br The interrelationship between obesity and

The interrelationship between obesity and galanin Numerous studies revealed that obesity and galanin may promote each other. On the one hand, galanin may increase the possibility of obesity of subjects via boosting their appetite and food intake. Acute injection with galanin or its agonist, galanin (1–16), into the paraventricular nucleus (PVN) of the hypothalamus, significantly increased appetite, food intake and body weight of subjects in the behavioral phenotype [15], [17], [18]. The effect of galanin on feeding behavior is blocked by its antagonists M40 and C7. Moreover, galanin knockout (Gal-KO) mice consumed far less resveratrol than controls [1]. Fat intake was significantly lower in the Gal-KO group treated with phosphate-buffered saline by mini-osmotic pumps into the lateral ventricle as compared to galanin-treated Gal-KO animals. Chronic administration of galanin into the lateral ventricle of Gal-KO animals partially reversed the fat avoidance phenotype. While the homozygous galanin-transgenic mice increased their total serum cholesterol, total serum triglycerides, visceral adiposity and body weight [58]. The beneficial effects of galanin on obesity were independent of any changes in food intake or horizontal activity, as galanin contributed to a reduction in heat production and metabolic rate. The galanin-mediated signaling pathways activate adipogenesis and suppress thermogenesis, resulting in obesity in mice [37]. On the other hand, obesity may also affect the plasma galanin levels of subjects. The plasma galanin levels are elevated in fat women and decreased in thin women [6]. Also in obese young women than normally menstruating women [54]. The plasma galanin levels were significantly higher in obese women with BMI over 31 [6]. The obese women with anorexia nervosa had a significant increase in plasma galanin concentration as compared with controls, suggesting that the increase in galanin levels is relative to their obese, not their food intake [7]. Galanin mRNA and galanin protein levels were also enhanced in PVN of obesity-prone rats fed with high-fat diet as compared with the obesity-prone rats fed with high-carbohydrate diet or obesity-resistant rats fed with high-fat diet [16]. In addition, male Sprague-Dawley rats fed with high-fat diet from birth day were divided into obesity-prone or obesity-resistant groups identified by weight-gain scores (8–10g/day vs. 5–7g/day) [43]. In their maturity obesity-prone and obesity-resistant subgroups became obese or remained lean respectively. At day 100 of age the obesity-prone rats had rapider weight gain, 50% greater adiposity and higher galanin levels in PVN than obesity-resistant animals. These suggest that it is obesity itself, rather than high-fat diet, that potentiates galanin secretion. Intriguingly, there was a significant increase (40–220%) in galanin concentration with age in the arcuate and dorsomedial nuclei of obese male Zucker rats than lean controls [54]. But galanin levels were globally lower in obese than in lean rats (−15% to −25%) at 2 weeks of age in PVN and at 4 weeks of age in the arcuate nucleus. These suggest that galanin is not an early player in the development of obesity and it is likely that obesity itself results in increasing galanin concentration.
The interrelationship between galanin and pain threshold Recently, a number of persistent pain models have been developed for the nociceptive research. The first is cyclophosphamine-induced cystitis, which is taken as an animal model of visceral pain [49]. Cyclophosphamide, an alkylating agent, may be metabolized by the liver to phosphoramide mustard and acrolein. The latter has been linked to the development of hemorrhagic cystitis resulting in dysuria and hematuria [8]. The second is Freund's adjuvants which may induce animal models of chronic inflammation pain [4], [14], [23], [67]. The third is allodynia pain which is a hypersensitive reaction that may result from central sensitization. Allodynia may be caused by temperature or physical stimuli, some populations of stem cells used to treat nerve damage including spinal cord injury [26]. The fourth is static mechanical allodynia which is a paradoxical painful hypoaesthesia. One etiology of which is lesions of A-beta fibers [65]. The last, the nerve ligation is a model of peripheral neuropathic pain with causaigia [38]. This model allows independent experimental manipulations of injured or intact spinal segments regarding mechanisms underlying causalgia.