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      Effect of nutritional counseling and long term isomaltulose based liquid formula (MHN-01) intake on metabolic syndrome

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          Abstract

          The isomaltulose based liquid formula (MHN-01), suppresses postprandial plasma glucose and insulin levels in healthy persons and patients with impaired glucose tolerance (IGT) or type 2 diabetes. MHN-01 intake as a part of breakfast also suppresses glucose and insulin levels after lunch, suggesting second meal effect. The objective of this study was to investigate the effects of nutritional counseling and long-term (24 weeks) MHN-01 ingestion on biomarkers of metabolic syndrome. Forty-one subjects with criteria of metabolic syndrome participated in this study composed with the control period (0–12 week) followed by nutritional counseling and the experimental period (12–36 week) followed by 200 kcal (837 kJ) of MHN-01 or dextrin-based standard balanced liquid formula (SBF) loading as a part of breakfast. In 16 of 41 subjects became to out of criteria for liquid formula loading study during control period (unqualified group). In the unqualified group, several biomarkers were improved. In experimental period, serum HbA 1c levels significantly increased in SBF group ( n = 12) but did not change in MHN-01 group ( n = 10). Thus, intake of 837 kJ MHN-01 as a part of breakfast may be effective for suppression of deteriorating glucose metabolism in metabolic syndrome.

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          Most cited references23

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          Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria.

          (2001)
          New diagnostic criteria for diabetes based on fasting blood glucose (FBG) level were approved by the American Diabetes Association. The impact of using FBG only has not been evaluated thoroughly. The fasting and the 2-hour glucose (2h-BG) criteria were compared with regard to the prediction of mortality. Existing baseline data on glucose level at fasting and 2 hours after a 75-g oral glucose tolerance test from 10 prospective European cohort studies including 15 388 men and 7126 women aged 30 to 89 years, with a median follow-up of 8.8 years, were analyzed. Hazards ratios for death from all causes, cardiovascular disease, coronary heart disease, and stroke were estimated. Multivariate Cox regression analyses showed that the inclusion of FBG did not add significant information on the prediction of 2h-BG alone (P>.10 for various causes), whereas the addition of 2h-BG to FBG criteria significantly improved the prediction (P<.001 for all causes and P<.005 for cardiovascular disease). In a model including FBG and 2h-BG simultaneously, hazards ratios (95% confidence intervals) in subjects with diabetes on 2h-BG were 1.73 (1.45-2.06) for all causes, 1.40 (1.02-1.92) for cardiovascular disease, 1.56 (1.03-2.36) for coronary heart disease, and 1.29 (0.66-2.54) for stroke mortality, compared with the normal 2h-BG group. Compared with the normal FBG group, the corresponding hazards ratios in subjects with diabetes on FBG were 1.21 (1.01-1.44), 1.20 (0.88-1.64), 1.09 (0.71-1.67), and 1.64 (0.88-3.07), respectively. The largest number of excess deaths was observed in subjects who had impaired glucose tolerance but normal FBG levels. The 2h-BG is a better predictor of deaths from all causes and cardiovascular disease than is FBG.
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            The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease.

            The glycemic index was proposed in 1981 as an alternative system for classifying carbohydrate-containing food. Since then, several hundred scientific articles and numerous popular diet books have been published on the topic. However, the clinical significance of the glycemic index remains the subject of debate. The purpose of this review is to examine the physiological effects of the glycemic index and the relevance of these effects in preventing and treating obesity, diabetes, and cardiovascular disease.
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              Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort.

              The aim of this study was to examine the relation between carbohydrate-related dietary factors, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. We examined cross-sectional associations between carbohydrate-related dietary factors, insulin resistance, and the prevalence of the metabolic syndrome in 2,834 subjects at the fifth examination (1991-1995) of the Framingham Offspring Study. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated using the following formula (fasting plasma insulin x plasma glucose)/22.5. The metabolic syndrome was defined using the National Cholesterol Education Program criteria. After adjustment for potential confounding variables, intakes of total dietary fiber, cereal fiber, fruit fiber, and whole grains were inversely associated, whereas glycemic index and glycemic load were positively associated with HOMA-IR. The prevalence of the metabolic syndrome was significantly lower among those in the highest quintile of cereal fiber (odds ratio [OR] 0.62; 95% CI 0.45-0.86) and whole-grain (0.67; 0.48-0.91) intakes relative to those in the lowest quintile category after adjustment for confounding lifestyle and dietary factors. Conversely, the prevalence of the metabolic syndrome was significantly higher among individuals in the highest relative to the lowest quintile category of glycemic index (1.41; 1.04-1.91). Total carbohydrate, dietary fiber, fruit fiber, vegetable fiber, legume fiber, glycemic load, and refined grain intakes were not associated with prevalence of the metabolic syndrome. Whole-grain intake, largely attributed to the cereal fiber, is inversely associated with HOMA-IR and a lower prevalence of the metabolic syndrome. Dietary glycemic index is positively associated with HOMA-IR and prevalence of the metabolic syndrome. Given that both a high cereal fiber content and lower glycemic index are attributes of whole-grain foods, recommendation to increase whole-grain intake may reduce the risk of developing the metabolic syndrome.
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                Author and article information

                Journal
                J Clin Biochem Nutr
                J Clin Biochem Nutr
                JCBN
                Journal of Clinical Biochemistry and Nutrition
                the Society for Free Radical Research Japan (Kyoto, Japan )
                0912-0009
                1880-5086
                September 2015
                6 August 2015
                : 57
                : 2
                : 140-144
                Affiliations
                [1 ]Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan
                [2 ]Department of Diabetes, Endocrinology and Nutrition, Kyoto University Graduate School of Medicine, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan
                [3 ]Department of Clinical Nutrition, School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan
                [4 ]Division of Endocrinology and Metabolism, Department of Medicine, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu, Shiga 520-2192, Japan
                [5 ]Department of Metabolism/Diabetes and Clinical Nutrition, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan
                [6 ]Division of Dietary Service, Nagasaki University Hospital, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan
                [7 ]Endocrinology and Metabolism, Tokushima University Medical and Dental Hospital, 2-50-1 Kuramoto-cho, Tokushima 770-8503, Japan
                [8 ]Director, Matsubara Mayflower Hospital, 944-55 Fujita, Kato, Hyogo 673-1462, Japan
                [9 ]Faculty of Statistic and Computer Science, College of Nursing Art and Science, University of Hyogo, 13-71 Kitaoji-cho, Akashi, Hyogo 673-8588, Japan
                [10 ]Food Science Research Labs., R&D Div., Meiji Co., Ltd., 540 Narita, Odawara, Kanagawa 250-0862, Japan
                Author notes
                *To whom correspondence should be addressed. E-mail: takeda.eiji@ 123456tokushima-u.ac.jp
                [†]

                Present address: Department of Nutrition and Life Sciences, Kanagawa Institute of Technology, 1030 Shimo-ogino, Atsugi, Kanagawa 243-0292, Japan

                Article
                jcbn14-132
                10.3164/jcbn.14-132
                4566023
                09f854ab-65ad-4cf7-bd68-2bb847dd98d4
                Copyright © 2015 JCBN

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 October 2014
                : 24 November 2014
                Categories
                Original Article

                Biochemistry
                postprandial hyperglycemia,insulin,diabetes,impaired glucose tolerance
                Biochemistry
                postprandial hyperglycemia, insulin, diabetes, impaired glucose tolerance

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