Human Nutrition Unit, Faculty of Medicine and Health Sciences, Institut d'Investigació Sanitària Pere Virgili, Rovira i Virgili University, Reus, Spain.
CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain.
Am J Clin Nutr. 2019 Jun 1;109(6):1738-1745. doi: 10.1093/ajcn/nqz048.
Telomere attrition may play an important role in the pathogenesis and severity of type 2 diabetes (T2D), increasing the probability of β cell senescence and leading to reduced cell mass and decreased insulin secretion. Nutrition and lifestyle are known factors modulating the aging process and insulin resistance/secretion, determining the risk of T2D.
The aim of this study was to evaluate the effects of pistachio intake on telomere length and other cellular aging-related parameters of glucose and insulin metabolism.
Forty-nine prediabetic subjects were included in a randomized crossover clinical trial. Subjects consumed a pistachio-supplemented diet (PD, 50 E% [energy percentage] carbohydrates and 33 E% fat, including 57 g pistachios/d) and an isocaloric control diet (CD, 55 E% carbohydrates and 30 E% fat) for 4 mo each, separated by a 2-wk washout period. DNA oxidation was evaluated by DNA damage (via 8-hydroxydeoxyguanosine). Leucocyte telomere length and gene expression related to either oxidation, telomere maintenance or glucose, and insulin metabolism were analyzed by multiplexed quantitative reverse transcriptase-polymerase chain reaction after the dietary intervention.
Compared with the CD, the PD reduced oxidative damage to DNA (mean: -3.5%; 95% CI: -8.07%, 1.05%; P = 0.009). Gene expression of 2 telomere-related genes (TERT and WRAP53) was significantly upregulated (164% and 53%) after the PD compared with the CD (P = 0.043 and P = 0.001, respectively). Interestingly, changes in TERT expression were negatively correlated to changes in fasting plasma glucose concentrations and in the homeostatic model assessment of insulin resistance.
Chronic pistachio consumption reduces oxidative damage to DNA and increases the gene expression of some telomere-associated genes. Lessening oxidative damage to DNA and telomerase expression through diet may represent an intriguing way to promote healthspan in humans, reversing certain deleterious metabolic consequences of prediabetes. This study was registered at clinicaltrials.gov as NCT01441921.
端粒损耗可能在 2 型糖尿病（T2D）的发病机制和严重程度中发挥重要作用，增加 β 细胞衰老的可能性，导致细胞数量减少和胰岛素分泌减少。营养和生活方式是调节衰老过程和胰岛素抵抗/分泌的已知因素，决定了 T2D 的风险。
本研究旨在评估开心果摄入对葡萄糖和胰岛素代谢相关端粒长度和其他细胞衰老参数的影响。
49 名糖尿病前期患者参与了一项随机交叉临床试验。受试者分别接受为期 4 个月的开心果补充饮食（PD，50%E[能量百分比]碳水化合物和 33%E 脂肪，包括 57 克开心果/天）和等热量对照饮食（CD，55%碳水化合物和 30%E 脂肪），两者之间间隔 2 周的洗脱期。通过 DNA 损伤（通过 8-羟基脱氧鸟苷）评估 DNA 氧化。在饮食干预后，通过多重定量逆转录-聚合酶链反应分析白细胞端粒长度以及与氧化、端粒维持或葡萄糖和胰岛素代谢相关的基因表达。
与 CD 相比，PD 降低了 DNA 氧化损伤（平均值：-3.5%；95%CI：-8.07%，1.05%；P=0.009）。与 CD 相比，PD 后与端粒相关的 2 个基因（TERT 和 WRAP53）的基因表达显著上调（164%和 53%）（P=0.043 和 P=0.001）。有趣的是，TERT 表达的变化与空腹血糖浓度和稳态模型评估的胰岛素抵抗呈负相关。
慢性开心果摄入可降低 DNA 的氧化损伤，并增加某些与端粒相关基因的表达。通过饮食减少 DNA 和端粒酶表达的氧化损伤可能代表一种促进人类健康寿命的有趣方法，逆转糖尿病前期的某些有害代谢后果。本研究在 clinicaltrials.gov 上注册为 NCT01441921。
