| Institution: | 1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada;2. Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada;3. Clinical Nutrition & Risk Factor Modification Center, St. Michael''s Hospital, Toronto, Ontario, Canada;4. Division of Endocrinology and Metabolism, St. Michael''s Hospital, Toronto, Ontario, Canada;5. College of Pharmacy and Nutrition, Division of Nutrition and Dietetics, University of Saskatchewan, Saskatoon, SK, Canada;6. Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada;1. Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan;2. Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan;1. Geriatric Unit, Department of Medicine, University of Padua, Italy;2. Community Hospital, Feltre, Italy;3. Warren Alpert Medical School of Brown University, Providence, RI, USA;1. Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy;2. Department of Biomolecular Sciences, University of Urbino “Carlo Bo”, Urbino, Italy;3. Department of Internal Medicine, University of Perugia, Italy;1. Laboratory of General Practice Research, IRCCS – Istituto di Ricerche Farmacologiche Mario Negri, Via Giuseppe La Masa, 19, 20156 Milan, Italy;2. Laboratory of Geriatric Neuropsychiatry, IRCCS – Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy;3. Diabetes Unit, “S. Maria della Misericordia” Hospital, Rovigo, Italy;4. Laboratory for Quality Assessment of Geriatric Therapies and Services, IRCCS – Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy;5. Regional Health Ministry, Lombardy Region, Milan, Italy;6. Diabetology Unit, Department of Internal Medicine, Ospedali Riuniti di Bergamo, Italy;1. Faculty of Nutrition, Federal University of Goiás (UFG), Goiânia, GO, Brazil;2. Labex Clinical Laboratory, Goiânia, GO, Brazil |
| Abstract: | Background and aimsNut consumption has been associated with decreased risk of coronary heart disease (CHD) and type 2 diabetes which has been largely attributed to their healthy fatty acid profile, yet this has not been ascertained. Therefore, we investigated the effect of nut consumption on serum fatty acid concentrations and how these relate to changes in markers of glycemic control and calculated CHD risk score in type 2 diabetes.Methods and results117 subjects with type 2 diabetes consumed one of three iso-energetic (mean 475 kcal/d) supplements for 12 weeks: 1. full-dose nuts (50–100 g/d); 2. half-dose nuts with half-dose muffins; and 3. full-dose muffins. In this secondary analysis, fatty acid concentrations in the phospholipid, triacylglycerol, free fatty acid, and cholesteryl ester fractions from fasting blood samples obtained at baseline and week 12 were analyzed using thin layer and gas chromatography. Full-dose nut supplementation significantly increased serum oleic acid (OA) and MUFAs compared to the control in the phospholipid fraction (OA: P = 0.036; MUFAs: P = 0.024). Inverse associations were found with changes in CHD risk versus changes in OA and MUFAs in the triacylglycerol (r = ?0.256, P = 0.011; r = ?0.228, P = 0.024, respectively) and phospholipid (r = ?0.278, P = 0.006; r = ?0.260, P = 0.010, respectively) fractions. In the cholesteryl ester fraction, change in MUFAs was inversely associated with markers of glycemic control (HbA1c: r = ?0.250, P = 0.013; fasting blood glucose: r = ?0.395, P < 0.0001).ConclusionNut consumption increased OA and MUFA content of the serum phospholipid fraction, which was inversely associated with CHD risk factors and 10-year CHD risk.Clinical Trial Reg. No.NCT00410722, clinicaltrials.gov. |
