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      The Association of Metabolic Syndrome and Urolithiasis

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          Abstract

          There has been an increasing prevalence of kidney stones over the last 2 decades worldwide. Many studies have indicated a possible association between metabolic syndrome and kidney stone disease, particularly in overweight and obese patients. Many different definitions of metabolic syndrome have been suggested by various organizations, although the definition by the International Diabetes Federation (IDF) is universally considered as the most acceptable definition. The IDF definition revolves around 4 core components: obesity, dyslipidemia, hypertension, and diabetes mellitus. Several hypotheses have been proposed to explain the pathophysiology of urolithiasis resulting from metabolic syndrome, amongst which are the insulin resistance and Randall's plaque hypothesis. Similarly the pathophysiology of calcium and uric acid stone formation has been investigated to determine a connection between the two conditions. Studies have found many factors contributing to urolithiasis in patients suffering from metabolic syndrome, out of which obesity, overweight, and sedentary lifestyles have been identified as major etiological factors. Primary and secondary prevention methods therefore tend to revolve mainly around lifestyle improvements, including dietary and other preventive measures.

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          Most cited references39

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          2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults

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            Dietary fat, insulin sensitivity and the metabolic syndrome.

            Insulin resistance is the pathogenetic link underlying the different metabolic abnormalities clustering in the metabolic syndrome. It can be induced by different environmental factors, including dietary habits. Consumption of energy-dense/high fat diets is strongly and positively associated with overweight that, in turn, deteriorates insulin sensitivity, particularly when the excess of body fat is located in abdominal region. Nevertheless the link between fat intake and overweight is not limited to the high-energy content of fatty foods; the ability to oxidize dietary fat is impaired in some individuals genetically predisposed to obesity. Insulin sensitivity is also affected by the quality of dietary fat, independently of its effects on body weight. Epidemiological evidence and intervention studies clearly show that in humans saturated fat significantly worsen insulin-resistance, while monounsaturated and polyunsaturated fatty acids improve it through modifications in the composition of cell membranes which reflect at least in part dietary fat composition. A recent multicenter study (KANWU) has shown that shifting from a diet rich in saturated fatty acids to one rich in monounsaturated fat improves insulin sensitivity in healthy people while a moderate alpha-3 fatty acids supplementation does not affect insulin sensitivity. There are also other features of the metabolic syndrome that are influenced by different types of fat, particularly blood pressure and plasma lipid levels. Most studies show that alpha-3 fatty acids reduce blood pressure in hypertensive but not in normotensive subjects while shifting from saturated to monounsaturated fat intake reduces diastolic blood pressure. In relation to lipid abnormalities alpha-3 fatty acids reduce plasma triglyceride levels but in parallel, increase LDL cholesterol. Substitution of unsaturated fat for saturated fat not only reduces LDL cholesterol but contributes also to reduce plasma triglycerides in insulin resistant individuals. In conclusion, there is evidence available in humans indicating that dietary fat quality influences insulin sensitivity and associated metabolic abnormalities. Therefore, prevention of the metabolic syndrome has to be targeted: (1) to correct overweight by reducing the energy density of the habitual diet (i.e., fat intake) and (2) to improve insulin sensitivity and associated metabolic abnormalities through a reduction of dietary saturated fat, partially replaced, when appropriate, by monounsaturated and polyunsaturated fats. Copyright 2004 Elsevier Ltd.
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              Fruit and vegetable intakes, C-reactive protein, and the metabolic syndrome.

              Limited data on the relation between the risk of the metabolic syndrome and fruit and vegetable intakes and inflammatory marker concentrations are available. We evaluated the relation between fruit and vegetable intakes and C-reactive protein (CRP) concentrations and the prevalence of the metabolic syndrome. Fruit and vegetable intakes were assessed with the use of a validated semiquantitative food-frequency questionnaire in a cross-sectional study of 486 Tehrani female teachers aged 40-60 y. Anthropometric measurements were made and blood pressure was assessed according to standard methods. Fasting blood samples were taken for biochemical measurements. The metabolic syndrome was defined on the basis of the National Cholesterol Education Program Adult Treatment Panel III guidelines. The reported mean daily fruit and vegetable intakes were 228 +/- 79 and 186 +/- 88 g/d, respectively. Both fruit and vegetable intakes were inversely associated with plasma CRP concentrations. After statistical control for age, body mass index, and waist circumference, mean plasma CRP concentrations across increasing quintile categories of fruit intakes were 1.94, 1.79, 1.65, 1.61, and 1.56 mg/L and of vegetable intakes were 2.03, 1.82, 1.58, 1.52, and 1.47 mg/L (P for trend < 0.01 for both). These inverse associations remained significant after additional control for other potential confounding variables and dietary factors. After control for potential confounders, persons in the highest quintile of fruit intake had a 34% (95% CI: 20%, 46%) lower and those in the highest quintile of vegetables intake had a 30% (95% CI: 16%, 39%) lower chance of having the metabolic syndrome than did those in the lowest quintiles. Higher intakes of fruit and vegetables are associated with a lower risk of the metabolic syndrome; the lower risk may be the result of lower CRP concentrations. These findings support current dietary recommendations to increase daily intakes of fruit and vegetables as a primary preventive measure against cardiovascular disease.
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                Author and article information

                Journal
                Int J Endocrinol
                Int J Endocrinol
                IJE
                International Journal of Endocrinology
                Hindawi Publishing Corporation
                1687-8337
                1687-8345
                2015
                22 March 2015
                : 2015
                : 570674
                Affiliations
                1Department of Urology, University Hospital Southampton NHS Trust, Southampton SO16 6YD, UK
                2Department of Biochemical Pathology, University Hospital Southampton NHS Trust, Southampton SO16 6YD, UK
                Author notes

                Academic Editor: Faustino R. Perez-Lopez

                Article
                10.1155/2015/570674
                4385647
                25873954
                833fb7e8-58ff-4cfc-8cf9-157558bc93d4
                Copyright © 2015 Yee V. Wong et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 December 2014
                : 21 February 2015
                : 24 February 2015
                Categories
                Review Article

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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