Jie Li1,2, Andrea J Glenn3,4,5, Qingling Yang1, Ding Ding1, Lingling Zheng1, Wei Bao6, Jeannette Beasley7, Erin LeBlanc8, Kenneth Lo9, JoAnn E Manson10, Lawrence Philips11, Lesley Tinker12, Simin Liu1,2,13. 1. Global Health Research Center, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. 2. Department of Epidemiology and Center for Global Cardiometabolic Health, School of Public Health, Brown University, Providence, RI. 3. Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada. 4. Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, St. Michael's Hospital, Toronto, Ontario, Canada. 5. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA. 6. Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China. 7. Division of General Internal Medicine and Clinical Innovation, New York University Langone Health, New York, NY. 8. Kaiser Permanente Center for Health Research, Portland, OR. 9. Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong Special Administrative Region, China. 10. Brigham and Women's Hospital, Harvard Medical School, and Harvard T.H. Chan School of Public Health, Boston, MA. 11. Division of Endocrinology, Emory University, Atlanta, GA. 12. Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA. 13. Departments of Surgery and Medicine, The Warren Alpert Medical School, Brown University, Providence, RI.
Abstract
OBJECTIVE: Whether and how dietary protein intake is linked to type 2 diabetes (T2D) remains unclear. The aim of this study was to investigate the associations of protein intake with development of T2D and the potential mediating roles of T2D biomarkers. RESEARCH DESIGN AND METHODS: We included 108,681 postmenopausal women without T2D at baseline from the Women's Health Initiative (WHI) (primary cohort) and 34,616 adults without T2D from the U.K. Biobank (UKB) (replication cohort). Cox proportional hazard models were used for estimation of protein-T2D associations. Mediation analysis was performed to assess the mediating roles of biomarkers in case-control studies nested in the WHI. RESULTS: In the WHI, 15,842 incident T2D cases were identified during a median follow-up of 15.8 years. Intake of animal protein was associated with increased T2D risk (hazard ratio in comparing the highest to the lowest quintile = 1.31 [95% CI 1.24-1.37]) and plant protein with decreased risk (0.82 [0.78-0.86]). Intakes of red meat, processed meat, poultry, and eggs were associated with increased T2D risk and whole grains with decreased risk. Findings from the UKB were similar. These findings were materially attenuated after additional adjustment for BMI. Substituting 5% energy from plant protein for animal protein was associated with 21% decreased T2D risk (0.79 [0.74-0.84]), which was mediated by levels of hs-CRP, interleukin-6, leptin, and SHBG. CONCLUSIONS: Findings from these two large prospective cohorts support the notion that substituting plant protein for animal protein may decrease T2D risk mainly by reducing obesity-related inflammation.
OBJECTIVE: Whether and how dietary protein intake is linked to type 2 diabetes (T2D) remains unclear. The aim of this study was to investigate the associations of protein intake with development of T2D and the potential mediating roles of T2D biomarkers. RESEARCH DESIGN AND METHODS: We included 108,681 postmenopausal women without T2D at baseline from the Women's Health Initiative (WHI) (primary cohort) and 34,616 adults without T2D from the U.K. Biobank (UKB) (replication cohort). Cox proportional hazard models were used for estimation of protein-T2D associations. Mediation analysis was performed to assess the mediating roles of biomarkers in case-control studies nested in the WHI. RESULTS: In the WHI, 15,842 incident T2D cases were identified during a median follow-up of 15.8 years. Intake of animal protein was associated with increased T2D risk (hazard ratio in comparing the highest to the lowest quintile = 1.31 [95% CI 1.24-1.37]) and plant protein with decreased risk (0.82 [0.78-0.86]). Intakes of red meat, processed meat, poultry, and eggs were associated with increased T2D risk and whole grains with decreased risk. Findings from the UKB were similar. These findings were materially attenuated after additional adjustment for BMI. Substituting 5% energy from plant protein for animal protein was associated with 21% decreased T2D risk (0.79 [0.74-0.84]), which was mediated by levels of hs-CRP, interleukin-6, leptin, and SHBG. CONCLUSIONS: Findings from these two large prospective cohorts support the notion that substituting plant protein for animal protein may decrease T2D risk mainly by reducing obesity-related inflammation.
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