Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8841318 | Neuroscience Letters | 2018 | 24 Pages |
Abstract
Patients with spinal cord injury (SCI) have an increased risk for developing type 2 diabetes. It is unknown whether the pancreatic-islet microvascular vasomotion is involved. We used female C57BL/6 mice and a 100-kilodyne T10 Infinite Horizons contusion SCI (or T10 laminectomy) to detect blood glucose and pancreatic-islet microvascular vasomotion. Blood glucose obtained from tail vein was detected using one Touch UltraEasy glucometer. Glucose tolerance test was performed by d-glucose administration intraperitoneally. Functional status of pancreatic-islet microvascular vasomotion was determined by laser Doppler monitoring. Expressions of insulin and glucagon were determined by immunohistochemistry. Expression of VEGF-A was determined by immunohistochemistry and Western blotting. Our result demonstrated that blood glucose was significantly increased at 4âh postinjury compared to that in sham group, with continuous higher blood glucose until 4 days postinjury (pâ<â0.05). SCI mice at day 7 and day 14 had significantly impaired glucose tolerance following glucose administration (pâ<â0.01). Average blood perfusion, amplitude, frequency, and relative velocity of vasomotion were significantly lower at 6âh postinjury than those in the sham group (pâ<â0.05), which were gradually upregulated over time. The expression of insulin was decreased, while the expression of glucagon was increased at 6âh postinjury. Similarly, the expression of VEGF-A was significantly decreased at 6âh postinjury, compared to that in sham group (pâ<â0.05), with slight increases by 14 days postinjury. Our study suggests that the functional status of pancreatic-islet microvascular vasomotion is impaired after injury, which may have implications for developing effective therapeutic interventions for SCI.
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Authors
Yingli Jing, Mingming Liu, Fan Bai, Di Li, Degang Yang,