metabolicsyndrome:epidemiology,pathophysiology,and

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Hindawi Publishing Corporation Journal of Nutrition and Metabolism Volume 2012, Article ID 584541, 1 page doi:10.1155/2012/584541 Editorial Metabolic Syndrome: Epidemiology, Pathophysiology, and Nutrition Intervention Isaias Dichi, 1 Andr´ ea Name Colado Sim˜ ao, 2 elio Vannucchi, 3 Rui Curi, 4 and Philip C. Calder 5 1 Department of Internal Medicine, University of Londrina, 86038-440 Londrina, PR, Brazil 2 Department of Pathology and Clinical Analysis, University of Londrina, 86038-440 Londrina, PR, Brazil 3 Department of Internal Medicine and Clinical Nutrition, University of S˜ ao Paulo (USP), 14049-900 Ribeir˜ ao Preto, SP, Brazil 4 Department of Biomedical Sciences and Physiology, University of S˜ ao Paulo (USP), S˜ ao Paulo, 14049-900 Ribeir˜ ao Preto, SP, Brazil 5 School of Medicine, University of Southampton, IDS Building, MP887 Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK Correspondence should be addressed to Isaias Dichi, [email protected] Received 7 March 2012; Accepted 7 March 2012 Copyright © 2012 Isaias Dichi 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. Metabolic syndrome (MetS) comprises pathological con- ditions that include insulin resistance, arterial hyperten- sion, visceral adiposity, and dyslipidemia, which favor the development of cardiovascular (CV) diseases. MetS is rising in developed and in developing countries, in male and female subjects, and in adults, adolescents, and children. Although obesity and insulin resistance comprise the leading causes of MetS, many other pathophysiological mechanisms, like proinflammatory adipocitokines, hyperuricemia, nitric oxide, and oxidative stress may contribute to the potential cardiovascular risk factors related to the syndrome. On the other hand, increases in anti-inflammatory adipocitokine, as adiponectin, and antioxidant mechanisms could give some CV protection. Nutritional intervention has been attempted to attenuate the detrimental or increase the beneficial mechanisms in order to decrease the potential risk of hypertension, glucose intolerance and diabetes, lipid disorders, and abdominal obesity, which are the main clinical features of MetS. In the present special issue on MetS, original research articles as well as review articles contribute to the continuing eorts to understand the pathophysiology underlying MetS and the development of strategies to treat these conditions through nutrition intervention. Several aspects of pathophysiology and nutrition inter- vention will be found in this special issue on MetS. Four articles evaluate the role of inflammation and adipocytokines on the syndrome. T. Di Chiara et al. have proposed in their review that hypoadiponectinemia is the most interesting new hypothesis to explain the pathophysiology of MetS; the review by Emanuela et al. also proposes inflammatory status as a link between obesity and MetS; L. Pala et al. in a case-control study assessed the relationship among sev- eral adipokines (adiponectin, retinol-binding protein 4, adipocyte fatty acid binding protein, and visfatin) and inci- dent CV diseases, and A. N. C. Sim˜ ao et al. evaluated several markers related to MetS and their association to adiponectin levels. All together, these papers reinforce the suggestion that hypoadiponectinemia may exert a fundamental role in the passage from visceral obesity to MetS. The review article from H. La Guardia et al. examines the link between MetS and chronic kidney disease, exploring both pathophysiology and intervention strategies. Nutritional intervention is also evaluated in A. Branchi’s et al. and M. Waling’s et al. studies. In the former, post- prandial changes in serum lipoproteins and blood glucose were evaluated in two dierent mixed meals (low-fat or low- carbohydrate diets). In the later, the eects after one-year family-based intervention were assessed on anthropometrics and metabolic markers in overweight and obese children. Isaias Dichi Andr´ ea Name Colado Sim˜ ao elio Vannucchi Rui Curi Philip C. Calder

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Page 1: MetabolicSyndrome:Epidemiology,Pathophysiology,and

