The lifetime risk for Type-2 diabetes mellitus remains higher in people with spinal cord injuries than in the able-bodied population. However, the mechanisms driving this disparity remain poorly understood. The goal of the current study was to evaluate the impact of a palatable high-fat diet (HFD) on glycemic regulation using a rodent model of moderate thoracic contusion. Animals were placed on either Chow or HFD and tolerance to glucose, insulin, and ENSURE mixed meal were investigated. Important targets in the gut-brain axis were investigated. HFD consumption equally induced weight gain in SCI and naïve rats over CH rats. Elevated blood glucose was observed during intraperitoneal GTT in HFD-fed rats over CH-fed rats. ITT was unremarkable amongst the three groups. Gavage of ENSURE resulted in high GLP-1 release from SCI rats over naïve controls. An elevation in terminal total GLP-1 was measured, with a marked reduction in circulating dipeptidyl peptidase 4 (DPP4), the GLP-1 cleaving enzyme, in SCI rats, compared to naïve. Increased glucagon mRNA in the pancreas and reduced immunoreactive glucagon-positive staining in the pancreas in SCI rats compared to controls suggested increased glucagon turnover. Finally, GLP-1 receptor gene expression in the ileum, the primary source of GLP-1 production and release, in SCI rats suggests the responsivity of the gut to altered circulating GLP-1 in the body. In conclusion, the actions of GLP-1 and its preprohormone, glucagon, are markedly uncoupled from their actions on glucose control in the SCI rat. More work is required to understand GLP-1 in the human.

The information, practices and views in this article are those of the author(s) and do not necessarily reflect the opinion of the Royal Geographical Society (with IBG).

Chronic spinal cord injury (SCI) results in an increased predisposition to various metabolic problems that can be exacerbated by consuming a diet rich in calories and saturated fat. In addition, gastrointestinal symptoms have been reported after SCI, including intestinal dysbiosis of the gut microbiome. The effects of both diet and SCI on the gut microbiome of adult male Long Evans rats euthanized 16 weeks after injury was investigated. The rats were either thoracic spinal contused or received sham procedures. After 12 weeks of either a low-fat or high-fat diet, cecal contents were analyzed, revealing significant microbial changes to every taxonomic level below the kingdom level. Shannon alpha diversity analyses demonstrated a significant difference in diversity between the groups based on the surgical condition of the rats. SCI produced a unique signature of changes in commensal bacteria that were significantly different than Sham. Specific changes in commensal bacteria as a result of diet manipulation had high fidelity with reports in the literature, such as Clostridia, Thiohalorhabdales, and Pseudomonadales. In addition, novel changes in commensal bacteria were identified that are unique dietary influences on SCI. Linear regression analysis on body fat and lean mass showed that a consequence of chronic SCI produces uncoupled associations between some commensal bacteria and body composition. In conclusion, despite tightly controlling the protein content and varying the carbohydrate and fat contents, Sham and SCI rats respond uniquely to diet. These data provide potential direction for therapeutic modulation of the microbiome to improve health and wellness following SCI.

No abstract

No abstract