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      Dietary Acid Load and Cardiometabolic Risk Factors—A Narrative Review

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          Abstract

          The Western, diet rich in acidogenic foods (e.g., meat, fish and cheese) and low in alkaline foods (e.g., vegetables, fruits and legumes), is deemed to be a cause of endogenous acid production and elevated dietary acid load (DAL), which is a potential cause of metabolic acidosis. Multiple authors have suggested that such a dietary pattern increases the excretion of calcium and magnesium, as well as cortisol secretion. In addition, it is associated with decreased citrate excretion. All of these seem to increase blood pressure and insulin resistance and may contribute to the development of cardiometabolic disorders. However, there are inconsistencies in the results of the studies conducted. Therefore, this narrative literature review aims to present the outcomes of studies performed in recent years that investigated the association between DAL and the following cardiometabolic risk factors: blood pressure, hypertension, carbohydrate metabolism and lipid profile. Study outcomes are divided into (i) statistically significant positive association, (ii) statistically significant inverse association, and (iii) no statistically significant association.

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          Most cited references68

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          2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk

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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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              Impact of Dietary Fiber Consumption on Insulin Resistance and the Prevention of Type 2 Diabetes.

              Large prospective cohort studies consistently show associations of a high dietary fiber intake (>25 g/d in women and >38 g/d in men) with a 20-30% reduced risk of developing type 2 diabetes (T2D), after correction for confounders. It is less well recognized that these effects appear to be mainly driven by high intakes of whole grains and insoluble cereal fibers, which typically are nonviscous and do not relevantly influence postprandial glucose responses [i.e., glycemic index (GI)] or are strongly fermented by the gut microbiota in the colon. In contrast, a dietary focus on soluble, viscous, gel-forming, more readily fermentable fiber intakes derived from fruit and certain vegetables yields mixed results and generally does not appear to reduce T2D risk. Although disentangling types of fiber-rich foods and separating these from possible effects related to the GI is an obvious challenge, the common conclusion that key metabolic effects of high-fiber intake are explained by mechanisms that should mainly apply to the soluble, viscous type can be challenged. More recently, studies in humans and animal models focused on gaining mechanistic insights into why especially high-cereal-fiber (HCF) diets appear to improve insulin resistance (IR) and diabetes risk. Although effects of HCF diets on weight loss are only moderate and comparable to other types of dietary fibers, possible novel mechanisms have emerged, which include the prevention of the absorption of dietary protein and modulation of the amino acid metabolic signature. Here we provide an update of our previous review from 2008, with a focus on mechanistic insights of how HCF diets may improve IR and the risk of developing T2D.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                07 November 2020
                November 2020
                : 12
                : 11
                : 3419
                Affiliations
                Department of Clinical Dietetics, Faculty of Health Sciences, Medical University of Warsaw, E Ciołka Str. 27, 01-445 Warsaw, Poland; jostrowska@ 123456wum.edu.pl (J.O.); dorota.szostak-wegierek@ 123456wum.edu.pl (D.S.-W.)
                Author notes
                [* ]Correspondence: jjaniszewska@ 123456wum.edu.pl ; Tel.: +48-22-572-09-31
                Author information
                https://orcid.org/0000-0003-1040-8766
                Article
                nutrients-12-03419
                10.3390/nu12113419
                7695144
                33171835
                966e96ae-a846-4298-b07f-4c39c85173bb
                © 2020 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
                : 15 October 2020
                : 04 November 2020
                Categories
                Review

                Nutrition & Dietetics
                dietary acid load,hypertension,insulin resistance,type 2 diabetes mellitus,lipid profile

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