背景:肥胖中过多的脂肪堆积,由于饮食不均衡,会导致代谢和神经系统疾病,并增加患焦虑和抑郁的风险。
目的:评估饮食干预(DI)对5-羟色胺能系统的影响,肥胖小鼠脑源性神经营养因子(BDNF)表达与行为的关系.
方法:雄性C57BL/6小鼠,5周大,接受高脂饮食(HFD)10周以诱导肥胖。在这段时间之后,八个星期,这些动物中有一半接受对照饮食(CD),组肥胖(OB)+对照饮食(OB+CD,n=10),还有一半人继续接受HFD,组肥胖+HFD(OB+HFD,n=10)。在第八周的干预结束时,进行了行为测试(蔗糖偏好测试,开放领域,新颖的物体识别,高架加上迷宫和尾部悬挂)。每周评估体重和食物摄入量。内脏肥胖,海马和下丘脑BDNF蛋白的表达,5-HT1A(5-HT1A血清素受体)和TPH2(血清素合成的关键酶),在安乐死后进行评估。
结果:饮食干预涉及在8周内从HFD变为CD,有效减少体重增加,肥胖,和快感缺失的行为。在OB+HFD组中,我们在开阔的田野中看到了较低的蔗糖偏好和较短的行进距离,与OB+CD小鼠相比,下丘脑中的前BDNF表达增加。然而,TPH2和5-HT1A的水平保持不变。
结论:HFD模型诱导肥胖和快感缺乏,但是饮食干预成功地改善了这些情况。
BACKGROUND: The excessive fat accumulation in obesity, resulting from an unbalanced diet, can lead to metabolic and neurological disorders and increase the risk of developing anxiety and depression.
OBJECTIVE: Assess the impact of dietary intervention (DI) on the serotonergic system, brain-derived neurotrophic factor (BDNF) expression and behaviors of obese mice.
METHODS: Male C57BL/6 mice, 5 weeks old, received a high-fat diet (HFD) for 10 weeks for the induction of obesity. After this period, for 8 weeks, half of these animals received a control diet (CD), group obese (OB) + control diet (OB + CD, n = 10), and another half continued being fed HFD, group obese + HFD (OB + HFD, n = 10). At the end of the eighth week of intervention, behavioral tests were performed (sucrose preference test, open field, novel object recognition, elevated plus maze and tail suspension). Body weight and food intake were assessed weekly. Visceral adiposity, the hippocampal and hypothalamic protein expression of BDNF, 5-HT1A (5-HT1A serotonin receptor) and TPH2 (key enzyme in serotonin synthesis), were evaluated after euthanasia.
RESULTS: The dietary intervention involved changing from a HFD to a CD over an 8-week period, effectively reduced body weight gain, adiposity, and anhedonia-like behavior. In the OB + HFD group, we saw a lower sucrose preference and shorter traveled distance in the open field, along with increased pro-BDNF expression in the hypothalamus compared to the OB + CD mice. However, the levels of TPH2 and 5-HT1A remained unchanged.
CONCLUSIONS: The HFD model induced both obesity and anhedonia, but the dietary intervention successfully improved these conditions.