Adipose tissue derived cytokines, such as the anti-inflammatory adiponectin play a significant role in a variety of disease conditions. Adiponectin is reduced with obesity and in type 2 diabetes patients; both conditions associated with development of co-morbid pain. This study set out to characterise expression of adiponectin in spinal cord in rodent models of genetic obesity (Zucker rats), experimentally-induced obesity (high fat diet (HFD) fed rats), and type 2 diabetes, and to determine if changes are associated with alterations in nociceptive pain.Responses to thermal and mechanical stimulation of the hindpaw were assessed in adult male Zucker fatty rats and lean littermates (n=6/group), adult male Wistar rats fed a high fat (22%) diet for 16 weeks and injected intraperitoneally (i.p) with either low dose of streptozotocin (STZ; 30 mg/kg; (n=6), a model of type 2 diabetes (T2D rats), or vehicle (HFD rats; n=6), and control rats fed a normal diet and injected with vehicle citrate buffer (i.p; n = 6). Animals were euthanased by schedule 1 killing and spinal cord and plasma collected. Blood glucose, insulin and total cellular cholesterol were measured, and expression of adiponectin mRNA analysed in spinal cord using real-time PCR (n=6 per group). Data were analysed using an ANOVA with post-hoc Tukey’s test.Obese Zucker rats were significantly heavier than lean controls (551 ± 35g vs. 377 ± 27g; P<0.01), as were HFD rats (502 ± 12g vs. 444 ± 7g for controls; P<0.01). Both obese Zucker and HFD rats had elevated plasma cholesterol and insulin levels (all P<0.01 vs. controls), but were normoglycaemic. After an initial weight gain, T2D rats had significant weight loss (410 ± 12 vs. 473 ± 4g for controls; P < 0.01), and had elevated blood glucose and cholesterol levels (P<0.05 and P<0.01 vs. controls); insulin levels were unchanged. T2D rats displayed significant thermal and mechanical hyperalgesia (P <0.01 vs. controls); nociceptive responses were unchanged in Obese Zucker and HFD rats. Real-time PCR analysis revealed a significant down-regulation in spinal adiponectin in T2D rats (8 fold decrease; P < 0.05 vs. control rats), and in obese Zucker rats (2.4 fold decrease; P < 0.05 vs. lean rats, but not in HFD rats.The increased pain sensitivity and altered adipokine expression profile in rats with type 2 diabetes fits the hypothesis that changes in key adipokines, at the spinal level may underlie pain with diabetes, although further studies are necessary to confirm a causative role.