致动脉粥样硬化饮食和高蛋白/不饱和脂肪酸饮食对加速衰老模型 SAMP8 表型的不同影响

IF 3.2 Q2 CLINICAL NEUROLOGY Neurology International Pub Date : 2024-09-23 DOI:10.3390/neurolint16050080
Jesús Llanquinao, Claudia Jara, Daniela Cortés-Díaz, Bredford Kerr, Cheril Tapia-Rojas
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引用次数: 0

摘要

背景/目的:人们对衰老进行了广泛的研究,并越来越关注通过神经生物学方法对记忆损伤进行研究。线粒体功能障碍是衰老的一个标志,也是衰老表型的一个因素;因此,线粒体干预似乎至关重要。饮食是改变线粒体的生理学近似方法,可影响与年龄相关的表型。研究方法我们研究了两种由低碳水化合物和高脂肪组成的膳食,它们在蛋白质量和一次性脂肪类型上有所不同--致动脉粥样硬化膳食可可(高蛋白/高饱和脂肪/高胆固醇)和南海滩膳食(极高蛋白/高不饱和脂肪)--这两种膳食对 3 个月大的衰老加速小鼠模型(SAMP8)种子的氧化应激、线粒体状态和海马依赖性记忆的影响,为期 3 个月,以确定它们的促进或抗衰老作用。研究结果尽管可可饮食名声不好,但它能减少活性氧(ROS)含量,而不会影响能量状态和依赖海马的空间敏锐度。与 "南海滩饮食 "的有益影响相反,它却诱导了一种促衰老表型,增加了氧化损伤和 NMDA 的 NR2B 亚基水平,损害了能量和空间敏锐度。令人惊讶的是,尽管这两种饮食都出现了负面变化,但却导致了细微的记忆损伤,这表明代偿机制被激活,防止了更严重的认知能力下降。结论我们的研究结果表明,通常被认为是好的饮食可能对衰老的发生不利。此外,可能是由于非老龄动物大脑的可塑性,它们能补偿损伤,防止出现更严重的表型。然而,这些无声的变化可能会导致或增加高龄时出现病变的风险。
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Contrasting Effects of an Atherogenic Diet and High-Protein/Unsaturated Fatty Acids Diet on the Accelerated Aging Mouse Model SAMP8 Phenotype.

Background/Objectives: Aging has been extensively studied, with a growing interest in memory impairment by a neurobiological approach. Mitochondrial dysfunction is a hallmark of aging, contributing to the aging phenotype; therefore, mitochondrial interventions seem fundamental. The diet is a physiological approximation for modifying mitochondria, which could impact the age-related phenotype. Methods: We studied two diets with low-carbohydrate and high-fat compositions, differing in the amount of protein and the fat type disposable-the atherogenic diet Cocoa (high protein/high saturated fat/high cholesterol) and the South Beach diet (very high-protein/high-unsaturated fat)-on oxidative stress, mitochondrial state, and hippocampus-dependent memory in 3-month-old Senescence-Accelerated Mouse Model (SAMP8) seed over 3 months to determine their pro- or anti-aging effects. Results: Despite its bad reputation, the Cocoa diet reduces the reactive oxygen species (ROS) content without impacting the energy state and hippocampus-dependent spatial acuity. In contrast to the beneficial impact proposed for the South Beach diet, it induced a pro-aging phenotype, increasing oxidative damage and the levels of NR2B subunit of the NMDA, impairing energy and spatial acuity. Surprisingly, despite the negative changes observed with both diets, this led to subtle memory impairment, suggesting the activation of compensatory mechanisms preventing more severe cognitive decline. Conclusions: Our results demonstrated that diets usually considered good could be detrimental to the onset of aging. Also, probably due to the brain plasticity of non-aged animals, they compensate for the damage, preventing a more aggravated phenotype. Nevertheless, these silent changes could predispose or increase the risk of suffering pathologies at advanced age.

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来源期刊
Neurology International
Neurology International CLINICAL NEUROLOGY-
CiteScore
3.70
自引率
3.30%
发文量
69
审稿时长
11 weeks
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