Impaired AMPK ‑CGRP signaling in the central nervous system contributes to enhanced neuropathic pain in high‑fat diet‑induced obese rats, with or without nerve injury.

Impaired AMPK‑CGRP signaling in the central nervous system contributes to enhanced neuropathic pain in high‑fat diet‑induced obese rats, with or without nerve injury. Mol Med Rep. 2019 Jun 06;: Authors: Guo X, Tao X, Tong Q, Li T, Dong D, Zhang B, Zhao M, Song T Abstract Obesity is associated with increased sensitivity to pain, including neuropathic pain, but the precise mechanisms are not fully understood. Recent evidence has revealed that AMP‑activated protein kinase (AMPK) in the central nervous system (CNS) regulates the neuropeptide calcitonin gene‑related peptide (CGRP), a principal neurotransmitter of the class C nerve fiber, which serves an important role in initiating and maintaining neuropathic pain. AMPK has been demonstrated to be downregulated in the CNS in obesity. The present study hypothesized that obesity may lead to increased sensitivity to neuropathic pain by downregulating AMPK and upregulating CGRP expression levels in the CNS. Sprague‑Dawley rats consuming a high‑fat diet (HF) for 12 weeks developed obesity; they exhibited significantly decreased levels of phospho (p)‑AMPK and increased CGRP expression levels in the spinal cord (SC) and dorsal root ganglion (DRG), respectively, compared with rats consuming a low‑fat (LF) diet. HF‑fed rats that underwent spared nerve injury (SNI) also exhibited lower p‑AMPK and higher CGRP expression levels in the SC and DRG, compared with the corresponding...
Source: Molecular Medicine Reports - Category: Molecular Biology Tags: Mol Med Rep Source Type: research