Neurocognitive and developmental perspectives of obesity.
Neurocognitive and developmental perspectives of obesity.
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肥胖的神经认知和发育观点。
DOI：
10.1016/j.ijdevneu.2017.11.005
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Hommel,JonathanD
中科院分区：
文献类型：
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作者：
Hommel,JonathanD
本期《国际发育神经科学杂志》特别版的重点是“肥胖的神经认知和发育视角”。肥胖是一个全球性的健康问题，全世界有超过 6 亿成年人肥胖，超过 4000 万五岁以下儿童肥胖。全球肥胖率继续上升，而且没有明显稳定的迹象，这进一步加剧了这个问题。尽管能量稳态受到大脑的严格调节，但饮食引起的肥胖正在导致神经认知功能障碍也变得越来越明显。本特别版重点阐述大脑功能与能量稳态之间的复杂关系，以增进我们对这一全球问题的理解。在 Guarnieri 等人的第一份手稿中，评估了高脂肪饮食对 microRNA-155 (mir-155)（一种重要的炎症分子调节剂）的影响。饮食引起的肥胖使伏隔核中的 mir-155 水平降低了 80% 以上，伏隔核是与奖励和动机行为密切相关的大脑区域。与野生型对照相比，mir-155 的敲除导致小鼠消耗更多的高脂肪饮食，从而导致体重显着增加。在敲除小鼠中没有观察到新陈代谢的变化，表明mir-155是食物摄入和体重的新型调节剂。探索发育过程中必需营养素 omega-3 多不饱和脂肪酸围产期饮食缺乏的行为和代谢后果。这导致大脑中的 omega-3 多不饱和脂肪酸减少。此外，这些动物对蔗糖奖励的敏感性升高，高脂肪饮食导致体重增加，活动减少，焦虑样行为增加。这项工作极大地增强了我们对营养缺乏对能量平衡和行为影响的理解。神经肽 Y (NPY) 和阿片黑皮质素原 (POMC) 是大脑中调节能量平衡的神经肽。克莱因等人。已经证明，怀孕小鼠接触高脂肪饮食会改变胚胎大脑中 NPY 和 POMC 的表达。这些发现对怀孕期间高脂肪饮食导致的胚胎大脑代谢重编程具有深远的影响。尽管出生体重过高或过低与多种神经发育障碍有关，但母亲营养在这些疾病中的作用却知之甚少。在这里，灭霸等人。发现母体蛋白质消耗低（胎儿生长欠佳和出生体重低的模型）会减少与奖励相关的大脑区域中 mu-阿片受体和多巴胺 D1 受体的结合。这可能会导致一些与低出生体重相关的行为异常。此外，小笠原等人。研究人员探索了母亲食物限制以及后代高热量饮食对第三代小鼠能量稳态的多代影响。当受到脂多糖的攻击时，多个大脑区域的神经胶质原纤维酸性蛋白的表达发生改变。为了更好地了解肥胖的潜在行为机制，需要进一步探索摄入行为模型。在本期中，约翰逊回顾了舔行为的使用；通过评估舔的微观结构，可以识别和量化舔的发作和爆发。这种行为反映了液体的适口性，并允许研究避免食物和接受食物的潜在神经生物学机制。肥胖在导致认知功能障碍中的作用已成为一个突出的研究领域。这是 …
This special edition of the International Journal of Developmental Neuroscience is focused on “Neurocognitive and Developmental Perspectives of Obesity”. Obesity is a global health concern with over 600 million obese adults around the world and over 40 million obese children under the age of five. Further adding to the problem, global obesity rates continue to rise with no obvious signs of stabilization. Although energy homeostasis is heavily regulated by the brain, it is also becoming more apparent that diet-induced obesity is causing neurocognitive dysfunction. This special edition focuses on elucidating the complex relationship between brain function and energy homeostasis to advance our understanding of this global problem. In the first manuscript by Guarnieri et al., the effects of a high-fat diet on microRNA-155 (mir-155), an important molecular regulator of inflammation, were evaluated. Diet-induced obesity reduced the levels of mir-155 by over 80% in the nucleus accumbens, a brain region closely associated with reward and motivated behavior. Knockout of mir-155 caused mice to consume more of a high-fat diet compared to wild type controls resulting in significant body weight gain. No changes in metabolism were observed in the knockout mice, indicating that mir-155 is a novel regulator of food intake and body weight.Auguste et al. explore the behavioral and metabolic consequences of perinatal dietary deficiency of the essential nutrient omega-3 polyunsaturated fatty acid during development. This resulted in reduced omega-3 polyunsatureated fatty acids in the brain. Furthermore, these animals had elevated sensitivity to sucrose reward, elevated weight gain on a high-fat diet, decreased activity, and increased anxiety-like behavior. This work greatly enhances our understanding of the effects of nutrient deficiency on energy balance and behavior. Neuropeptide Y (NPY) and proopiomelanocortin (POMC) are neuropeptides in the brain which regulate energy balance. Klein et al. have demonstrated that exposure of a pregnant mouse to a high-fat diet alters expression of NPY and POMC in the brains of embryos. These findings have profound implications for metabolic reprogramming in embryonic brains resulting from the consumption of a high fat diet during pregnancy. Although birthweight that is either too high or too low is associated with multiple neurodevelopmental disorders, the role of maternal nutrition in these disorders is poorly understood. Here, Thanos et al. discovered that low maternal protein consumption, a model for suboptimal fetal growth and small birth weitht, have decreased binding of mu-opioid receptor and dopamine D1 receptor in reward-associated brain regions. This may contribute to some of the behavioral abnormalities associated with low birthweight. Furthermore, Ogassawara et al. have explored multigenerational effects of maternal food restriction followed by a hypercaloric diet for the offspring on energy homeostasis in third generation mice. When challenged with lipopolysaccharide, the expression of glial fibrillary acidic protein was altered in multiple brain regions. In order to better understand underlying behavioral mechanisms of obesity, models of ingestive behavior need to be further explored. In this issue, Johnson has reviewed the use of licking behavior; by evaluating the microstructure of licking, licking bouts and bursts can be identified and quantified. This behavior reflects the palatability of the liquid and allows for the study of the underlying neurobiological mechanisms of food avoidance and food acceptance. The role of obesity in causing cognitive dysfunction has become a prominent area of research. It is …