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      Improved insulin sensitivity and lower postprandial triglyceride concentrations after cold-pressed turnip rapeseed oil compared to cream in patients with metabolic syndrome

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          Abstract

          Background

          The aim of this study was to compare acute effects of turnip rapeseed oil rich with mono- and polyunsaturated fatty acids and cream on postprandial triglyceride levels and post-glucose load measures of insulin sensitivity in population of men with metabolic syndrome.

          Methods

          This open-label balanced crossover study included 37 men with metabolic syndrome. They underwent an oral glucose-fat tolerance test where they ingested 75 g of glucose with either 240 mL of cream or 84 mL of turnip rapeseed oil depending on the study arm. Hourly postprandial blood samples were drawn up to 5 h after this oral glucose-fat tolerance test to determine the changes in triglyceride concentrations and to measure insulin sensitivity. Changes in insulin sensitivity were calculated with different insulin sensitivity indices (OGIS, Stumvoll, Gutt and McAuley scores) derived from measured insulin and glucose concentrations. The oral glucose-fat tolerance test was preceded by a period during which the participants consumed a daily portion of either 35 mL of turnip rapeseed oil or 37.5 g of butter depending on the study arm in addition to their habitual diets. Both dietary periods lasted from 6 to 8 weeks. After an 8-week wash-out period the subjects crossed over to the other study arm and underwent the same process with the other fat adjunct.

          Results

          The area under the curve for hourly triglyceride concentrations was 16% smaller after turnip rapeseed oil than after cream (13.86 [interquartile range 8.54] vs. 16.41 [9.09] mmol/l, p < 0.001). The insulin sensitivity markers of OGIS (324 [38.97] vs. 377 [68.38] p < 0.001), Stumvoll score (0.079 [0.029] vs. 0.085 [0.029], p = 0.038) and Gutt score (67.0 ± 2.78 vs. 78.8 ± 4.97 p = 0.001) were higher after turnip rapeseed oil period than after butter period. There was a non-significant change in the McAuley score.

          Conclusion

          Dietary turnip rapeseed oil improved postprandially measured insulin sensitivity and triglyceride concentrations compared to cream and butter. This provides a possible efficient dietary mean to treat cardiovascular risk factors.

          Trial registration ClinicalTrials.gov NCT01119690 (05-06-2010)

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          Most cited references32

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          Glucose clamp technique: a method for quantifying insulin secretion and resistance.

          Methods for the quantification of beta-cell sensitivity to glucose (hyperglycemic clamp technique) and of tissue sensitivity to insulin (euglycemic insulin clamp technique) are described. Hyperglycemic clamp technique. The plasma glucose concentration is acutely raised to 125 mg/dl above basal levels by a priming infusion of glucose. The desired hyperglycemic plateau is subsequently maintained by adjustment of a variable glucose infusion, based on the negative feedback principle. Because the plasma glucose concentration is held constant, the glucose infusion rate is an index of glucose metabolism. Under these conditions of constant hyperglycemia, the plasma insulin response is biphasic with an early burst of insulin release during the first 6 min followed by a gradually progressive increase in plasma insulin concentration. Euglycemic insulin clamp technique. The plasma insulin concentration is acutely raised and maintained at approximately 100 muU/ml by a prime-continuous infusion of insulin. The plasma glucose concentration is held constant at basal levels by a variable glucose infusion using the negative feedback principle. Under these steady-state conditions of euglycemia, the glucose infusion rate equals glucose uptake by all the tissues in the body and is therefore a measure of tissue sensitivity to exogenous insulin.
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            Metabolic syndrome with and without C-reactive protein as a predictor of coronary heart disease and diabetes in the West of Scotland Coronary Prevention Study.

            The National Cholesterol Education Program (NCEP) recently proposed a simple definition for metabolic syndrome. Information on the prospective association of this definition for coronary heart disease (CHD) and type 2 diabetes is currently limited. We used a modified NCEP definition with body mass index in place of waist circumference. Baseline assessments in the West of Scotland Coronary Prevention Study were available for 6447 men to predict CHD risk and for 5974 men to predict incident diabetes over 4.9 years of follow-up. Mean LDL cholesterol was similar but C-reactive protein was higher (P<0.0001) in the 26% of men with the syndrome compared with those without. Metabolic syndrome increased the risk for a CHD event [univariate hazard ratio (HR)=1.76 (95% CI, 1.44 to 2.15)] and for diabetes [univariate HR=3.50 (95% CI 2.51 to 4.90)]. Metabolic syndrome continued to predict CHD events (HR=1.30, 95% CI, 1.00 to 1.67, P=0.045) in a multivariate model incorporating conventional risk factors. Men with 4 or 5 features of the syndrome had a 3.7-fold increase in risk for CHD and a 24.5-fold increase for diabetes compared with men with none (both P<0.0001). C-reactive protein enhanced prognostic information for both outcomes. With pravastatin, men with the syndrome had similar risk reduction for CHD as compared with those without (HR, 0.73 and 0.69; pravastatin versus placebo). A modified NCEP metabolic syndrome definition predicts CHD events, and, more strikingly, new-onset diabetes, and thus helps identify individuals who may receive particular benefit from lifestyle measures to prevent these diseases.
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              Pathogenesis of NIDDM. A balanced overview.

