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Effect of different exercise intensities on the pancreas of animals with metabolic syndrome

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      Abstract

      Introduction

      Metabolic syndrome (MS) comprises several metabolic disorders that are risk factors for cardiovascular disease and has its source connected to the accumulation of visceral adipose tissue (VAT) and development of insulin resistance. Despite studies showing beneficial results of exercise on several risk factors for cardiovascular disease, studies evaluating the effects of different intensities of exercise training on the pancreas with experimental models are scarce.

      Methods

      In total, 20 Wistar rats were used, divided into four groups: control (C), metabolic syndrome (MS and without exercise), metabolic syndrome and practice of walking (MSWalk), and metabolic syndrome and practice of running (MSRun). The applied procedures were induction of MS by fructose in drinking water; experimental protocol of walking and running; weighing of body mass and VAT; sacrifice of animals with blood collection and removal of organs and processing of samples for light microscopy using the analysis of volume densities (Vv) of the studied structures.

      Results

      Running showed a reduction of VAT weight (−54%), triglyceride levels (−40%), Vv[islet] (−62%), Vv[islet.cells] (−22%), Vv[islet.insterstitial] (−44%), and Vv[acinar.insterstitial] (−24%) and an increase of Vv[acini] (+21%) and Vv[acinar.cells] (+22%). Regarding walking, we observed a decrease of VAT weight (−34%) and triglyceride levels (−27%), an increase of Vv[islet.cells] (+72%) and Vv[acinar.cells] (+7%), and a decrease of Vv[acini] (−4%) and Vv[acinar.insterstitial] (−16%) when compared with those in the MS group.

      Conclusion

      Our results suggest that the experimental model with low-intensity exercise (walking) seems to be more particularly recommended for preventing morphological and metabolic disorders occurring in the MS.

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      Most cited references 34

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      The metabolic syndrome.

      The metabolic syndrome is a common metabolic disorder that results from the increasing prevalence of obesity. The disorder is defined in various ways, but in the near future a new definition(s) will be applicable worldwide. The pathophysiology seems to be largely attributable to insulin resistance with excessive flux of fatty acids implicated. A proinflammatory state probably contributes to the syndrome. The increased risk for type 2 diabetes and cardiovascular disease demands therapeutic attention for those at high risk. The fundamental approach is weight reduction and increased physical activity; however, drug treatment could be appropriate for diabetes and cardiovascular disease risk reduction.
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        Abdominal obesity and metabolic syndrome.

        Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance or full-blown diabetes, and increased risk of developing cardiovascular disease. Proposed criteria for identifying patients with metabolic syndrome have contributed greatly to preventive medicine, but the value of metabolic syndrome as a scientific concept remains controversial. The presence of metabolic syndrome alone cannot predict global cardiovascular disease risk. But abdominal obesity - the most prevalent manifestation of metabolic syndrome - is a marker of 'dysfunctional adipose tissue', and is of central importance in clinical diagnosis. Better risk assessment algorithms are needed to quantify diabetes and cardiovascular disease risk on a global scale.
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          Combination of high-fat diet-fed and low-dose streptozotocin-treated rat: a model for type 2 diabetes and pharmacological screening.

          The objective of the present study was to develop a rat model that replicates the natural history and metabolic characteristics of human type 2 diabetes and is also suitable for pharmacological screening. Male Sprague-Dawley rats (160-180 g) were divided into two groups and fed with commercially available normal pellet diet (NPD) (12% calories as fat) or in-house prepared high-fat diet (HFD) (58% calories as fat), respectively, for a period of 2 weeks. The HFD-fed rats exhibited significant increase in body weight, basal plasma glucose (PGL), insulin (PI), triglycerides (PTG) and total cholesterol (PTC) levels as compared to NPD-fed control rats. Besides, the HFD rats showed significant reduction in glucose disappearance rate (K-value) on intravenous insulin glucose tolerance test (IVIGTT). Hyperinsulinemia together with reduced glucose disappearance rate (K-value) suggested that the feeding of HFD-induced insulin resistance in rats. After 2 weeks of dietary manipulation, a subset of the rats from both groups was injected intraperitoneally with low dose of streptozotocin (STZ) (35 mg kg(-1)). Insulin-resistant HFD-fed rats developed frank hyperglycemia upon STZ injection that, however, caused only mild elevation in PGL in NPD-fed rats. Though there was significant reduction in PI level after STZ injection in HFD rats, the reduction observed was only to a level that was comparable with NPD-fed control rats. In addition, the levels of PTG and PTC were further accentuated after STZ treatment in HFD-fed rats. In contrast, STZ (35 mg kg(-1), i.p.) failed to significantly alter PI, PTG and PTC levels in NPD-fed rats. Thus, these fat-fed/STZ-treated rats simulate natural disease progression and metabolic characteristics typical of individuals at increased risk of developing type 2 diabetes because of insulin resistance and obesity. Further, the fat-fed/STZ-treated rats were found to be sensitive for glucose lowering effects of insulin sensitizing (pioglitazone) as well as insulinotropic (glipizide) agents. Besides, the effect of pioglitazone and glipizide on the plasma lipid parameters (PTG and PTC) was shown in these diabetic rats. The present study represents that the combination of HFD-fed and low-dose STZ-treated rat serves as an alternative animal model for type 2 diabetes simulating the human syndrome that is also suitable for testing anti-diabetic agents for the treatment of type 2 diabetes.
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            Author and article information

            Affiliations
            [1 ]Laboratório de Estudos Morfoquantitativo e Imunohistoquímico, Universidade São Judas Tadeu, São Paulo, Brazil
            [2 ]Faculdade de Medicina do ABC, Santo André, São Paulo, Brazil
            [3 ]Departamento de Ciências Biológicas, Universidade Federal de São Paulo, São Paulo, Brazil
            [4 ]Instituto Dante Pazzanese de Cardiologia, São Paulo, Brazil
            Author notes
            Correspondence: Fernando Luiz Affonso Fonseca, Laboratório de Análises Clínicas da Faculdade de Medicina do ABC Av. Príncipe de Gales, 821. CEP: 09060-650; Santo André-SP, Brazil, Email profferfonseca@ 123456gmail.com
            Journal
            Diabetes Metab Syndr Obes
            Diabetes Metab Syndr Obes
            Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
            Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy
            Dove Medical Press
            1178-7007
            2015
            13 February 2015
            : 8
            : 115-120
            4335626 10.2147/DMSO.S74436 dmso-8-115
            © 2015 Amaral et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

            The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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            Original Research

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