It has been widely suggested that saturated fat consumption has fuelled the current obesity epidemic. Macronutrient choices appear to be important not only as potential factors influencing obesity, but also independently as risk factors for diabetes, cardiovascular disease and cancer. The neuropeptide galanin has previously been implicated in the regulation of fat intake, although its precise role has been contested. The present study investigated mice with targeted knockout of the galanin gene (GKO). We demonstrate that, when only a high fat diet (HFD) was available, wild-type (WT) animals consumed significantly more energy than the GKO mice (89.85 +/- 4.57 kJ/day versus 76.84 +/- 3.55 kJ/day, P < 0.001, n = 17 versus 15). Consistent with this, WT animals gained more body weight when fed the HFD than GKO animals (3.48 +/- 0.44 g versus 2.02 +/- 0.62 g, P < 0.001, n = 17 versus 15). In a macronutrient choice scenario, WT mice ate almost three-fold more fat than GKO animals (0.63 +/- 0.02 g versus 0.23 +/- 0.01 g, P < 0.001, n = 18 versus 24). Chronic administration of galanin by mini-osmotic pumps into the lateral ventricle of GKO animals partially reversed the fat avoidance phenotype. Fat intake was significantly lower in the phosphate-buffered saline-treated GKO group compared to galanin-treated GKO animals (0.32 +/- 0.01 g versus 0.38 +/- 0.01 g, P < 0.005, n = 17 versus 17). These data are compatible with the hypothesis that galanin specifically regulates fat intake, and implies that an antagonist to one or more of the galanin receptor subtype(s) may be of use in the treatment of some forms of obesity.

译文

:已被广泛认为,饱和脂肪的消耗助长了当前的肥胖病流行。大量营养素的选择不仅作为影响肥胖的潜在因素,而且作为糖尿病,心血管疾病和癌症的危险因素,也很重要。神经肽甘丙肽以前曾参与脂肪摄入的调节,尽管其确切作用已受到争议。本研究调查了有针对性地敲除甘丙肽基因(GKO)的小鼠。我们证明,当只有高脂饮食(HFD)可用时,野生型(WT)动物比GKO小鼠消耗的能量要多得多(89.85 /-4.57 kJ /天,而76.84 /-3.55 kJ /天,P < 0.001,n = 17对15)。与此相一致,野生型动物饲喂HFD时比GKO动物获得更多的体重(3.48±0.44 g对2.02±0.62 g,P <0.001,n = 17对15)。在选择大量营养素的情况下,野生型小鼠的脂肪摄入几乎是GKO动物的三倍(0.63 /-0.02克对0.23 /-0.01克,P <0.001,n = 18对24)。通过微型渗透泵向GKO动物的侧脑室长期施用甘丙肽会部分逆转避免脂肪的表型。与甘丙肽治疗的GKO动物相比,磷酸盐缓冲盐水治疗的GKO组的脂肪摄入量显着降低(0.32 / 0.01 g对0.38 / 0.01 g,P <0.005,n = 17对17)。这些数据与甘丙肽特异性地调节脂肪摄入的假设是相容的,并且暗示针对一种或多种甘丙肽受体亚型的拮抗剂可以用于治疗某些形式的肥胖症。

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