Castillo-Vazquez Selma Karime, Palacios-González Berenice, Vela-Amieva Marcela, Ibarra-González Isabel, Morales Ricardo, García-delaTorre Paola, Sánchez-García Sergio, García-Peña Carmen, Reyes-Chilpa Ricardo, Medina-Campos Raúl Hernán, Hernández-Pineda Jessica, Gomez-Verjan Juan Carlos, Rivero-Segura Nadia Alejandra
Dirección de Investigación, Instituto Nacional de Geriatría, Ciudad de México 10200, Mexico.
Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México, Ciudad Universitaria, Ciudad de México 04510, Mexico.
Metabolites. 2025 Jun 19;15(6):417. doi: 10.3390/metabo15060417.
BACKGROUND/OBJECTIVES: Insomnia has been widely associated with cognitive impairment (CI). However, the relationship between the two entities (insomnia and CI) is poorly understood. In this context, adults with insomnia show metabolic changes, including alterations in the catabolism of branched-chain amino acids, glycerophospholipids, and glutathione and glutamate biosynthesis. Nevertheless, aging itself induces metabolic changes that may be amplified by chronic diseases that compromise the health of the elderly. Therefore, in the present study we aim to characterise metabolomic profiles of insomnia and CI alone in order to address a significant gap in current research regarding the pathways through which insomnia may lead to CI in older persons.
In this study we perform a targeted metabolomics analysis (UPLC-MS) on 80 serum samples from the Cohort of Obesity, Sarcopenia, and Frailty of Older Mexican Adults (COSFOMA); these samples were classified into four groups (control, insomnia, CI, and insomnia + CI).
Our results show that insomnia increases the concentration of acylcarnitines (C10, C8, C14, C12:1, C18:1 and C18) as compared to CI group, while older persons with CI show a decrease the concentration of the acylcarnitines C16, C10 and C8. Finally, individuals with both conditions (insomnia + CI) show that only the concentration of the acylcarnitine C16 decreases compared to controls.
Taken together, our results shed light on the relevance of insomnia on lipid metabolism in older persons.
背景/目的：失眠与认知障碍（CI）密切相关。然而，人们对这两者（失眠和认知障碍）之间的关系了解甚少。在这种情况下，患有失眠症的成年人会出现代谢变化，包括支链氨基酸、甘油磷脂的分解代谢以及谷胱甘肽和谷氨酸生物合成的改变。然而，衰老本身会引发代谢变化，而慢性疾病可能会加剧这种变化，从而影响老年人的健康。因此，在本研究中，我们旨在单独描述失眠和认知障碍的代谢组学特征，以填补当前研究中关于失眠可能导致老年人认知障碍的途径方面的重大空白。
在本研究中，我们对来自墨西哥老年成年人肥胖、肌肉减少症和衰弱队列（COSFOMA）的80份血清样本进行了靶向代谢组学分析（超高效液相色谱-质谱联用，UPLC-MS）；这些样本被分为四组（对照组、失眠组、认知障碍组和失眠 + 认知障碍组）。
我们的结果表明，与认知障碍组相比，失眠会增加酰基肉碱（C10、C8、C14、C12:1、C18:1和C18）的浓度，而患有认知障碍的老年人酰基肉碱C16、C10和C8的浓度会降低。最后，同时患有这两种疾病（失眠 + 认知障碍）的个体表明，与对照组相比，只有酰基肉碱C16的浓度降低。
综上所述，我们的结果揭示了失眠对老年人脂质代谢的影响。
