| Objective:Current studies have shown that white adipose tissue inflammation is one of the causative factors of type 2 diabetes.However,changes in white adipose tissue inflammation after weight loss metabolic surgery remain unclear,and changes in diabetes-related hormones during postoperative circulation may be associated with changes in inflammation.The purpose of this study was to determine the changes in the subcutaneous white adipose tissue and visceral white adipose tissue inflammatory state after metabolic surgery,the changes in diabetes-related hormones in the circulation,and to study the effects of related hormones on the inflammatory state of macrophages.Material and Methods:A retrospective analysis of patients with type 2 diabetes who underwent duodenal jejunal bypass with sleeve gastrectomy(DJB-SG)was performed.The changes of body weight,body mass index,fasting blood glucose,glycated hemoglobin,homeostatic model assessment of insulin resistence,and C-peptide were analyzed 3 days pre-and 12 months post-surgery.Analysis of insulin,gastric inhibitory polypeptide,leptin,plasminogen activator inhibitor-1,resistin,glucagon-like peptide-1,visfatin,glucagon and ghrelin at 3 days pre-surgery and 3 and 12 months post-surgery.Then,DJB-SG surgery was performed on Goto-kakisaki rats.Body weight,fasting blood glucose,homeostatic model assessment of insulin resistence,and changes in ghrelin were compared between the surgical group and the sham operation group every 2 weeks,Oral Glucose Tolerance Test were compared pre-and 8 weeks post-surgery.8 weeks after surgery,the rats were sacrificed,visceral and subcutaneous white adipose tissue was collected from greater omentum and groin,respectively.The changes of tumor necrosis factor-?(TNF-?)and Cluster of differentiation 68(CD68)expression in visceral white adipose tissue and subcutaneous white adipose tissue were analyzed using Immunohistochemistry Paraffin Staining.The changes of cell surface antigens CD 11c,CD206 and secretory factors TNF-a and interleukin-10(IL-10)were detected after treating RAW264.7 cells with ghrelin and its antagonist.Results:Postoperative patients'body mass index,fasting blood glucose,hemoglobin,homeostatic model assessment of insulin resistence were significantly reduced(P<0.05),C-peptide did not change significantly;circulating ghrelin,leptin,plasminogen activator inhibitor-1 and insulin levels were significantly reduced at 1 year after surgery(P<0.05),gastric inhibitory polypeptide was significantly reduced at 3 days pre-and 12 months post-surgery.Goto-kakisaki rats showed significant reduction in body weight,fasting blood glucose,and homeostatic model assessment of insulin resistence(P<0.05),and elevation of insulin(P<0.05),from 4 weeks after surgery,oral glucose tolerance test showed significant reduction(P<0.05)at 8 weeks after surgery;the level of ghrelin was also significantly reduced in the circulation from 4 weeks after surgery(P<0.05).In addition,the expression of TNF-? and CD68 in rat visceral white adipose tissue was significantly decreased(P<0.05),and there was no significant change in white adipose tissue.In vitro,ghrelin significantly down-regulated the secretion of TNF-a in RAW264.7(P<0.05),which was blocked by its antagonist.There were no significant changes in CD11c,CD206,and IL-10.Conclusion:Both retrospective analysis and animal models confirmed that DJB-SG surgery can significantly reduce body weight and blood sugar.In vivo,DJB-SG surgery significantly reduced circulating ghrelin,leptin,plasminogen activator inhibitor-1 and insulin levels in patients.Circulating ghrelin and inflammatory status of visceral white adipose tissue in rats were also decreased.In vitro,experiments showed that high doses of ghrelin acted on its receptors,significantly reducing the secretion of TNF-a by RAW264.7,suggesting that the reduction of ghrelin level after surgery can not directly affect macrophages and reduce the secretion of TNF-a,it is not one of the direct causes of metabolic surgery to improve the inflammatory state of adipose tissue. |
PDF Full Text Request