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      Exercise training prevents diastolic dysfunction induced by metabolic syndrome in rats

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          Abstract

          OBJECTIVE:

          High fructose consumption contributes to the incidence of metabolic syndrome and, consequently, to cardiovascular outcomes. We investigated whether exercise training prevents high fructose diet-induced metabolic and cardiac morphofunctional alterations.

          METHODS:

          Wistar rats receiving fructose overload (F) in drinking water (100 g/l) were concomitantly trained on a treadmill (FT) for 10 weeks or kept sedentary. These rats were compared with a control group (C). Obesity was evaluated by the Lee index, and glycemia and insulin tolerance tests constituted the metabolic evaluation. Blood pressure was measured directly (Windaq, 2 kHz), and echocardiography was performed to determine left ventricular morphology and function. Statistical significance was determined by one-way ANOVA, with significance set at p<0.05.

          RESULTS:

          Fructose overload induced a metabolic syndrome state, as confirmed by insulin resistance (F: 3.6±0.2 vs. C: 4.5±0.2 mg/dl/min), hypertension (mean blood pressure, F: 118±3 vs. C: 104±4 mmHg) and obesity (F: 0.31±0.001 vs. C: 0.29±0.001 g/mm). Interestingly, fructose overload rats also exhibited diastolic dysfunction. Exercise training performed during the period of high fructose intake eliminated all of these derangements. The improvements in metabolic parameters were correlated with the maintenance of diastolic function.

          CONCLUSION:

          The role of exercise training in the prevention of metabolic and hemodynamic parameter alterations is of great importance in decreasing the cardiac morbidity and mortality related to metabolic syndrome.

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          Most cited references90

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          Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

          Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.
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            Fructose, weight gain, and the insulin resistance syndrome.

            This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic beta cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.
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              Fructose, insulin resistance, and metabolic dyslipidemia

              Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.
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                Author and article information

                Journal
                Clinics (Sao Paulo)
                Clinics (Sao Paulo)
                Clinics
                Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
                1807-5932
                1980-5322
                July 2012
                : 67
                : 7
                : 815-820
                Affiliations
                [I ]Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, Hypertension Unit, Heart Institute (InCor), Sao Paulo/SP, Brazil.
                [II ]Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, Cardiomiopathy Unit, Heart Institute (InCor), Sao Paulo/SP, Brazil.
                [III ]Human Movement Laboratory, Sao Judas Tadeu University, Sao Paulo/SP, Brazil.
                [IV ]Laboratory of Translational Physiology, Nove de Julho University, Sao Paulo Sao Paulo/SP, Brazil.
                [V ]Center of Biological Sciences and Health, Mackenzie Presbyterian University, Sao Paulo/SP, Brazil.
                Author notes

                Mostarda C performed and coordinated the experiments. Moraes-Silva IC and Machi JF participated in the data discussion and helped draft the manuscript. Salemi VM performed the echocardiography evaluation. Rodrigues B, De Angelis K and Farah VM participated in the design and data discussion and helped draft the manuscript. Irigoyen MC conceived the study and participated in its design and coordination.

                E-mail: hipirigoyen@ 123456incor.usp.br Tel.: 55 11 2661-5327
                Article
                cln_67p815
                10.6061/clinics/2012(07)18
                3400174
                22892928
                aec42dea-a40a-46b7-8b5b-980159ebe92a
                Copyright © 2012 Hospital das Clínicas da FMUSP

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 December 2011
                : 5 February 2012
                : 14 March 2012
                Page count
                Pages: 6
                Categories
                Basic Research

                Medicine
                insulin resistance,diastolic function,metabolic syndrome,cardiac hypertrophy,exercise training

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