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Obesity and aging: Molecular mechanisms and therapeutic approaches.

肥胖和衰老: 分子机制和治疗方法。

  • 影响因子:0
  • DOI:10.1016/j.arr.2021.101268
  • 作者列表:"Santos AL","Sinha S
  • 发表时间:2021-05-01
Abstract

:The epidemic of obesity is a major challenge for health policymakers due to its far-reaching effects on population health and potentially overwhelming financial burden on healthcare systems. Obesity is associated with an increased risk of developing acute and chronic diseases, including hypertension, stroke, myocardial infarction, cardiovascular disease, diabetes, and cancer. Interestingly, the metabolic dysregulation associated with obesity is similar to that observed in normal aging, and substantial evidence suggests the potential of obesity to accelerate aging. Therefore, understanding the mechanism of fat tissue dysfunction in obesity could provide insights into the processes that contribute to the metabolic dysfunction associated with the aging process. Here, we review the molecular and cellular mechanisms underlying both obesity and aging, and how obesity and aging can predispose individuals to chronic health complications. The potential of lifestyle and pharmacological interventions to counter obesity and obesity-related pathologies, as well as aging, is also addressed.

摘要

: 肥胖的流行是卫生政策制定者面临的主要挑战,因为它对人口健康产生了深远的影响,并可能给医疗保健系统带来巨大的财政负担。肥胖与发展急性和慢性疾病的风险增加有关,包括高血压、中风、心肌梗塞、心血管疾病、糖尿病和癌症。有趣的是,与肥胖相关的代谢失调与正常衰老中观察到的相似,大量证据表明肥胖可能加速衰老。因此,了解肥胖中脂肪组织功能障碍的机制可以提供有助于与衰老过程相关的代谢功能障碍的过程的见解。在这里,我们回顾了肥胖和衰老的分子和细胞机制,以及肥胖和衰老如何使个体易患慢性健康并发症。还讨论了生活方式和药物干预对对抗肥胖和肥胖相关病理以及衰老的潜力。

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影响因子:2.68
发表时间:2021-02-01
DOI:10.1080/14656566.2020.1814255
作者列表:["Sawada H","Oeda T","Kohsaka M","Tomita S","Umemura A","Park K","Yamamoto K","Kiyohara K"]

METHODS:BACKGROUND:Cholinergic neurotransmission regulates neuroinflammation in Parkinson disease (PD). RESEARCH DESIGN AND METHODS:The authors conducted a delayed-start study of donepezil for cognitive decline in non-demented PD patients. The study consisted of a 96-week randomized placebo-controlled double-blind phase 1, followed by a 24-week donepezil extension phase 2. The primary outcome measure was a change in the Mini-Mental State Examination (MMSE) at week 120. RESULTS:A total of 98 patients were randomly allocated to the early-start (donepezil-to-donepezil) and delayed-start (placebo-to-donepezil) groups. Mean (SD) of the baseline MMSE was 27.6 (2.0) and 28.0 (2.1), respectively. MMSE change at week 120 was better in the early-start group than in the delayed-start group, but the difference was not significant. The MMSE declined in apolipoprotein ε4 carriers, but not in non-carriers, and the factor interaction (intervention × ε4 genotype) was highly significant (P < 0.001). Analyzed with the interaction, the difference was significant (group difference 1.95 [0.33 to 3.57], P = 0.018). The MMSE decline slope in phase 1 was significantly better in the early-start group than in the delayed-start group (P = 0.048). CONCLUSIONS:Cognitive function deteriorated in ε4 carriers, but not in non-carriers, and early-start donepezil may postpone cognitive decline in the former.

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影响因子:2.06
发表时间:2021-03-24
DOI:10.1007/s11033-021-06299-9
作者列表:["Louvrier A","Terranova L","Meyer C","Meyer F","Euvrard E","Kroemer M","Rolin G"]

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