Objective: Using multiple isotopically labeled tracers, we aimed to determine the underlying kinetic changes responsible for hypoglycinemia in obesity by: 1) Comparing glycine kinetics between participants with morbid obesity (BMI ≥ 32.5 kg/m2) to those with healthy weight (BMI < 25 kg/m2), and 2) Comparing glycine kinetic changes in participants with morbid obesity after bariatric surgery. Methods: [1,2-13C2] glycine, [2,3,3-2H3] serine, and [2H5] phenylalanine were infused to compare the glycine kinetic parameters between 21 participants with morbid obesity and 21 controls with healthy weight. Participants with morbid obesity then underwent bariatric surgery and 17 were re-studied 6 months later. Data were analyzed by non-parametric methods and presented as median (interquartile range). Results: Compared to controls, participants with morbid obesity had significantly lower plasma glycine concentrations at 163 (153-171) vs. 201 (172-227) µmol/L and significantly reduced de novo glycine synthesis rate at 86.2 (64.5-111) vs.124 (103-159) µmol·kg LBM-1·h1, p < 0.001. Following surgery, body weight and insulin resistance decreased and this was accompanied by significant increases in plasma glycine concentration to 210 (191-243) µmol/L as well as the de novo glycine synthesis rate to 127 (98.3-133) µmol·kg LBM-1·h-1, p < 0.001 vs. baseline. Conclusion: Hypoglycinemia in participants with morbid obesity was associated with impaired de novo glycine synthesis. The increase in plasma glycine concentration and de novo glycine synthesis plus the marked improvement in insulin resistance after bariatric surgery suggest that hypoglycinemia may be secondary to impaired glycine synthesis because of obesity-induced insulin resistance. Clinical Trial Registration: [https://tinyurl.com/6wfj7yss], identifier [NCT04660513].