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      Effect of Nutrient and Micronutrient Intake on Chylomicron Production and Postprandial Lipemia

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          Abstract

          Postprandial lipemia, which is one of the main characteristics of the atherogenic dyslipidemia with fasting plasma hypertriglyceridemia, low high-density lipoprotein cholesterol and an increase of small and dense low-density lipoproteins is now considered a causal risk factor for atherosclerotic cardiovascular disease and all-cause mortality. Postprandial lipemia, which is mainly related to the increase in chylomicron production, is frequently elevated in individuals at high cardiovascular risk such as obese or overweight patients, type 2 diabetic patients and subjects with a metabolic syndrome who share an insulin resistant state. It is now well known that chylomicron production and thus postprandial lipemia is highly regulated by many factors such as endogenous factors: circulating factors such as hormones or free fatty acids, genetic variants, circadian rhythms, or exogenous factors: food components, dietary supplements and prescription drugs. In this review, we focused on the effect of nutrients, micronutrients and phytochemicals but also on food structure on chylomicron production and postprandial lipemia.

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          Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

          Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.
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            Overproduction of very low-density lipoproteins is the hallmark of the dyslipidemia in the metabolic syndrome.

            Insulin resistance is a key feature of the metabolic syndrome and often progresses to type 2 diabetes. Both insulin resistance and type 2 diabetes are characterized by dyslipidemia, which is an important and common risk factor for cardiovascular disease. Diabetic dyslipidemia is a cluster of potentially atherogenic lipid and lipoprotein abnormalities that are metabolically interrelated. Recent evidence suggests that a fundamental defect is an overproduction of large very low-density lipoprotein (VLDL) particles, which initiates a sequence of lipoprotein changes, resulting in higher levels of remnant particles, smaller LDL, and lower levels of high-density liporotein (HDL) cholesterol. These atherogenic lipid abnormalities precede the diagnosis of type 2 diabetes by several years, and it is thus important to elucidate the mechanisms involved in the overproduction of large VLDL particles. Here, we review the pathophysiology of VLDL biosynthesis and metabolism in the metabolic syndrome. We also review recent research investigating the relation between hepatic accumulation of lipids and insulin resistance, and sources of fatty acids for liver fat and VLDL biosynthesis. Finally, we briefly discuss current treatments for lipid management of dyslipidemia and potential future therapeutic targets.
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              Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review.

              To review systematically the evidence for an effect of long chain and shorter chain omega 3 fatty acids on total mortality, cardiovascular events, and cancer. Electronic databases searched to February 2002; authors contacted and bibliographies of randomised controlled trials (RCTs) checked to locate studies. Review of RCTs of omega 3 intake for (3) 6 months in adults (with or without risk factors for cardiovascular disease) with data on a relevant outcome. Cohort studies that estimated omega 3 intake and related this to clinical outcome during at least 6 months were also included. Application of inclusion criteria, data extraction, and quality assessments were performed independently in duplicate. Of 15,159 titles and abstracts assessed, 48 RCTs (36,913 participants) and 41 cohort studies were analysed. The trial results were inconsistent. The pooled estimate showed no strong evidence of reduced risk of total mortality (relative risk 0.87, 95% confidence interval 0.73 to 1.03) or combined cardiovascular events (0.95, 0.82 to 1.12) in participants taking additional omega 3 fats. The few studies at low risk of bias were more consistent, but they showed no effect of omega 3 on total mortality (0.98, 0.70 to 1.36) or cardiovascular events (1.09, 0.87 to 1.37). When data from the subgroup of studies of long chain omega 3 fats were analysed separately, total mortality (0.86, 0.70 to 1.04; 138 events) and cardiovascular events (0.93, 0.79 to 1.11) were not clearly reduced. Neither RCTs nor cohort studies suggested increased risk of cancer with a higher intake of omega 3 (trials: 1.07, 0.88 to 1.30; cohort studies: 1.02, 0.87 to 1.19), but clinically important harm could not be excluded. Long chain and shorter chain omega 3 fats do not have a clear effect on total mortality, combined cardiovascular events, or cancer.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                08 June 2019
                June 2019
                : 11
                : 6
                : 1299
                Affiliations
                [1 ]Aix-Marseille Université, Faculty of Medicine, 27 Boulevard Jean Moulin, 13385 Marseille, France; Charles.DESMARCHELIER@ 123456univ-amu.fr (C.D.); Patrick.BOREL@ 123456univ-amu.fr (P.B.); denis.lairon@ 123456orange.fr (D.L.); Marie.MARANINCHI@ 123456univ-amu.fr (M.M.)
                [2 ]C2VN (Center for Cardiovascular and Nutrition Research), Faculty of Medicine, 27 Boulevard Jean Moulin, 13385 Marseille, France
                [3 ]INSERM, Faculty of Medicine, 27 Boulevard Jean Moulin, 13385 Marseille, France
                [4 ]INRA, Faculty of Medicine, 27 Boulevard Jean Moulin, 13385 Marseille, France
                [5 ]APHM (Assistance Publique-Hôpitaux de Marseille), CHU Conception, 147 Boulevard Baille, 13385 Marseille, France
                Author notes
                [* ]Correspondence: RVALERO@ 123456mail.ap-hm.fr ; Tel.: +33-491-383-650
                Author information
                https://orcid.org/0000-0001-9970-7089
                https://orcid.org/0000-0001-9977-3238
                https://orcid.org/0000-0002-6645-1811
                https://orcid.org/0000-0002-2176-3280
                Article
                nutrients-11-01299
                10.3390/nu11061299
                6627366
                31181761
                fe723833-8f43-4270-8f3c-1e353d381446
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 30 April 2019
                : 04 June 2019
                Categories
                Review

                Nutrition & Dietetics
                carbohydrates,cardiovascular disease,cholesterol,fibers,food structure,lipids,polyphenols,proteins,triglycerides,vitamins

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