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马尔默饮食与癌症队列中唾液淀粉酶基因座()拷贝数变异与淀粉摄入量对葡萄糖稳态的交互作用。

Interaction Effect Between Copy Number Variation in Salivary Amylase Locus () and Starch Intake on Glucose Homeostasis in the Malmö Diet and Cancer Cohort.

作者信息

Hamid Aida Koder, Andersson-Assarsson Johanna, Ericson Ulrika, Sonestedt Emily

机构信息

Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.

Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

出版信息

Front Nutr. 2021 Jan 7;7:598850. doi: 10.3389/fnut.2020.598850. eCollection 2020.

Abstract

Salivary amylase initiates the digestion of starch and it has been hypothesized that salivary amylase may play a role in the development of insulin resistance and type 2 diabetes. The aim was to examine the interaction between copy number variation in the salivary amylase gene and starch intake. We studied 3,624 adults without diabetes or elevated blood glucose in the Malmö Diet Cancer cohort. We assessed the associations and interactions between starch intake, copies and glucose homeostasis traits (i.e., fasting plasma glucose, insulin and HOMA-IR) and risk of type 2 diabetes over an average of 18 follow-up years. copy number was not associated with glucose, insulin or HOMA-IR. We observed a significant interaction between starch intake and copies on insulin and HOMA-IR after adjusting for potential confounders ( < 0.05). The inverse association between starch intake and insulin and HOMA-IR was stronger in the group with 10 or more copies ( < 0.001). In addition, we observed an inverse association between starch intake and type 2 diabetes in the group with 10 or more copies ( = 0.003), but not in the other groups. This cross-sectional observational study suggests that copy numbers might interact with starch intake on glucose homeostasis traits. Interventional studies are required to determine whether individuals with high copy numbers may benefit from a high starch intake.

摘要

唾液淀粉酶启动淀粉的消化,并且有假说认为唾液淀粉酶可能在胰岛素抵抗和2型糖尿病的发生发展中起作用。目的是研究唾液淀粉酶基因拷贝数变异与淀粉摄入量之间的相互作用。我们在马尔默饮食与癌症队列中研究了3624名无糖尿病或血糖升高的成年人。我们评估了淀粉摄入量、拷贝数与葡萄糖稳态特征(即空腹血糖、胰岛素和稳态模型评估胰岛素抵抗指数)之间的关联和相互作用,以及在平均18年的随访期间2型糖尿病的风险。拷贝数与血糖、胰岛素或稳态模型评估胰岛素抵抗指数无关。在调整潜在混杂因素后,我们观察到淀粉摄入量与拷贝数在胰岛素和稳态模型评估胰岛素抵抗指数方面存在显著的相互作用(P<0.05)。在拷贝数为10个或更多的组中,淀粉摄入量与胰岛素和稳态模型评估胰岛素抵抗指数之间的负相关更强(P<0.001)。此外,我们观察到在拷贝数为10个或更多的组中,淀粉摄入量与2型糖尿病之间存在负相关(P=0.003),但在其他组中未观察到。这项横断面观察性研究表明,拷贝数可能在葡萄糖稳态特征方面与淀粉摄入量相互作用。需要进行干预性研究来确定高拷贝数个体是否可能从高淀粉摄入量中获益。

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