Greer Andrew W, Boisclair Yves R, Stankiewicz Miroslaw, McAnulty Robin W, Jay Nigel P, Sykes Andrew R
Lincoln University, Canterbury, New Zealand.
Br J Nutr. 2009 Oct;102(7):954-7. doi: 10.1017/S0007114509359115.
The hypothesis that increases in the concentration of the anorectic peptide leptin may be responsible for the immune-mediated reduction in feed intake (FI) during gastrointestinal parasitism in sheep was investigated. In a 2 x 2 x 2 factorial design, the first factor was age at the start of infection (5 months old v. 17 months old). The second factor was parasite infection (no infection v. administration of eighty L3 infective Trichostrongylus colubriformis larvae/kg live weight (LW) per d three times per week for 77 d). The third factor was immunosuppressive therapy with a corticosteroid (no therapy or weekly intramuscular injection of 40 mg methylprednisolone acetate/30 kg LW). Relative to their uninfected counterparts, a 20 % reduction in FI per unit LW (FI/LW; g DM/kg LW) was observed in infected non-suppressed 5-month-old lambs from 21 to 63 d post-infection (P < 0.001) but not in comparable17-month-old ewes or in corticosteroid-treated lambs or ewes (P>0.05 for all), allowing the suggestion that the anorexia was a consequence of the developing immune response. The reduction in FI/LW in 5-month-old lambs was not associated with an increase in plasma leptin concentration. Furthermore, plasma leptin concentrations were greater in corticosteroid-treated animals (P < 0.001) and in 17-month-old animals (P < 0.001), none of which displayed an infection-induced reduction in FI/LW. Plasma leptin was positively correlated with carcass fat percentage in both 5-month-old (P = 0.016) and 17-month-old (P < 0.001) animals and did not appear to provide a direct feedback mechanism that restricted energy intake. The results do not support the hypothesis that an increase in circulating leptin is directly responsible for the immune-mediated anorexia in lambs during T. colubriformis infection.
在绵羊胃肠道寄生虫感染期间，厌食肽瘦素浓度的升高可能是免疫介导的采食量（FI）减少的原因。采用2×2×2析因设计，第一个因素是感染开始时的年龄（5月龄对17月龄）。第二个因素是寄生虫感染（未感染对每周三次、连续77天每天每千克活体重（LW）接种80条蛇形毛圆线虫L3感染性幼虫）。第三个因素是用皮质类固醇进行免疫抑制治疗（未治疗或每周一次肌肉注射每30千克LW 40毫克醋酸甲泼尼龙）。相对于未感染的对照动物，感染但未接受治疗的5月龄羔羊在感染后21至63天，每单位LW的FI（FI/LW；克干物质/千克LW）降低了20%（P<0.001），但在17月龄的母羊或接受皮质类固醇治疗的羔羊或母羊中未观察到这种情况（所有P>0.05），这表明厌食是免疫反应发展的结果。5月龄羔羊FI/LW的降低与血浆瘦素浓度的升高无关。此外，接受皮质类固醇治疗的动物（P<0.001）和17月龄的动物（P<0.001）血浆瘦素浓度更高，但这些动物均未出现感染诱导的FI/LW降低。5月龄（P = 0.016）和17月龄（P<0.001）动物的血浆瘦素与胴体脂肪百分比呈正相关，且似乎未提供限制能量摄入的直接反馈机制。结果不支持循环瘦素增加直接导致蛇形毛圆线虫感染期间羔羊免疫介导的厌食这一假说。
