Obesity as a Neuroendocrine Reprogramming.

Obesity as a Neuroendocrine Reprogramming.
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肥胖是一种神经内分泌重编程。

DOI:
10.3390/medicina57010066
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发表时间:
2021-01-13
期刊:
Medicina (Kaunas, Lithuania)
影响因子:
--
通讯作者:
St-Amand J
St-Amand J
中科院分区:
其他
文献类型:
--
作者:
Ghanemi A;Yoshioka M;St-Amand J

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肥胖症代表了由于能量摄入和能量消耗之间的平衡被打破而导致过量脂肪积累的健康问题。阐明肥胖形成的分子和细胞途径仍然是理解肥胖和开发其治疗方法所面临的主要挑战。在这种情况下,这种观点提出肥胖作为选定的神经和内分泌模式的重编程器,以适应肥胖状态所代表的新的代谢失衡。事实上,在肥胖发展过程中,能量平衡转向增加能量储存,主要但不仅限于脂肪组织。肥胖所代表的这些新的代谢模式需要在神经内分泌系统的控制下通过不同的调节信号在不同的细胞和代谢水平上发生变化。因此,存在涉及不同机制的神经内分泌变化,例如神经可塑性和激素敏感性,因此,神经内分泌系统在代谢功能方面的改变与伴随肥胖诱导的代谢表型的变化相适应。这种内分泌重新编程可以解释为什么一旦肥胖建立,减肥就具有挑战性,因为这意味着违背新的内源性代谢参考,这是由能量代谢相关神经内分泌调节的新"设置"产生的。研究肥胖作为神经内分泌重编程器的分类概念可以优化我们对潜在机制的理解,重要的是,揭示肥胖分子发病机制的一些奥秘,以及将抗肥胖疗法的药理学研究集中在神经生物学突触可塑性和激素相互作用敏感性上。
Obesity represents a health problem resulting from a broken balance between energy intake and energy expenditure leading to excess fat accumulation. Elucidating molecular and cellular pathways beyond the establishment of obesity remains the main challenge facing the progress in understanding obesity and developing its treatment. Within this context, this opinion presents obesity as a reprogrammer of selected neurological and endocrine patterns in order to adapt to the new metabolic imbalance represented by obesity status. Indeed, during obesity development, the energy balance is shifted towards increased energy storage, mainly but not only, in adipose tissues. These new metabolic patterns that obesity represents require changes at different cellular and metabolic levels under the control of the neuroendocrine systems through different regulatory signals. Therefore, there are neuroendocrine changes involving diverse mechanisms, such as neuroplasticity and hormonal sensitivity, and, thus, the modifications in the neuroendocrine systems in terms of metabolic functions fit with the changes accompanying the obesity-induced metabolic phenotype. Such endocrine reprogramming can explain why it is challenging to lose weight once obesity is established, because it would mean to go against new endogenous metabolic references resulting from a new “setting” of energy metabolism-related neuroendocrine regulation. Investigating the concepts surrounding the classification of obesity as a neuroendocrine reprogrammer could optimize our understanding of the underlying mechanisms and, importantly, reveal some of the mysteries surrounding the molecular pathogenesis of obesity, as well as focusing the pharmacological search for antiobesity therapies on both neurobiology synaptic plasticity and hormonal interaction sensitivity.
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