Neuroscience Research Center, Qom University of Medical Sciences, Qom, Iran.
Neuroscience Research Center, Guilan University of Medical Sciences, Rasht, Iran.
Clin Nutr ESPEN. 2020 Dec;40:376-382. doi: 10.1016/j.clnesp.2020.07.019. Epub 2020 Aug 24.
Alteration in the insulin signaling could contribute to the development of Alzheimer's disease (AD) through metabolic or inflammatory processes, adipokines could affect insulin dysregulation. This study aimed to investigate whether there is a correlation between serum adiponectin level alteration and insulin resistance with the presence and severity of AD, compared to normal controls.
This analytical observational study was conducted on 60 non-overweight and non-diabetic participants who were assigned to AD patients (n = 34) and healthy volunteers (n = 26). The diagnosis and severity of dementia were evaluated by the same protocol, and the Mini-Mental Score Exam (MMSE) questionnaire was utilized to collect the data. Moreover, adiponectin concentration, fasting blood sugar, and plasma insulin levels were measured using enzyme-linked immunosorbent assay. Furthermore, the homeostasis model assessment for insulin resistance (HOMA-IR) was utilized in this study.
The mean ages of the AD patients and control participants were 71.35 and 70.46, respectively. In addition, the mean values of the serum adiponectin level of the participants were 9660 and 12,730 ng/mL in control and AD groups, respectively (P ≤ 0.05). Additionally, the insulin resistance (IR) was 2.90 and 5.10 in the control and AD groups, respectively (P ≤ 0.05). According to the results, there was a significant positive correlation between serum adiponectin level and HOMA-IR in the AD group; however, no significant correlation was observed between serum adiponectin level and MMSE score in this group. The MMSE score of AD patients significantly decreased by 1.2 times with an increase in each score of the IR (P ≤ 0.05).
A significant direct positive correlation was observed between the serum adiponectin level and IR among the AD patients. However, a significant decrease in cognition levels was detected following an increase in IR scores of the AD patients.
胰岛素信号的改变可能通过代谢或炎症过程导致阿尔茨海默病（AD）的发生，脂肪因子也可能影响胰岛素失调。本研究旨在比较非超重和非糖尿病患者，探讨血清脂联素水平改变与胰岛素抵抗与 AD 的发生和严重程度之间的相关性。
本分析性观察研究纳入了 60 名非超重和非糖尿病患者，分为 AD 患者（n=34）和健康志愿者（n=26）。采用相同的方案评估痴呆的诊断和严重程度，使用 Mini-Mental 评分量表（MMSE）问卷收集数据。此外，使用酶联免疫吸附试验测量脂联素浓度、空腹血糖和血浆胰岛素水平。此外，本研究还使用了稳态模型评估胰岛素抵抗（HOMA-IR）。
AD 患者和对照组参与者的平均年龄分别为 71.35 岁和 70.46 岁。此外，对照组和 AD 组参与者血清脂联素水平的平均值分别为 9660 和 12730ng/mL（P≤0.05）。此外，对照组和 AD 组的胰岛素抵抗（IR）分别为 2.90 和 5.10（P≤0.05）。结果表明，AD 组血清脂联素水平与 HOMA-IR 呈显著正相关；然而，在该组中，血清脂联素水平与 MMSE 评分之间没有显著相关性。AD 患者的 MMSE 评分显著下降 1.2 倍，IR 评分每增加 1 分（P≤0.05）。
AD 患者血清脂联素水平与 IR 呈显著直接正相关。然而，AD 患者的认知水平显著下降，IR 评分增加。
