Tasnim Nishat, Khan Nawsheen, Gupta Aditi, Neupane Purushottam, Mehta Aashna, Shah Shahtaj A, Dey Rohit C
North Bengal Medical College, Sirajgonj, Rajshahi, Bangladesh.
Caribbean Medical University, Curaçao, The Netherlands.
Ann Med Surg (Lond). 2023 May 4;85(6):2906-2915. doi: 10.1097/MS9.0000000000000766. eCollection 2023 Jun.
Obesity and cognitive decline including dementia and Alzheimer's Disease (AD) affect millions worldwide. Several studies have shown that obese individuals suffer from cognitive decline. Here, we suggest that adiponectin and leptin, protein hormones secreted by white adipose tissue explain the relationship between obesity and cognitive decline. We systematically searched PubMed and World Health Organization (WHO) websites with the keywords obesity and dementia and compiled literature that explains how adiponectin and leptin impact obesity and cognitive decline. Full-text, free-access articles on PubMed published after 2009 have been included. Whereas articles published before 2009, books, and reports were excluded. We concentrated on mechanisms via which adiponectin and leptin affect energy expenditure, fatty acid catabolism, satiety, hunger, Body Mass Index (BMI), neurogenesis, and brain structures that lead to the development of cognitive dysfunction. Moreover, we hypothesized that adiponectin and leptin hormones explain how obesity and dementia are connected. After compiling the research studies, we summarized that adiponectin and leptin negatively correlate to BMI. Adiponectin arbitrates energy expenditure and fatty acid catabolism to prevent obesity. In the presence of adiponectin, hippocampal cells proliferate, whereas neurogenesis is reduced in its absence. However, leptin prevents obesity by promoting satiety, reducing hunger, and increasing insulin sensitivity. It also has neuroprotective effects thus reducing the risk of developing cognitive decline. So, physical exercise, diet alteration, weight reduction, adiponectin, and leptin supplementation should be carried out to protect against obesity-induced cognitive decline. Therefore, further research studies should be done in this area.
肥胖以及包括痴呆症和阿尔茨海默病（AD）在内的认知衰退影响着全球数百万人。多项研究表明，肥胖个体存在认知衰退问题。在此，我们认为脂联素和瘦素这两种由白色脂肪组织分泌的蛋白质激素可以解释肥胖与认知衰退之间的关系。我们用关键词“肥胖症”和“痴呆症”系统地搜索了PubMed和世界卫生组织（WHO）网站，并汇编了解释脂联素和瘦素如何影响肥胖症和认知衰退的文献。纳入了2009年之后在PubMed上发表的全文、可免费获取的文章。而2009年之前发表的文章、书籍和报告则被排除在外。我们专注于脂联素和瘦素影响能量消耗、脂肪酸分解代谢、饱腹感、饥饿感、体重指数（BMI）、神经发生以及导致认知功能障碍发展的脑结构的机制。此外，我们假设脂联素和瘦素激素可以解释肥胖症和痴呆症是如何关联的。在汇编研究之后，我们总结出脂联素和瘦素与BMI呈负相关。脂联素调节能量消耗和脂肪酸分解代谢以预防肥胖。在有脂联素的情况下，海马体细胞会增殖，而在其缺乏时神经发生会减少。然而，瘦素通过促进饱腹感、减少饥饿感和提高胰岛素敏感性来预防肥胖。它还具有神经保护作用，从而降低发生认知衰退的风险。因此，应该进行体育锻炼、改变饮食、减轻体重、补充脂联素和瘦素以预防肥胖引起的认知衰退。所以，该领域应开展进一步的研究。
