Zheng Peiwen, Wang Fan, Li Hui, Chen Hanlu, Li Mengtong, Ma Haozheng, He Jue, Chen Li, Liu Yanlong, Xu Haiyun
School of Mental Health, Wenzhou Medical University, The Affiliated Kangning Hospital, Wenzhou, China.
Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China.
Endocr Connect. 2024 May 27;13(6). doi: 10.1530/EC-24-0016. Print 2024 Jun 1.
This study aimed to reveal associations between metabolic hormones in cerebral spinal fluid (CSF) and cigarette smoking-induced weight gain and to explore the underlying mechanism.
A total of 156 adult men were included, comprising active smokers and nonsmokers. In addition to demographic information and body mass index (BMI), plasma levels of ApoA1 and ApoB, high-density lipoprotein, low-density lipoprotein, cholesterol, triglyceride, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase in the participants were measured. Moreover, the metabolic hormones adiponectin, fibroblast growth factor 21 (FGF21), ghrelin, leptin, and orexin A, as well as the trace elements iron and zinc in CSF, were assessed.
Compared to nonsmokers, active smokers showed higher BMI, and elevated CSF levels of FGF21, Zn, and Fe, but decreased levels of metabolic hormones adiponectin, ghrelin, leptin, and orexin A. Negative correlations existed between CSF FGF21 and ghrelin, between CSF Zn and ghrelin, as well as between CSF Fe and orexin A in active smokers. Furthermore, elevated CSF FGF21 and Zn predicted ghrelin level decrease in the smokers.
These data relate smoking-induced weight gain to its neurotoxic effect on the neurons that synthesize metabolic hormones such as adiponectin, ghrelin, leptin, or orexin A in the brain, by disrupting mitochondrial function and causing oxidative stress in the neurons.
本研究旨在揭示脑脊液(CSF)中的代谢激素与吸烟导致的体重增加之间的关联,并探究其潜在机制。
共纳入156名成年男性,包括现吸烟者和非吸烟者。除人口统计学信息和体重指数(BMI)外,还测量了参与者血浆中的载脂蛋白A1和载脂蛋白B、高密度脂蛋白、低密度脂蛋白、胆固醇、甘油三酯、丙氨酸转氨酶、天冬氨酸转氨酶和γ-谷氨酰转移酶水平。此外,还评估了脑脊液中的代谢激素脂联素、成纤维细胞生长因子21(FGF21)、胃饥饿素、瘦素和食欲素A,以及微量元素铁和锌。
与非吸烟者相比,现吸烟者的BMI更高,脑脊液中FGF21、锌和铁的水平升高,但代谢激素脂联素、胃饥饿素、瘦素和食欲素A的水平降低。现吸烟者脑脊液中的FGF21与胃饥饿素之间、锌与胃饥饿素之间以及铁与食欲素A之间存在负相关。此外,脑脊液中FGF21和锌的升高预示着吸烟者胃饥饿素水平降低。
这些数据表明,吸烟导致体重增加与其对大脑中合成脂联素、胃饥饿素、瘦素或食欲素A等代谢激素的神经元产生神经毒性作用有关,其机制是破坏线粒体功能并在神经元中引起氧化应激。