              Non-insulin-dependent diabetes mellitus (NIDDM) results from an imbalance between insulin sensitivity and insulin secretion. Both longitudinal and cross-sectional studies have demonstrated that the earliest detectable abnormality in NIDDM is an impairment in the body's ability to respond to insulin. Because the pancreas is able to appropriately augment its secretion of insulin to offset the insulin resistance, glucose tolerance remains normal. With time, however, the beta-cell fails to maintain its high rate of insulin secretion and the relative insulinopenia (i.e., relative to the degree of insulin resistance) leads to the development of impaired glucose tolerance and eventually overt diabetes mellitus. The cause of pancreatic "exhaustion" remains unknown but may be related to the effect of glucose toxicity in a genetically predisposed beta-cell. Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered beta-cell function in NIDDM. Insulin resistance in NIDDM involves both hepatic and peripheral, muscle, tissues. In the postabsorptive state hepatic glucose output is normal or increased, despite the presence of fasting hyperinsulinemia, whereas the efficiency of tissue glucose uptake is reduced. In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. The accelerated rate of hepatic glucose output is due entirely to augmented gluconeogenesis. In muscle many cellular defects in insulin action have been described including impaired insulin-receptor tyrosine kinase activity, diminished glucose transport, and reduced glycogen synthase and pyruvate dehydrogenase. The abnormalities account for disturbances in the two major intracellular pathways of glucose disposal, glycogen synthesis, and glucose oxidation. In the earliest stages of NIDDM, the major defect involves the inability of insulin to promote glucose uptake and storage as glycogen. Other potential mechanisms that have been put forward to explain the insulin resistance, include increased lipid oxidation, altered skeletal muscle capillary density/fiber type/blood flow, impaired insulin transport across the vascular endothelium, increased amylin, calcitonin gene-related peptide levels, and glucose toxicity.
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                Author and article information

                Contributors
                harri.saarinen@fimnet.fi
                sari.husgafvel@phsotey.fi
                hanna.pohjantahti-maaroos@kuh.fi
                marja.wallenius45@gmail.com
                ari.palomaki@khshp.fi
                Journal
                Diabetol Metab Syndr
                Diabetol Metab Syndr
                Diabetology & Metabolic Syndrome
                BioMed Central (London )
                1758-5996
                4 May 2018
                4 May 2018
                2018
                : 10
                : 38
                Affiliations
                [1 ]ISNI 0000 0004 0628 3152, GRID grid.413739.b, Central Hospital of Kanta-Häme, ; Ahvenistontie 20, 13530 Hämeenlinna, Finland
                [2 ]Linnan Klinikka, Raatihuoneenkatu 10, 13100 Hämeenlinna, Finland
                [3 ]Central Hospital of Päijät-Häme, Keskussairaalankatu 7, 15850 Lahti, Finland
                [4 ]ISNI 0000 0004 0628 207X, GRID grid.410705.7, Heart Center, , Kuopio University Hospital, ; P.O. Box 1777, 70211 Kuopio, Finland
                [5 ]ISNI 0000 0001 2314 6254, GRID grid.5509.9, Faculty of Medicine and Life Sciences, , University of Tampere, ; 33014 Tampere, Finland
                Author information
                http://orcid.org/0000-0002-9807-6681
                Article
                340
                10.1186/s13098-018-0340-7
                5935965
                e23822c9-e3d6-4aa0-955f-7cce0fc38f40
                © The Author(s) 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 1 January 2018
                : 23 April 2018
                Categories
                Research
                Custom metadata
                © The Author(s) 2018

                Nutrition & Dietetics
                metabolic syndrome,polyunsaturated fatty acids,monounsaturated fatty acids,turnip rapeseed oil,insulin resistance,triglycerides,diabetes mellitus

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