Neuroscience and Neurochemistry

Biography

Biography: Sharron Dolan

Abstract

Obese individuals are more likely to be affected by chronic pain, however, the biological mechanisms underpinning this comorbidity are not known. A causal link may be dysregulated secretion of inflammatory adipokines both from expanding adipose tissue and centrally. The aim of this study was to characterize altered pain processing and changes in inflammatory cytokine expression in spinal cord in rodent models of obesity. Responses to thermal and mechanical stimulation of the hind paw were assessed in adult male Wistar rats fed a high fat diet (HFD; 22%) or normal diet for 16 weeks (n=6/group) in absence of inflammation, and then in response to intradermal hind paw injection of carrageenan (3%; 50μl), a model of acute inflammation. Spinal cord was collected and adipokine mRNA expression, cholesterol and triglycerides (TAGs) measured using real-time PCR and ELISA. Rats fed a HFD gained significantly more weight than controls (502 ± 12g vs. 444 ± 7g; P<0.01), and displayed plasma hyperinsulaemia and hypercholesterolaemia (both P<0.05 vs. controls) but normoglycaemia. Acute nociceptive responses were unchanged in obese rats but they displayed potentiated mechanical and thermal hyperalgesia and increased paw edema (all P<0.05 vs. lean controls) in response to carrageenan. Significant changes in levels of resistin C reactive protein, TGFβ and visfatin (but not IL1β or TNFβ) were detected in obese rat spinal cord. The increased pain and inflammation in obese rats fits with the hypothesis that obesity is a chronic low-grade inflammatory disorder, producing a state where responses to inflammatory challenge are potentiated. The altered adipokine profile observed suggests adipokines may be useful biomarkers for monitoring initiation and progression of pain with obesity, or even be involved in the development of co-morbid pain in obese individuals.