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Kuopio, Finland

Torro nen R.,Institute of Public Health and Clinical Nutrition | Kolehmainen M.,Institute of Public Health and Clinical Nutrition | Sarkkinen E.,Institute of Public Health and Clinical Nutrition | Sarkkinen E.,Oy Foodfiles Ltd | And 4 more authors.
Journal of Nutrition | Year: 2013

Starch in white wheat bread (WB) induces high postprandial glucose and insulin responses. For rye bread (RB), the glucose response is similar, whereas the insulin response is lower. In vitro studies suggest that polyphenol-rich berries may reduce digestion and absorption of starch and thereby suppress postprandial glycemia, but the evidence in humans is limited. We investigated the effects of berries consumed with WB or RB on postprandial glucose and insulin responses. Healthy females (n = 13-20) participated in 3 randomized, controlled, crossover, 2-h meal studies. They consumedWB or RB, both equal to 50 g available starch, with 150 g whole-berry pur ée or the same amount of bread without berries as reference. In study 1, WB was served with strawberries, bilberries, or lingonberries and in study 2 with raspberries, cloudberries, or chokeberries. In study 3, WB or RB was served with a mixture of berries consisting of equal amounts of strawberries, bilberries, cranberries, and blackcurrants. Strawberries, bilberries, lingonberries, and chokeberries consumed with WB and the berry mixture consumed with WB or RB significantly reduced the postprandial insulin response. Only strawberries (36%) and the berry mixture (with WB, 38%; with RB, 19%) significantly improved the glycemic profile of the breads. These results suggest than when WB is consumed with berries, less insulin is needed for maintenance of normal or slightly improved postprandial glucose metabolism. The lower insulin response to RB compared with WB can also be further reduced by berries. ©2013 American Society for Nutrition. Source

Kohler A.,Ludwig Maximilians University of Munich | Sarkkinen E.,Oy Foodfiles Ltd | Sarkkinen E.,University of Eastern Finland | Tapola N.,Oy Foodfiles Ltd | Niskanen T.,Oy Foodfiles Ltd
Lipids in Health and Disease | Year: 2015

Background: Krill contains two marine omega-3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), mainly bound in phospholipids. Typical products from krill are krill oil and krill meal. Fish oils contain EPA and DHA predominantly bound in triglycerides. The difference in the chemical binding of EPA and DHA has been suggested to affect their bioavailability, but little is known on bioavailability of EPA and DHA in krill meal. This study was undertaken to compare the acute bioavailability of two krill products, krill oil and krill meal, with fish oil in healthy subjects. Methods: A randomized, single-dose, single-blind, cross-over, active-reference trial was conducted in 15 subjects, who ingested krill oil, krill meal and fish oil, each containing approx. 1 700 mg EPA and DHA. Fatty acid compositions of plasma triglycerides and phospholipids were measured repeatedly for 72 hours. The primary efficacy analysis was based on the 72 hour incremental area under the curve (iAUC) of EPA and DHA in plasma phospholipid fatty acids. Results: A larger iAUC for EPA and DHA in plasma phospholipid fatty acids was detected after krill oil (mean 89.08∈±∈33.36% × h) than after krill meal (mean 44.97∈±∈18.07% x h, p∈<∈0.001) or after fish oil (mean 59.15∈±∈22.22% × h, p=0.003). Mean iAUC's after krill meal and after fish oil were not different. A large inter-individual variability in response was observed. Conclusion: EPA and DHA in krill oil had a higher 72-hour bioavailability than in krill meal or fish oil. Our finding that bioavailabilities of EPA and DHA in krill meal and fish oil were not different argues against the interpretation that phospholipids are better absorbed than triglycerides. Longer-term studies using a parameter reflecting tissue fatty acid composition, like erythrocyte EPA plus DHA are needed. Trial registration: NCT02089165 © 2015 Köhler et al.; licensee BioMed Central. Source

Sarkkinen E.S.,Oy Foodfiles Ltd | Sarkkinen E.S.,University of Eastern Finland | Kastarinen M.J.,Central Hospital Central Finland | Kastarinen M.J.,University of Eastern Finland | And 7 more authors.
Nutrition Journal | Year: 2011

Background: High salt intake is linked to hypertension whereas a restriction of dietary salt lowers blood pressure (BP). Substituting potassium and/or magnesium salts for sodium chloride (NaCl) may enhance the feasibility of salt restriction and lower blood pressure beyond the sodium reduction alone. The aim of this study was to determine the feasibility and effect on blood pressure of replacing NaCl (Regular salt) with a novel mineral salt [50% sodium chloride and rich in potassium chloride (25%), magnesium ammonium potassium chloride, hydrate (25%)] (Smart Salt). Methods. A randomized, double-blind, placebo-controlled study was conducted with an intervention period of 8-weeks in subjects (n = 45) with systolic (S)BP 130-159 mmHg and/or diastolic (D)BP 85-99 mmHg. During the intervention period, subjects consumed processed foods salted with either NaCl or Smart Salt. The primary endpoint was the change in SBP. Secondary endpoints were changes in DBP, daily urine excretion of sodium (24-h dU-Na), potassium (dU-K) and magnesium (dU-Mg). Results: 24-h dU-Na decreased significantly in the Smart Salt group (-29.8 mmol; p = 0.012) and remained unchanged in the control group: resulting in a 3.3 g difference in NaCl intake between the groups. Replacement of NaCl with Smart Salt resulted in a significant reduction in SBP over 8 weeks (-7.5 mmHg; p = 0.016). SBP increased (+3.8 mmHg, p = 0.072) slightly in the Regular salt group. The difference in the change of SBP between study groups was significant (p < 0.002). Conclusions: The substitution of Smart Salt for Regular salt in subjects with high normal or mildly elevated BP resulted in a significant reduction in their daily sodium intake as well as a reduction in SBP. Trial Registration. ISRCTN: ISRCTN01739816. © 2011 Sarkkinen et al; licensee BioMed Central Ltd. Source

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