Division of Food and Nutrition Science, Department of Life Sciences, Chalmers University of Technology, Gothenburg, Sweden.
Division of Food and Nutrition Science, Department of Life Sciences, Chalmers University of Technology, Gothenburg, Sweden.
Am J Clin Nutr. 2024 May;119(5):1280-1292. doi: 10.1016/j.ajcnut.2024.02.012. Epub 2024 Feb 23.
Consumption of processed red meat has been associated with increased risk of developing type 2 diabetes (T2D), but challenges in dietary assessment call for objective intake biomarkers.
This study aimed to investigate metabolite biomarkers of meat intake and their associations with T2D risk.
Fasting plasma samples were collected from a case-control study nested within Västerbotten Intervention Program (VIP) (214 females and 189 males) who developed T2D after a median follow-up of 7 years. Panels of biomarker candidates reflecting the consumption of total, processed, and unprocessed red meat and poultry were selected from the untargeted metabolomics data collected on the controls. Observed associations were then replicated in Swedish Mammography clinical subcohort in Uppsala (SMCC) (n = 4457 females). Replicated metabolites were assessed for potential association with T2D risk using multivariable conditional logistic regression in the discovery and Cox regression in the replication cohorts.
In total, 15 metabolites were associated with ≥1 meat group in both cohorts. Acylcarnitines 8:1, 8:2, 10:3, reflecting higher processed meat intake [r > 0.22, false discovery rate (FDR) < 0.001 for VIP and r > 0.05; FDR < 0.001 for SMCC) were consistently associated with higher T2D risk in both data sets. Conversely, lysophosphatidylcholine 17:1 and phosphatidylcholine (PC) 15:0/18:2 were associated with lower processed meat intake (r < -0.12; FDR < 0.023, for VIP and r < -0.05; FDR < 0.001, for SMCC) and with lower T2D risk in both data sets, except for PC 15:0/18:2, which was significant only in the VIP cohort. All associations were attenuated after adjustment for BMI (kg/m).
Consistent associations of biomarker candidates involved in lipid metabolism between higher processed red meat intake with higher T2D risk and between those reflecting lower intake with the lower risk may suggest a relationship between processed meat intake and higher T2D risk. However, attenuated associations after adjusting for BMI indicates that such a relationship may at least partly be mediated or confounded by BMI.
食用加工红肉与 2 型糖尿病（T2D）风险增加有关，但饮食评估中的挑战需要客观的摄入量生物标志物。
本研究旨在探讨肉类摄入量的代谢物生物标志物及其与 T2D 风险的关联。
从嵌套在 Västerbotten 干预计划（VIP）中的病例对照研究中采集空腹血浆样本（214 名女性和 189 名男性），这些人在中位随访 7 年后患上了 T2D。从对照组收集的非靶向代谢组学数据中选择反映总肉、加工肉和未加工肉和家禽摄入量的生物标志物候选物。然后在乌普萨拉的瑞典乳腺 X 线摄影临床亚队列（SMCC）（n=4457 名女性）中对观察到的关联进行复制。在发现队列中使用多变量条件逻辑回归和复制队列中的 Cox 回归，评估复制的代谢物与 T2D 风险的潜在关联。
总共，有 15 种代谢物与两个队列中的≥1 种肉类组相关。酰基肉碱 8:1、8:2、10:3，反映较高的加工肉摄入量[r>0.22，VIP 的错误发现率（FDR）<0.001 和 r>0.05；SMCC 的 FDR<0.001]与两个数据集的更高 T2D 风险一致相关。相反，溶血磷脂酰胆碱 17:1 和磷脂酰胆碱（PC）15:0/18:2 与较低的加工肉摄入量（r<−0.12；VIP 的 FDR<0.023 和 r<−0.05；SMCC 的 FDR<0.001）和两个数据集的较低 T2D 风险相关，除了 PC 15:0/18:2，它仅在 VIP 队列中显著。所有关联在调整 BMI（kg/m）后均减弱。
脂质代谢中涉及更高加工红肉摄入量与更高 T2D 风险之间以及反映更低摄入量与更低风险之间的生物标志物候选物的一致关联可能表明加工肉摄入量与更高 T2D 风险之间存在关系。然而，调整 BMI 后关联减弱表明，这种关系至少部分可能由 BMI 介导或混淆。
