RESUMEN
Metabolic surgery is superior to lifestyle intervention in reducing weight and lowering glycemia and recently suggested as treatment for type 2 diabetes mellitus. Especially Roux-en-Y gastric bypass (RYGB) has been focus for much research, but still the mechanisms of action are only partly elucidated. We suggest that several mechanisms might be mediated by sphingolipids like sphingomyelin. We measured serum sphingomyelin before and up to 2 years after RYGB surgery in 220 patients, divided before surgery in one non-diabetic subgroup and two diabetic subgroups, one of which contained patients obtaining remission of type 2 diabetes after RYGB, while patients in the other still had diabetes after RYGB. Pre- and postoperative sphingomyelin levels were compared within and between groups. Sphingomyelin levels were lower in diabetic patients than in non-diabetic patients before surgery. Following RYGB, mean sphingomyelin concentration fell significantly in the non-diabetic subgroup and the preoperative difference between patients with and without diabetes disappeared. Changes in diabetic subgroups were not significant. Relative to bodyweight, an increase in sphingomyelin was seen in all subgroups, irrespective of diabetes status. We conclude that RYGB has a strong influence on sphingomyelin metabolism, as seen reflected in changed serum levels. Most significantly, no differences between the two diabetic subgroups were detected after surgery, which might suggest that patients in both groups still are in a "diabetic state" using the non-diabetic subgroup as a reference.
RESUMEN
BACKGROUND: In obesity, which is a major contributor to insulin resistance and diabetes, the circulating level of S100A8/A9 (calprotectin) is elevated and declines after Roux-en-Y gastric bypass surgery (RYGB). However, studies on S100A8/A9 and the pathophysiological mechanisms in insulin resistance and diabetes are few and contradictory. METHODS: We studied 48 subjects who underwent RYGB, comprising a non-diabetic control group and two diabetic groups in whom diabetes either regressed or persisted, 6-12 months post-surgically. S100A8/A9, interleukin 6 (IL-6) as well as other inflammatory and diabetes-related markers were measured pre- and post-surgically. RESULTS: Significant and similar decreases of BMI were found in all groups. S100A8/A9 and IL-6 decreased significantly in the group with diabetes remission and in the control group, but not in the group with persistent diabetes. The relative changes in S100A8/A9 and IL-6 correlated significantly (r = 0.905, p = 0.005) only in the group with persistent diabetes. In contrast, leukocyte count and C-reactive protein correlated significantly to S100A8/A9 only in the control group. CONCLUSION: Our study is suggestive of S100A8/A9 and IL-6 being related to a persistent diabetes status post-surgically and of different pathophysiological mechanisms being involved in the post-surgical changes in the three groups, despite similar decreases in BMI.