肥胖症与抑郁症:肥胖症与抑郁症:共同的联系和可能的目标

Srikanth Jitte, Saritha Keluth, Priya Bisht, Pranay Wal, Sanjiv Singh, Krishna Murti, Nitesh Kumar
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引用次数: 0

摘要

抑郁症是导致残疾的主要原因之一,它的长期表现会使代谢性疾病的治疗变得更加困难。肥胖与抑郁症的发作有关,而抑郁症与腹部肥胖和食物质量受损密切相关。本综述旨在研究肥胖与抑郁症之间可能存在的联系,以及消除这种联系的目标。撰写本稿件时参考了 Pubmed 和 Scopus 上的研究成果。肥胖与抑郁症有关,抑郁症患者更倾向于增加体重,从而导致不良的饮食决定和久坐不动的生活方式。脂肪因子包括脂肪连素、抵抗素和瘦素,是脂肪组织的分泌产物。目前正在对这些脂肪因子进行研究,以进一步了解肥胖与抑郁之间的内在联系。胃泌素是一种肠道激素,可控制肥胖和抑郁。此外,胃泌素水平升高会产生类似抗焦虑和抗抑郁的效果。肠道微生物群会影响人的新陈代谢功能,如从难以消化的营养成分中提取热量并储存在脂肪组织中,从而导致肥胖,肠道微生物可能会通过神经、内分泌和免疫信号系统等相互连接的途径与中枢神经系统相连。肠道细菌导致的大脑活动改变与抑郁症发作有关。人们普遍认为,包括多巴胺、血清素和去甲肾上腺素在内的单胺类物质具有控制情绪和食欲的功能。情绪信号会刺激下丘脑中的弓状神经元,这些神经元直接参与情绪调节和进食。肽类激素 GLP-1(胰高血糖素样肽-1)似乎对抑郁脑的神经炎症缺陷、神经发生、突触功能障碍和神经递质分泌差异具有医疗调节作用。肠道微生物群除了参与传统的消化道功能调节外,还可能在情绪和认知调节方面发挥作用。本综述探讨了肥胖相关的大脑低度轻度炎症会导致慢性抑郁和认知障碍的概念。
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Obesity and Depression: Common Link and Possible Targets.

Depression is among the main causes of disability, and its protracted manifestations could make it even harder to treat metabolic diseases. Obesity is linked to episodes of depression, which is closely correlated to abdominal adiposity and impaired food quality. The present review is aimed at studying possible links between obesity and depression along with targets to disrupt it. Research output in Pubmed and Scopus were referred for writing this manuscript. Obesity and depression are related, with the greater propensity of depressed people to gain weight, resulting in poor dietary decisions and a sedentary lifestyle. Adipokines, which include adiponectin, resistin, and leptin are secretory products of the adipose tissue. These adipokines are now being studied to learn more about the connection underlying obesity and depression. Ghrelin, a gut hormone, controls both obesity and depression. Additionally, elevated ghrelin levels result in anxiolytic and antidepressant-like effects. The gut microbiota influences the metabolic functionalities of a person, like caloric processing from indigestible nutritional compounds and storage in fatty tissue, that exposes an individual to obesity, and gut microorganisms might connect to the CNS through interconnecting pathways, including neurological, endocrine, and immunological signalling systems. The alteration of brain activity caused by gut bacteria has been related to depressive episodes. Monoamines, including dopamine, serotonin, and norepinephrine, have been widely believed to have a function in emotions and appetite control. Emotional signals stimulate arcuate neurons in the hypothalamus that are directly implicated in mood regulation and eating. The peptide hormone GLP-1(glucagon-like peptide- 1) seems to have a beneficial role as a medical regulator of defective neuroinflammation, neurogenesis, synaptic dysfunction, and neurotransmitter secretion discrepancy in the depressive brain. The gut microbiota might have its action in mood and cognition regulation, in addition to its traditional involvement in GI function regulation. This review addressed the concept that obesity-related low-grade mild inflammation in the brain contributes to chronic depression and cognitive impairments.

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