Epidemiological data from the last decades point to an exponential growth in the number of obese people. Different behavioral factors, mainly associated with food consumption, appear to contribute significantly to its development. Concomitant with increased obesity rates, an increase in the consumption of fructose has been observed; therefore, fructose consumption has been implicated as an important obesogenic factor. However, changes in brain activity due to fructose consumption are possible, especially in relation to hypothalamic satiety mechanisms. In addition, the obese state may provide an environment of chronic inflammation and further contribute to the discontinuation of satiety mechanisms in the hypothalamus. We briefly review the intrinsic alterations to the increased adipose tissue, its connections with the hypothalamus in the control of energy signaling mechanisms and, consequently, the participation of fructose as a co‐adjuvant or trigger. Presenting the current context with clinical trials involving human and animal studies, we seek to contribute to a better understanding of the role of fructose in the progression of obesity.

中文翻译：

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果糖能否影响通过下丘脑改变介导的肥胖的发展？

过去几十年的流行病学数据表明，肥胖人数呈指数增长。主要与食物消费相关的不同行为因素似乎对其发展做出了重大贡献。随着肥胖率的增加，已经观察到果糖消耗量的增加；因此，果糖消耗被认为是一个重要的致肥胖因素。然而，由于果糖消耗而导致大脑活动的变化是可能的，特别是与下丘脑饱腹感机制有关。此外，肥胖状态可能会提供慢性炎症的环境，并进一步导致下丘脑饱腹感机制的中断。我们简要回顾了增加的脂肪组织的内在改变，它与下丘脑在能量信号机制的控制中的联系，因此，果糖作为辅助佐剂或触发器的参与。通过涉及人类和动物研究的临床试验呈现当前背景，我们寻求有助于更好地了解果糖在肥胖进展中的作用。