Abstract
Background : Immunological and inflammatory mechanisms play a key role in the development and progression of type 2 diabetes mellitus. Aim : To raise the hypothesis that alterations in immunological parameters occur after duodenojejunal bypass surgery combined with ileal interposition without gastrectomy, and influences the insulin metabolism of betacells.Methods : Seventeen patients with type 2 diabetes mellitus under clinical management were submitted to surgery and blood samples were collected before and six months after surgery for evaluation of the serum profile of proinflammatory (IFN-γ, TNF-α, IL-17A) and anti-inflammatory cytokines (IL-4, IL-10). In addition, anthropometric measures, glucose levels and insulin use were evaluated in each patient. Results : No changes in the expression pattern of proinflammatory cytokines were observed before and after surgery. In contrast, there was a significant decrease in IL-10 expression, which coincided with a reduction in the daily insulin dose, glycemic index, and BMI of the patients. Early presentation of food to the ileum may have induced the production of incretins such as GLP-1 and PYY which, together with glycemic control, contributed to weight loss, diabetes remission and the consequent good surgical prognosis of these patients. In addition, the control of metabolic syndrome was responsible for the reduction of IL-10 expression in these patients. Conclusion : These findings suggest the presence of low-grade inflammation in these patients during the postoperative period, certainly as a result of adequate glycemic control and absence of obesity, contributing to a good outcome of surgery.
Highlights
Diabetes mellitus is a chronic disease characterized by relative or absolute insulin deficiency and consequent glucose intolerance
Immunological and inflammatory mechanisms play a key role in the development and progression of type 2 diabetes mellitus[16]
Herder et al.[11] showed that elevated TGF-β1 concentrations indicate an increased risk of progression to type 2 diabetes and that subclinical inflammation leads to insulin resistance and pancreatic beta-cell dysfunction
Summary
Diabetes mellitus is a chronic disease characterized by relative or absolute insulin deficiency and consequent glucose intolerance. Herder et al.[11] showed that elevated TGF-β1 concentrations indicate an increased risk of progression to type 2 diabetes and that subclinical inflammation leads to insulin resistance and pancreatic beta-cell dysfunction. According to Kopp et al.[12], elevated levels of C-reactive protein and IL-6 indicate chronic subclinical inflammation and are associated with metabolic syndrome and cardiovascular diseases. Taken together, these results suggest a bidirectional relationship between insulin resistance and inflammation, i.e., any chronic inflammatory process induces insulin resistance which, in turn, enhances the inflammatory process[6]. A variety of treatment options exist for the management of insulin resistance, including a multidisciplinary clinical approach designed to promote weight loss, pharmacological
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