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Neuregulin 1 affects leptin levels, food intake and weight gain in normal-weight, but not obese, db/db mice

机译:神经调节蛋白1影响正常体重而非肥胖的db / db小鼠的瘦素水平,食物摄入量和体重增加

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摘要

Aim. - Studies in vitro have highlighted the potential involvement of neuregulin 1 (NRG1) in the regulation of energy metabolism. This effect has also been suggested in vivo, as intracerebroventricular injection of NRG1 reduces food intakes and weight gain in rodents. Thus, it was hypothesised that NRG1 might affect serum leptin levels in mice. Methods. - Weight, food intakes, energy expenditure, spontaneous physical activity and serum leptin levels were evaluated in normal-weight C57BL/6JRJ mice following intraperitoneal administration of NRG1 (50 mu g/kg, three times/week) or saline for 8 weeks. Based on the results of this first experiment, leptin-resistant obese db/db mice were then given NRG1 for 8 weeks. Results. - Leptin serum concentrations were six times higher in C57BL/6JRJ mice treated with NRG1 than in the animals given saline. NRG1 treatment also reduced weight gain by 10% and food intakes by 15% compared with saline treatment, while energy expenditure remained unchanged. In db/db mice, serum leptin concentrations, weight gain, food intakes, energy expenditure and spontaneous physical activity were not altered by NRG1 treatment. Conclusion. - The decrease in food intakes and weight gain associated with NRG1 treatment in C57BL/6JRJ mice may be partly explained by increased leptin levels, whereas db/db mice were not affected by the treatment, suggesting resistance to NRG1 in this pathological state.
机译:目标。 -体外研究强调了神经调节蛋白1(NRG1)可能参与能量代谢的调节。还已经在体内暗示了这种作用,因为脑室内注射NRG1会减少啮齿动物的食物摄入和体重增加。因此,假设NRG1可能影响小鼠的血清瘦素水平。方法。 -在体重正常的C57BL / 6JRJ小鼠腹膜内施用NRG1(50μg / kg,3次/周)或生理盐水8周后,评估体重,食物摄入,能量消耗,自发体力活动和血清瘦素水平。根据第一个实验的结果,对瘦素抵抗型肥胖db / db小鼠进行NRG1干预8周。结果。 -用NRG1处理的C57BL / 6JRJ小鼠的瘦素血清浓度是生理盐水中的六倍。与盐水处理相比,NRG1处理还使体重增加减少了10%,食物摄入减少了15%,而能量消耗保持不变。在db / db小鼠中,NRG1处理不会改变血清瘦素浓度,体重增加,食物摄入,能量消耗和自发体力活动。结论。 -在C57BL / 6JRJ小鼠中,与NRG1治疗相关的食物摄入量减少和体重增加可以部分由瘦素水平升高来解释,而db / db小鼠不受该治疗影响,表明在这种病理状态下对NRG1有抗性。

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