Purpose <p>Dicarbonyls are reactive precursors of advanced glycation end-products. They are formed during food processing, and endogenously in humans during glycolysis and lipid peroxidation. Higher plasma dicarbonyls, particularly methylglyoxal (MGO), promote insulin resistance and type 2 diabetes, but the association between dietary dicarbonyls intake and type 2 diabetes is unknown. This study examined the associations between dietary dicarbonyls and type 2 diabetes incidence.</p> Methods <p>11,995 incident type 2 diabetes cases and a sub-cohort of 15,797 controls from the prospective multi-center European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct cohort were included. Intakes of three major dicarbonyls MGO, glyoxal [GO], and 3-deoxyglucosone [3-DG] were estimated at baseline using dietary questionnaires. Type 2 diabetes risk according to dietary dicarbonyl intake was estimated by multivariable-adjusted hazard ratios from Prentice-weighted Cox-regression analyses.</p> Results <p>Higher intakes of MGO (sample-specific mean intake 3.4 ± 1.3&#xa0;mg/d) and 3-DG (13.8 ± 10.5) were associated with lower incidence of type 2 diabetes (HR 0.92 [95% CI 0.90–0.95] for 1 SD higher MGO intake and 0.93 [0.90–0.95] for 1 SD higher 3-DG intake). No associations were observed for dietary GO.</p> Conclusion <p>Participants who consumed more dietary dicarbonyls MGO and 3-DG had a lower risk to develop type 2 diabetes. This protective association contrasts with the harmful effects on type 2 diabetes risk reported for endogenously formed dicarbonyls.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Higher intake of dietary dicarbonyl compounds is associated with lower incidence of type 2 diabetes: European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study

  • Kim Maasen,
  • Ana-Lucia Mayen,
  • Claudia Hana,
  • Viktoria Knaze,
  • Marleen M. J. van Greevenbroek,
  • Simone J. P. M. Eussen,
  • Charlotte Debras,
  • Coen D. A. Stehouwer,
  • Anne Tjønneland,
  • Cecilie Kyrø,
  • Daniel B. Ibsen,
  • Christina C. Dah,
  • Francesca Mancini,
  • Nasser Laouali,
  • Mariem Hajji,
  • Matthias B. Schulze,
  • Rashmita Bajracharya,
  • Verena Katzke,
  • Giovanna Masala,
  • Fabrizio Pasanisi,
  • Lorenzo Milani,
  • Valeria Pala,
  • Marta Farràs Mañé,
  • Conchi Moreno-Iribas,
  • Miguel Rodriguez-Barranco,
  • Sandra Milena Colorado Yohar,
  • Olatz Mokoroa,
  • Keren Papier,
  • Elisabete Weiderpass,
  • Heinz Freisling,
  • Nicholas J. Wareham,
  • Nita G. Forouhi,
  • Sofia Christakoudi,
  • Philippe Vangrieken,
  • Mazda Jenab,
  • Casper G. Schalkwijk

摘要

Purpose

Dicarbonyls are reactive precursors of advanced glycation end-products. They are formed during food processing, and endogenously in humans during glycolysis and lipid peroxidation. Higher plasma dicarbonyls, particularly methylglyoxal (MGO), promote insulin resistance and type 2 diabetes, but the association between dietary dicarbonyls intake and type 2 diabetes is unknown. This study examined the associations between dietary dicarbonyls and type 2 diabetes incidence.

Methods

11,995 incident type 2 diabetes cases and a sub-cohort of 15,797 controls from the prospective multi-center European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct cohort were included. Intakes of three major dicarbonyls MGO, glyoxal [GO], and 3-deoxyglucosone [3-DG] were estimated at baseline using dietary questionnaires. Type 2 diabetes risk according to dietary dicarbonyl intake was estimated by multivariable-adjusted hazard ratios from Prentice-weighted Cox-regression analyses.

Results

Higher intakes of MGO (sample-specific mean intake 3.4 ± 1.3 mg/d) and 3-DG (13.8 ± 10.5) were associated with lower incidence of type 2 diabetes (HR 0.92 [95% CI 0.90–0.95] for 1 SD higher MGO intake and 0.93 [0.90–0.95] for 1 SD higher 3-DG intake). No associations were observed for dietary GO.

Conclusion

Participants who consumed more dietary dicarbonyls MGO and 3-DG had a lower risk to develop type 2 diabetes. This protective association contrasts with the harmful effects on type 2 diabetes risk reported for endogenously formed dicarbonyls.