University of Cambridge Stroke Research Group, Neurology Unit, Department of Clinical Neurosciences, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK.
University of Cambridge Metabolic Research Laboratories and NIHR Cambridge Biomedical Research Centre, Welcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK.
Int J Obes (Lond). 2022 May;46(5):1059-1067. doi: 10.1038/s41366-021-00992-2. Epub 2022 Feb 10.
Obesity is a risk factor for both cardiovascular disease and dementia, but the mechanisms underlying this association are not fully understood. We examined associations between obesity, including estimates of central obesity using different modalities, with brain gray matter (GM) volume in the UK Biobank, a large population-based cohort study.
To determine relationships between obesity and the brain we used brain MRI, abdominal MRI, dual-energy X-ray absorptiometry (DXA), and bioelectric whole-body impedance. We determined whether obesity was associated with any change in brain gray matter (GM) and white matter (WM) volumes, and brain network efficiency derived from the structural connectome (wiring of the brain) as determined from diffusion-tensor MRI tractography. Using Waist-Hip Ratio (WHR), abdominal MRI and DXA we determined whether any associations were primarily with central rather than peripheral obesity, and whether associations were mediated by known cardiovascular risk factors. We analyzed brain MRI data from 15,634.
We found that central obesity, was associated with decreased GM volume (anthropometric data: p = 6.7 × 10, DXA: p = 8.3 × 10, abdominal MRI: p = 0.0006). Regional associations were found between central obesity and with specific GM subcortical nuclei (thalamus, caudate, pallidum, nucleus accumbens). In contrast, no associations were found with WM volume or structure, or brain network efficiency. The effects of central obesity on GM volume were not mediated by C-reactive protein or blood pressure, glucose, lipids.
Central body-fat distribution rather than the overall body-fat percentage is associated with gray matter changes in people with obesity. Further work is required to identify the factors that mediate the association between central obesity and GM atrophy.
肥胖是心血管疾病和痴呆的危险因素,但这种关联的机制尚不完全清楚。我们研究了肥胖症(包括使用不同模态评估的中心性肥胖)与英国生物库(一项大型基于人群的队列研究)中脑灰质(GM)体积之间的关联。
为了确定肥胖与大脑之间的关系,我们使用了脑 MRI、腹部 MRI、双能 X 射线吸收法(DXA)和生物电阻抗全身成像法。我们确定了肥胖是否与脑灰质(GM)和脑白质(WM)体积的任何变化有关,以及是否与从弥散张量 MRI 示踪术确定的结构连接组学(大脑的连接)得出的脑网络效率有关。我们使用腰臀比(WHR)、腹部 MRI 和 DXA 来确定这些关联是否主要与中心性肥胖而非外周性肥胖有关,以及这些关联是否通过已知的心血管风险因素来介导。我们分析了来自 15634 名参与者的脑 MRI 数据。
我们发现,中心性肥胖与 GM 体积减少有关(人体测量数据:p=6.7×10,DXA:p=8.3×10,腹部 MRI:p=0.0006)。在中心性肥胖与特定 GM 皮质下核(丘脑、尾状核、苍白球、伏隔核)之间发现了区域关联。相比之下,WM 体积或结构或脑网络效率与肥胖症之间没有关联。中心性肥胖对 GM 体积的影响不受 C 反应蛋白或血压、血糖、血脂的影响。
中心性体脂分布而不是体脂百分比与肥胖人群的 GM 变化有关。需要进一步的工作来确定介导中心性肥胖与 GM 萎缩之间关联的因素。