| First Author | Roy D | Year | 2024 |
| Journal | Cell Rep Med | Volume | 5 |
| Issue | 5 | Pages | 101525 |
| PubMed ID | 38663398 | Mgi Jnum | J:352357 |
| Mgi Id | MGI:7705628 | Doi | 10.1016/j.xcrm.2024.101525 |
| Citation | Roy D, et al. (2024) alpha2delta1-mediated maladaptive sensory plasticity disrupts adipose tissue homeostasis following spinal cord injury. Cell Rep Med 5(5):101525 |
| abstractText | Spinal cord injury (SCI) increases the risk of cardiometabolic disorders, including hypertension, dyslipidemia, and insulin resistance. Not only does SCI lead to pathological expansion of adipose tissue, but it also leads to ectopic lipid accumulation in organs integral to glucose and insulin metabolism. The pathophysiological changes that underlie adipose tissue dysfunction after SCI are unknown. Here, we find that SCI exacerbates lipolysis in epididymal white adipose tissue (eWAT). Whereas expression of the alpha2delta1 subunit of voltage-gated calcium channels increases in calcitonin gene-related peptide-positive dorsal root ganglia neurons that project to eWAT, conditional deletion of the gene encoding alpha2delta1 in these neurons normalizes eWAT lipolysis after SCI. Furthermore, alpha2delta1 pharmacological blockade through systemic administration of gabapentin also normalizes eWAT lipolysis after SCI, preventing ectopic lipid accumulation in the liver. Thus, our study provides insight into molecular causes of maladaptive sensory processing in eWAT, facilitating the development of strategies to reduce metabolic and cardiovascular complications after SCI. |
