Abstract

BackgroundObesity is characterized by low grade inflammation and an altered secretion of inflammatory cytokines from the adipose tissue. Weight loss has shown to reduce inflammation; however, changes in cytokine profiles during massive weight loss are not well described. The present study explored the hypothesis that Roux-en-Y gastric bypass (RYGB) reduces circulating levels of pro-inflammatory cytokines, while increasing anti-inflammatory cytokines in obese subjects with type 2 diabetes (T2D) and in obese normal glucose tolerant (NGT) subjects.MethodsThirteen obese subjects with T2D [weight; 129 ± 14 kg, glycated hemoglobin (HbA1c); 7.0 ± 0.9%, body mass index (BMI); 43.2 ± 5.3 kg/m2, mean ± SD] and twelve matched obese NGT subjects [weight; 127 ± 15 kg, HbA1c; 5.5 ± 0.4%, BMI; 41.5 ± 4.8 kg/m2, mean ± SD] were examined before, one week, three months, and one year after surgery. Interleukin (IL)-6, leptin, adiponectin, IL-8, transforming growth factor beta (TGF-β), and the incretin hormone glucagon-like peptide-1 (GLP-1) were measured in the fasting state and during a liquid meal. Insulin resistance was evaluated by HOMA-IR.ResultsWeight loss did not differ between the two groups. Before surgery, HbA1c was higher and HOMA-IR lower in T2D patients, however, converged to the values of NGT subjects one year after surgery. Circulating cytokine concentrations did not differ between the two groups at any time point. One week after surgery, circulating IL-6 and IL-8 were increased, while adiponectin and leptin were reduced compared with pre-surgical concentrations. Three months after surgery, IL-8 was increased, leptin was reduced, and no change was observed for IL-6, TGF-β, and adiponectin. One year after surgery, concentrations of IL-6, TGF-β, and leptin were significantly reduced compared to before surgery, while adiponectin was significantly increased.ConclusionsOne year after RYGB, fasting concentrations of IL-6 and leptin were reduced, while no changes were observed in IL-8. TGF-β was decreased and adiponectin increased in both T2D and NGT obese subjects. This study is the first to examine IL-8 and TGF-β in obese subject after RYGB. Resolution of inflammation could offer a potential explanation for the health improvement associated with major weight loss after bariatric surgery.Trial registrationhttp://www.clinicaltrials.gov (NCT01579981).

Highlights

  • Obesity is characterized by low grade inflammation and an altered secretion of inflammatory cytokines from the adipose tissue

  • Obesity is associated with chronic low-grade inflammation, which is thought to be involved in the development of obesity-related co-morbidities, such as insulin resistance, type 2 diabetes (T2D) and cardiovascular diseases (CVD) [1]

  • The adipose tissue is considered the prime organ for mediating obesity-induced inflammation by secreting high levels of pro-inflammatory molecules including interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) secreted by immune cells residing in the stromal vascular fraction

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Summary

Introduction

Obesity is characterized by low grade inflammation and an altered secretion of inflammatory cytokines from the adipose tissue. The present study explored the hypothesis that Roux-en-Y gastric bypass (RYGB) reduces circulating levels of pro-inflammatory cytokines, while increasing anti-inflammatory cytokines in obese subjects with type 2 diabetes (T2D) and in obese normal glucose tolerant (NGT) subjects. The adipose tissue is considered the prime organ for mediating obesity-induced inflammation by secreting high levels of pro-inflammatory molecules including interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α) secreted by immune cells residing in the stromal vascular fraction. This is thought to contribute to the development of insulin resistance and deterioration of glucose homeostasis [2,3,4]. Transforming growth factor beta (TGF-β), an immunoregulatory cytokine, has been found to be associated with obesity and T2D [22,23,24,25]

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