Psychopharmacology and Proteomics Laboratory, School of Psychology, The University of Sydney, Brennan MacCallum Building (A18), Sydney, NSW, 2006, Australia,
Neurochem Res. 2014 May;39(5):815-24. doi: 10.1007/s11064-014-1274-6. Epub 2014 Mar 15.
Obesity is a contemporary health problem of rapidly increasing prevalence. One possible cause of obesity is loss of control over consumption of highly palatable foodstuffs, perhaps mirroring the processes involved in drug addiction. Accordingly, the striatum may be a key neural substrate involved in both food and drug craving. We hypothesised here that prolonged exposure to 10% sucrose solution might cause neuroadaptations in the striatum that are analogous to those previously reported following prolonged exposure to alcohol or recreational drugs. Male Wistar rats were given constant access to 10% sucrose solution (in addition to normal lab chow and tap water) for 8 months and were compared with control rats receiving no sucrose access. Rats in the sucrose group typically drank more than 100 ml of sucrose solution per day and showed 13% greater body weight than controls at the end of the 8 months. Striatal dopamine (DA) concentrations were decreased in the sucrose group rats relative to controls. Differential expression of 18 proteins was identified in the striatum of the sucrose group rats relative to controls. Down regulated proteins included pyridoxal phosphate phosphatase, involved in DA synthesis, and glutathione transferase, involved in free radical scavenging. Up regulated proteins included prolactin (which is under negative regulation by DA) and adipose differentiation-related protein, involved in fat synthesis. We hypothesise that DA-related neuroadaptations in the striatum caused by prolonged sucrose intake may partly drive compulsive intake and seeking of high palatability foodstuffs, in a similar way to that observed with drug and alcohol addictions.
肥胖是一个日益严重的现代健康问题。肥胖的一个可能原因是对高美味食品的消费失去控制,这可能反映了成瘾过程。因此,纹状体可能是涉及食物和药物渴望的关键神经基质。在这里,我们假设长时间暴露于 10%蔗糖溶液可能会导致纹状体发生类似于长期暴露于酒精或娱乐性药物后所报道的神经适应性变化。雄性 Wistar 大鼠被给予持续接触 10%蔗糖溶液(除了正常的实验室饲料和自来水之外)8 个月,并与不接触蔗糖的对照组大鼠进行比较。蔗糖组大鼠通常每天饮用超过 100 毫升的蔗糖溶液,并且在 8 个月结束时体重比对照组大鼠增加了 13%。与对照组相比,蔗糖组大鼠的纹状体多巴胺(DA)浓度降低。与对照组相比,蔗糖组大鼠纹状体中有 18 种蛋白质的表达存在差异。下调的蛋白质包括参与 DA 合成的吡哆醛磷酸酶和参与自由基清除的谷胱甘肽转移酶。上调的蛋白质包括催乳素(受 DA 负调节)和脂肪分化相关蛋白,参与脂肪合成。我们假设,由于长时间摄入蔗糖而导致的纹状体中与 DA 相关的神经适应性变化,可能部分驱动了对高美味食物的强迫性摄入和寻求,类似于观察到的药物和酒精成瘾。