AI Article Synopsis
- Hyperadrenocorticism (HAC) in dogs affects insulin sensitivity and can lead to diabetes, influenced by changes in T cell activity and muscle tissue.
- This study investigated how the glucocorticoid dexamethasone alters metabolites in canine peripheral blood mononuclear cells (CnPBMCs) through advanced mass spectrometry techniques.
- Key findings revealed that dexamethasone elevated levels of certain glucose-related metabolites while decreasing others, indicating that glucocorticoids lower glucose metabolism and requirements in these cells.
Article Abstract
In dogs, hyperadrenocorticism (HAC) is associated with insulin resistance and diabetes does progress with HAC. There are significant differences in the transcriptomic and proteomic patterns of activated T cells, which parallel the findings in muscle tissues. The aim of this study was to assess how glucocorticoids affect intracellular metabolites in canine peripheral blood mononuclear cells (CnPBMCs) using dexamethasone. A total of 96 metabolites were identified by capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS). After incubation with dexamethasone, the metabolites glucose 1-phosphate, glucose 6-phosphate, fructose 6-phosphate, sedoheptulose 7-phosphate and acetyl-CoA were significantly increased. However, ATP, CTP, dATP, pyruvic acid and NADP(+) were significantly decreased. These results show that a glucocorticoid reduces the catabolic reaction of glucose and accordingly decreases the glucose requirements of CnPBMCs.
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| http://dx.doi.org/10.1016/j.tvjl.2015.10.054 | DOI Listing |
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