OBJECTIVEImprovements in diabetes after Roux-en-Y gastric bypass (RYGB) often occur days after surgery. Surgically induced hormonal changes and the restrictive postoperative diet are proposed mechanisms. We evaluated the contribution of caloric restriction versus surgically induced changes to glucose homeostasis in the immediate postoperative period.RESEARCH DESIGN AND METHODSPatients with type 2 diabetes planning to undergo RYGB participated in a prospective two-period study (each period involved a 10-day inpatient stay, and periods were separated by a minimum of 6 weeks of wash-out) in which patients served as their own controls. The presurgery period consisted of diet alone. The postsurgery period was matched in all aspects (daily matched diet) and included RYGB surgery. Glucose measurements were performed every 4 h throughout the study. A mixed-meal challenge test was performed before and after each period.RESULTSTen patients completed the study and had the following characteristics: age, 53.2 years (95% CI, 48.0–58.4); BMI, 51.2 kg/m2 (46.1–56.4); diabetes duration, 7.4 years (4.8–10.0); and HbA1c, 8.52% (7.08–9.96). Patients lost 7.3 kg (8.1–6.5) during the presurgery period versus 4.0 kg (6.2–1.7) during the postsurgery period (P = 0.01 between periods). Daily glycemia in the presurgery period was significantly lower (1,293.58 mg/dL·day [1,096.83–1,490.33) vs. 1,478.80 mg/dL·day [1,277.47–1,680.13]) compared with the postsurgery period (P = 0.02 between periods). The improvements in the fasting and maximum poststimulation glucose and 6-h glucose area under the curve (primary outcome) were similar during both periods.CONCLUSIONSGlucose homeostasis improved in response to a reduced caloric diet, with a greater effect observed in the absence of surgery as compared with after RYGB. These findings suggest that reduced calorie ingestion can explain the marked improvement in diabetes control observed after RYGB.

Purpose Roux-en-Y gastric bypass surgery is associated with an increased risk of nephrolithiasis but obesity itself is a known risk factor for kidney stones. To assess the mechanism(s) predisposing to nephrolithiasis after Roux-en-Y gastric bypass we compared urinary tract stone risk profiles in patients who underwent the procedure and normal obese individuals. Materials and Methods In this cross-sectional study urine and serum biochemistry was evaluated in 19 nonstone forming patients after Roux-en-Y gastric bypass and in 19 gender, age and body mass index matched obese controls without a history of nephrolithiasis. Results Compared with obese controls surgical patients had significantly higher mean ± SD urine oxalate (45 ± 21 vs 30 ± 11 mg daily, p = 0.01) and lower urine citrate (358 ± 357 vs 767 ± 307 mg daily, p <0.01). The prevalence of hyperoxaluria (47% vs 10.5%, p = 0.02) and hypocitraturia (63% vs 5%, p <0.01) was significantly higher in surgical patients, who also had significantly lower urine calcium than obese controls (115 ± 93 vs 196 ± 123 mg daily, p = 0.03). The calcium oxalate urine relative supersaturation ratio was not significantly different between the 2 groups. Conclusions Almost half of patients with Roux-en-Y gastric bypass without a history of nephrolithiasis showed hyperoxaluria or hypocitraturia. This prevalence was significantly higher than in body mass index matched controls. These risk factors were negated by lower urine calcium excretion in patients with Roux-en-Y gastric bypass.

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Both cyclooxygenase products, such as prostaglandin (PG) E2, and lipoxygenase products, such as leukotriene (LT) B4, are increased in colitis and have potent proinflammatory actions. We studied effects of specific inhibitors of cyclooxygenase and 5-lipoxygenase on the healing of acetic acid colitis in rats. Acetic acid colitis was induced 24 hr before enzyme inhibition began. Four days after induction of colitis, the area of gross colonic mucosal damage was determined by image analysis. Eicosanoid content in the intestinal lumen was quantitated by radioimmunoassay following chromatographic purification. Under these conditions, indomethacin significantly retarded the healing of colonic lesions and inhibited PGE2 by > 90% compared to placebo-treated colitis rats. AA861 had no effect on the healing of lesions, although > 75% inhibition of leukotriene synthesis was demonstrated. These results suggest that inhibition of endogenous colonic prostaglandins can impair healing mechanisms in acute colitis even after inflammation has developed. In contrast, inhibition of leukotriene synthesis did not affect healing.