Huang Xu-Feng, Yu Yinghua, Li Yulin, Tim South, Deng Chao, Wang Qing
Centre for Translational Neuroscience, School of Health Sciences, University of Wollongong, Northfield Avenue, Wollongong, 2522, Australia.
Neurochem Res. 2008 Sep;33(9):1881-8. doi: 10.1007/s11064-008-9661-5. Epub 2008 Mar 21.
This study examined changes in neuropeptide Y (NPY) Y2 receptor binding in the brains of C57BL/6 mice in response to different levels of high-fat diets via three dietary intervention methods: high-fat diet, switching from high- to low-fat diet and finally, energy restricted high-fat diet. Forty-five C57Bl/6 male mice were fed a high-fat diet for 8 weeks and then classified as diet-induced obese (DIO) or diet-resistant (DR) mice according to the highest and lowest body weight gainers, respectively. The DIO and DR mice were then randomly divided into three groups each and either continued on their high-fat diet ad libitum (DIO-H and DR-H), changed to a low-fat diet (DIO-L and DR-L) or pair-fed via energy restricted high-fat diet (DIO-P and DR-P) for a further 6 weeks. During the course of this study, body weight, energy intake and plasma peptide YY (PYY) were measured. The study revealed that the replacement of a high-fat diet with a low-fat diet was associated with a significant lowering of ventromedial hypothalamic (VMH) Y2 receptor binding in both the DIO-L and DR-L mice (-37%, -36%), and also a lowered plasma PYY level in the DIO-L mice (-25%). Despite a continued consumption of the high-fat diet, energy restricted pair feeding caused a lower VMH Y2 receptor binding in the obese mice (DIO-P) following weight loss compared to the DR-P mice (-14%). In conclusion, this study showed that changing diets from high- to low-fat can significantly lower the VMH Y2 receptor binding irrespective to the obesity phenotype. Energy restriction, even while on high-fat feeding, can cause a lower VMH Y2 receptor binding compared to DR mice even after body weight loss to similar levels. This suggests either a possible intrinsic nature of the DIO mice or a body weight set-point re-establishment to drive body weight regain.
本研究通过三种饮食干预方法，研究了C57BL/6小鼠大脑中神经肽Y（NPY）Y2受体结合情况随不同水平高脂饮食的变化：高脂饮食、从高脂饮食转换为低脂饮食以及最后能量限制高脂饮食。45只C57Bl/6雄性小鼠接受高脂饮食8周，然后分别根据体重增加最多和最少的小鼠分为饮食诱导肥胖（DIO）或饮食抵抗（DR）小鼠。然后将DIO和DR小鼠各随机分为三组，分别自由进食高脂饮食（DIO-H和DR-H）、改为低脂饮食（DIO-L和DR-L）或通过能量限制高脂饮食进行配对喂养（DIO-P和DR-P），持续6周。在本研究过程中，测量了体重、能量摄入和血浆肽YY（PYY）。研究表明，用低脂饮食替代高脂饮食与DIO-L和DR-L小鼠腹内侧下丘脑（VMH）Y2受体结合显著降低有关（分别降低37%、36%），并且DIO-L小鼠的血浆PYY水平也降低（降低25%）。尽管持续食用高脂饮食，但与DR-P小鼠相比，能量限制配对喂养使肥胖小鼠（DIO-P）体重减轻后VMH Y2受体结合降低（降低14%）。总之，本研究表明，从高脂饮食改为低脂饮食可显著降低VMH Y2受体结合，而与肥胖表型无关。即使在高脂喂养的情况下，能量限制也会导致VMH Y2受体结合比DR小鼠降低，即使体重减轻到相似水平。这表明要么是DIO小鼠可能具有内在特性，要么是体重设定点重新建立以推动体重恢复。
