Immune cell-mediated inflammation and the early improvements in glucose metabolism after gastric banding surgery
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The contribution of immune cells to the inflammasome that characterises type 2 diabetes mellitus and obesity is under intense research scrutiny. We hypothesised that early changes in glucose metabolism following gastric banding surgery may relate to systemic inflammation, particularly cell-mediated immunity.
Obese participants (BMI 43.4 ± 4.9 kg/m2, n = 15) with diabetes or impaired glucose tolerance (IGT) underwent laparoscopic adjustable gastric banding surgery. Measurements taken before, and at 2 and 12 weeks after surgery included: fasting glucose, glucose levels 2 h after a 75 g oral load, glucose incremental AUC, oral glucose insulin sensitivity index (OGIS), circulating immune cell numbers and activation, and adipokine levels. Subcutaneous and visceral adipose tissue were collected at surgery, and macrophage number and activation measured.
There were significant reductions in fasting and 2 h glucose, as well as improved OGIS at 2 and 12 weeks. At 12 weeks, 80% of the diabetic participants reverted to normal glucose tolerance or IGT, and all IGT participants had normalised glucose tolerance. The 12 week fall in fasting glucose was significantly related to baseline lymphocyte and T lymphocyte numbers, and to granulocyte activation, but also to the magnitude of the 12 week reduction in lymphocyte and T lymphocyte numbers and TNF-α levels. In a model that explained 75% of the variance in the change in fasting glucose, the 12 week change in T lymphocytes was independently associated with the 12 week fall in fasting glucose.
Rapid improvements in glucose metabolism after gastric banding surgery are related to reductions in circulating pro-inflammatory immune cells, specifically T lymphocytes. The contribution of immune cell-mediated inflammation to glucose homeostasis in type 2 diabetes and its improvement after bariatric surgery require further investigation.
KeywordsAdipokine Bariatric surgery Diabetes Glucose Immune cells Inflammation Insulin resistance Lymphocyte Obesity Tumour necrosis factor-α Weight loss
Impaired glucose tolerance
Oral glucose insulin sensitivity index
Subcutaneous adipose tissue
Visceral adipose tissue
Our thanks go to the staff of the Garvan Clinical Research Facility (particularly Angela Peris and Jennifer Hansen) and to all the volunteers who participated in the study.
This study was part-funded by a competitive, peer reviewed research grant from The Ladies Committee–Sister Bernice Award of the St Vincent’s Clinic Foundation and by philanthropic grants from the GP Harris Foundation and an anonymous donor. All researchers were independent of the funding bodies, which did not play any role in study design, data collection and analysis, and submission for publication.
Duality of interest
The authors declare that there is no duality of interest associated with this manuscript.
All authors contributed to study conception and design, data acquisition or analysis and interpretation, as well as to the drafting or critical revising of the manuscript for important intellectual content. All authors gave final approval of the version to be published.
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