Fretts Amanda M, Follis Jack L, Nettleton Jennifer A, Lemaitre Rozenn N, Ngwa Julius S, Wojczynski Mary K, Kalafati Ioanna Panagiota, Varga Tibor V, Frazier-Wood Alexis C, Houston Denise K, Lahti Jari, Ericson Ulrika, van den Hooven Edith H, Mikkilä Vera, Kiefte-de Jong Jessica C, Mozaffarian Dariush, Rice Kenneth, Renström Frida, North Kari E, McKeown Nicola M, Feitosa Mary F, Kanoni Stavroula, Smith Caren E, Garcia Melissa E, Tiainen Anna-Maija, Sonestedt Emily, Manichaikul Ani, van Rooij Frank J A, Dimitriou Maria, Raitakari Olli, Pankow James S, Djoussé Luc, Province Michael A, Hu Frank B, Lai Chao-Qiang, Keller Margaux F, Perälä Mia-Maria, Rotter Jerome I, Hofman Albert, Graff Misa, Kähönen Mika, Mukamal Kenneth, Johansson Ingegerd, Ordovas Jose M, Liu Yongmei, Männistö Satu, Uitterlinden André G, Deloukas Panos, Seppälä Ilkka, Psaty Bruce M, Cupples L Adrienne, Borecki Ingrid B, Franks Paul W, Arnett Donna K, Nalls Mike A, Eriksson Johan G, Orho-Melander Marju, Franco Oscar H, Lehtimäki Terho, Dedoussis George V, Meigs James B, Siscovick David S
Departments of Epidemiology, Cardiovascular Health Research Unit, University of Washington, Seattle, WA;
Department of Mathematics, Computer Science, and Cooperative Engineering, University of St. Thomas, Houston, TX;
Am J Clin Nutr. 2015 Nov;102(5):1266-78. doi: 10.3945/ajcn.114.101238. Epub 2015 Sep 9.
Recent studies suggest that meat intake is associated with diabetes-related phenotypes. However, whether the associations of meat intake and glucose and insulin homeostasis are modified by genes related to glucose and insulin is unknown.
We investigated the associations of meat intake and the interaction of meat with genotype on fasting glucose and insulin concentrations in Caucasians free of diabetes mellitus.
Fourteen studies that are part of the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium participated in the analysis. Data were provided for up to 50,345 participants. Using linear regression within studies and a fixed-effects meta-analysis across studies, we examined 1) the associations of processed meat and unprocessed red meat intake with fasting glucose and insulin concentrations; and 2) the interactions of processed meat and unprocessed red meat with genetic risk score related to fasting glucose or insulin resistance on fasting glucose and insulin concentrations.
Processed meat was associated with higher fasting glucose, and unprocessed red meat was associated with both higher fasting glucose and fasting insulin concentrations after adjustment for potential confounders [not including body mass index (BMI)]. For every additional 50-g serving of processed meat per day, fasting glucose was 0.021 mmol/L (95% CI: 0.011, 0.030 mmol/L) higher. Every additional 100-g serving of unprocessed red meat per day was associated with a 0.037-mmol/L (95% CI: 0.023, 0.051-mmol/L) higher fasting glucose concentration and a 0.049-ln-pmol/L (95% CI: 0.035, 0.063-ln-pmol/L) higher fasting insulin concentration. After additional adjustment for BMI, observed associations were attenuated and no longer statistically significant. The association of processed meat and fasting insulin did not reach statistical significance after correction for multiple comparisons. Observed associations were not modified by genetic loci known to influence fasting glucose or insulin resistance.
The association of higher fasting glucose and insulin concentrations with meat consumption was not modified by an index of glucose- and insulin-related single-nucleotide polymorphisms. Six of the participating studies are registered at clinicaltrials.gov as NCT0000513 (Atherosclerosis Risk in Communities), NCT00149435 (Cardiovascular Health Study), NCT00005136 (Family Heart Study), NCT00005121 (Framingham Heart Study), NCT00083369 (Genetics of Lipid Lowering Drugs and Diet Network), and NCT00005487 (Multi-Ethnic Study of Atherosclerosis).
近期研究表明，肉类摄入量与糖尿病相关表型有关。然而，肉类摄入量与葡萄糖及胰岛素稳态之间的关联是否会受到与葡萄糖和胰岛素相关基因的影响尚不清楚。
我们调查了无糖尿病的白种人中肉类摄入量以及肉类与基因型的相互作用对空腹血糖和胰岛素浓度的影响。
参与基因组流行病学心脏与衰老研究队列联盟的14项研究参与了此次分析。提供了多达50345名参与者的数据。通过研究内的线性回归和跨研究的固定效应荟萃分析，我们研究了：1）加工肉类和未加工红肉摄入量与空腹血糖和胰岛素浓度之间的关联；2）加工肉类和未加工红肉与空腹血糖或胰岛素抵抗相关遗传风险评分在空腹血糖和胰岛素浓度方面的相互作用。
在对潜在混杂因素进行调整后（不包括体重指数），加工肉类与较高的空腹血糖相关，未加工红肉与较高的空腹血糖和空腹胰岛素浓度均相关。每天每额外摄入50克加工肉类，空腹血糖升高0.021毫摩尔/升（95%置信区间：0.011，0.030毫摩尔/升）。每天每额外摄入100克未加工红肉，空腹血糖浓度升高0.037毫摩尔/升（95%置信区间：0.023，0.051毫摩尔/升），空腹胰岛素浓度升高0.049纳摩尔/升（95%置信区间：0.035，0.063纳摩尔/升）。在对体重指数进行额外调整后，观察到的关联减弱且不再具有统计学意义。在进行多重比较校正后，加工肉类与空腹胰岛素之间的关联未达到统计学意义。观察到的关联未受到已知影响空腹血糖或胰岛素抵抗的基因位点的影响。
较高的空腹血糖和胰岛素浓度与肉类消费之间的关联未因葡萄糖和胰岛素相关单核苷酸多态性指数而改变。六项参与研究已在clinicaltrials.gov注册，注册号分别为NCT0000513（社区动脉粥样硬化风险研究）、NCT00149435（心血管健康研究）、NCT00005136（家族心脏研究）、NCT00005121（弗雷明汉心脏研究）、NCT00083369（降脂药物与饮食网络遗传学研究）和NCT00005487（动脉粥样硬化多族裔研究）。
