Antioxidant Food Supplements and Obesity-Related Inflammation

Antioxidant Food Supplements and Obesity-Related Inflammation
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DOI:
10.2174/0929867311320180004
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发表时间:
2013-06-01
影响因子:
4.1
通讯作者:
Fuchs, D.
Fuchs, D.
中科院分区:
医学3区
文献类型:
--
作者:
Mangge, H.;Summers, K.;Fuchs, D.

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肥胖症的流行在世界范围内不断增长,并在很大程度上导致心血管疾病发病率的增加,心血管疾病是西方世界最常见的死亡原因。过量的食物摄入沿着体育锻炼不足是这种发展的基本动力。肥胖状态通常与瘦素水平的增加和慢性免疫介导的炎症有关。尽管瘦素水平高,瘦素反应,通常与饱腹感和饱足感,似乎是受损和个人继续消耗热量丰富的食物。抗氧化剂食品添加剂如亚硫酸钠、苯甲酸钠和姜黄素被证明可以抑制脂多糖处理的小鼠脂肪细胞中瘦素的释放。基于此,我们假设,过量食用食品添加剂引起的瘦素释放不足,可能导致中枢神经系统对瘦素的暴露减少,最终传播肥胖。另一方面,瘦素已被证明有利于Th 1型活动,最终降低色氨酸水平。色氨酸衍生物、5-羟色胺和褪黑激素通过几种机制诱导饱腹感/饱足感。在这种情况下,抗氧化剂抑制瘦素释放和Th 1型活性有利于增加血清素和褪黑激素水平。在这篇综述中所描述的机制中的分子高度整合在奖赏系统中,并且已经被牵连到肥胖的成瘾行为中。基于这些事实,将讨论抗氧化剂食品补充剂在使肥胖永久化的奖赏缺乏综合征的机制中的参与。
The obesity prevalence is growing worldwide and largely responsible for the increased incidence of cardiovascular disease, the most common cause of death in the western world. Excessive food intake along with insufficient physical exercise is the basic impetus for this development. The obese state is commonly associated with an increase in leptin levels and chronic immune-mediated inflammation. Despite high leptin levels, the leptin response, normally associated with satiety and satiation, seems to be impaired and individuals continue to consume calorie-rich food. Antioxidant food additives such as sodium sulphite, sodium benzoate and curcumin were shown to suppress the leptin release in lipopolysaccharide-treated murine adipocytes. Based on this, we hypothesize that the insufficient leptin release, caused by excessive consumption of food additives, may lead to a reduced exposure of the central nervous system to leptin and ultimately propagate obesity. On the other hand, leptin has been shown to favor Th1-type activity, which ultimately decreases tryptophan levels. Tryptophan derivatives, serotonin and melatonin, induce satiety/satiation through several mechanisms. In this context, the antioxidant suppression of leptin release and Th1-type activity is beneficial to increase serotonin and melatonin levels. The molecules in the mechanism described in this review are highly integrated in the reward system, and have been implicated in the addiction behavior of obesity. Based on these facts, the involvement of antioxidant food supplements in the mechanisms of the reward-deficiency syndrome which perpetuates obesity will be discussed.