Hindawi Publishing CorporationJournal of Nutrition and MetabolismVolume 2012, Article ID 584541, 1 pagedoi:10.1155/2012/584541

Editorial

Metabolic Syndrome: Epidemiology, Pathophysiology, andNutrition Intervention

Isaias Dichi,1 Andrea Name Colado Simao,2 Helio Vannucchi,3

Rui Curi,4 and Philip C. Calder5

1 Department of Internal Medicine, University of Londrina, 86038-440 Londrina, PR, Brazil2 Department of Pathology and Clinical Analysis, University of Londrina, 86038-440 Londrina, PR, Brazil3 Department of Internal Medicine and Clinical Nutrition, University of Sao Paulo (USP), 14049-900 Ribeirao Preto, SP, Brazil4 Department of Biomedical Sciences and Physiology, University of Sao Paulo (USP), Sao Paulo, 14049-900 Ribeirao Preto, SP, Brazil5 School of Medicine, University of Southampton, IDS Building, MP887 Southampton General Hospital, Tremona Road,Southampton SO16 6YD, UK

Correspondence should be addressed to Isaias Dichi, [email protected]

Received 7 March 2012; Accepted 7 March 2012

Copyright © 2012 Isaias Dichi 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.

Metabolic syndrome (MetS) comprises pathological con-ditions that include insulin resistance, arterial hyperten-sion, visceral adiposity, and dyslipidemia, which favor thedevelopment of cardiovascular (CV) diseases. MetS is risingin developed and in developing countries, in male andfemale subjects, and in adults, adolescents, and children.Although obesity and insulin resistance comprise the leadingcauses of MetS, many other pathophysiological mechanisms,like proinflammatory adipocitokines, hyperuricemia, nitricoxide, and oxidative stress may contribute to the potentialcardiovascular risk factors related to the syndrome. On theother hand, increases in anti-inflammatory adipocitokine,as adiponectin, and antioxidant mechanisms could givesome CV protection. Nutritional intervention has beenattempted to attenuate the detrimental or increase thebeneficial mechanisms in order to decrease the potentialrisk of hypertension, glucose intolerance and diabetes, lipiddisorders, and abdominal obesity, which are the main clinicalfeatures of MetS.

In the present special issue on MetS, original researcharticles as well as review articles contribute to the continuingefforts to understand the pathophysiology underlying MetSand the development of strategies to treat these conditionsthrough nutrition intervention.

Several aspects of pathophysiology and nutrition inter-vention will be found in this special issue on MetS. Fourarticles evaluate the role of inflammation and adipocytokineson the syndrome. T. Di Chiara et al. have proposed in their

review that hypoadiponectinemia is the most interestingnew hypothesis to explain the pathophysiology of MetS;the review by Emanuela et al. also proposes inflammatorystatus as a link between obesity and MetS; L. Pala et al. ina case-control study assessed the relationship among sev-eral adipokines (adiponectin, retinol-binding protein 4,adipocyte fatty acid binding protein, and visfatin) and inci-dent CV diseases, and A. N. C. Simao et al. evaluated severalmarkers related to MetS and their association to adiponectinlevels. All together, these papers reinforce the suggestion thathypoadiponectinemia may exert a fundamental role in thepassage from visceral obesity to MetS.

The review article from H. La Guardia et al. examinesthe link between MetS and chronic kidney disease, exploringboth pathophysiology and intervention strategies.

Nutritional intervention is also evaluated in A. Branchi’set al. and M. Waling’s et al. studies. In the former, post-prandial changes in serum lipoproteins and blood glucosewere evaluated in two different mixed meals (low-fat or low-carbohydrate diets). In the later, the effects after one-yearfamily-based intervention were assessed on anthropometricsand metabolic markers in overweight and obese children.

Isaias DichiAndrea Name Colado Simao

Helio VannucchiRui Curi

Philip C. Calder

Page 2: MetabolicSyndrome:Epidemiology,Pathophysiology,and

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