Duodenal-jejunal bypass surgery on type 2 diabetic rats reduces the expression of matrix metalloproteinase-9 and tissue inhibitor of matrix metalloproteinase-1 in the thoracic aorta

Author:

Wubulikasimu Maimaitiyusufu,Haifeng Han,Zhibo Yan,Xiang Zhang,Shaozhuang Liu,Guangyong Zhang,Aimaiti Kasimu,Sanyuan Hu

Abstract

Background Bariatric surgery offers a productive resolution of type 2 diabetes mellitus (T2DM). The development of T2DM vasculopathy is due to chronic inflammation, which increases matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) expression. This study sought to examine MMP-9 and TIMP-1 expression in the thoracic aorta after duodenal-jejunal bypass (DJB) surgery on a T2DM rat model induced by a high-fat diet and low dose streptozotocin (STZ). Methods Twenty-one T2DM Wistar rats induced by high-fat diet and low dose STZ were randomly divided into DJB and sham duodenal-jejunal bypass (S-DJB) groups. Ten Wistar rats were fed a normal diet as a control. Recovery of gastrointestinal function post-operation and resumption of a normal diet completed the experiment. Body weight, blood glucose, blood lipid levels, and MMP-9 and TIMP-1 expression levels in aortic endothelial cells were measured throughout. Results DJB rats showed significant weight loss 2 weeks post-operation compared with S-DJB rats. After surgery, DJB rats showed significant improvement and steady glycemic control with improved insulin sensitivity and glucose tolerance. They also exhibited improved lipid metabolism with a decrease in fasting free fatty acids (FFAs) and triglycerides (all P <0.05). Immunohistochemistry showed decreased MMP-9 and TIMP-1 expression 12 weeks after surgery (P < 0.01). Conclusions DJB surgery on an induced T2DM rat model improves blood glucose levels and lipids, following a high-fat diet and low dose STZ treatment. In addition, DJB decreased MMP-9 and TIMP-1 expression in vascular endothelial cells, which may play an important role in delaying the development of T2DM vascular disease.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

General Medicine

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