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      Seaweeds as Preventive Agents for Cardiovascular Diseases: From Nutrients to Functional Foods

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          Being naturally enriched in key nutrients and in various health-promoting compounds, seaweeds represent promising candidates for the design of functional foods. Soluble dietary fibers, peptides, phlorotannins, lipids and minerals are macroalgae’s major compounds that can hold potential in high-value food products derived from macroalgae, including those directed to the cardiovascular-health promotion. This manuscript revises available reported data focusing the role of diet supplementation of macroalgae, or extracts enriched in bioactive compounds from macroalgae origin, in targeting modifiable markers of cardiovascular diseases (CVDs), like dyslipidemia, oxidative stress, vascular inflammation, hypertension, hypercoagulability and activation of the sympathetic and renin-angiotensin systems, among others. At last, the review also describes several products that have been formulated with the use of whole macroalgae or extracts, along with their claimed cardiovascular-associated benefits.

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          Inflammation and Atherosclerosis

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            Diabetes, Hypertension, and Cardiovascular Disease

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              Adiponectin: action, regulation and association to insulin sensitivity.

              Adiponectin is a novel adipocyte-specific protein, which, it has been suggested, plays a role in the development of insulin resistance and atherosclerosis. Although it circulates in high concentrations, adiponectin levels are lower in obese subjects than in lean subjects. Apart from negative correlations with measures of adiposity, adiponectin levels are also reduced in association with insulin resistance and type 2 diabetes. Visceral adiposity has been shown to be an independent negative predictor of adiponectin. Thus, most features of the metabolic syndrome's negative associations with adiponectin have been shown. Adiponectin levels seem to be reduced prior to the development of type 2 diabetes, and administration of adiponectin has been accompanied by lower plasma glucose levels as well as increased insulin sensitivity. Furthermore, reduced expression of adiponectin has been associated with some degree of insulin resistance in animal studies indicating a role for hypoadiponectinaemia in relation to insulin resistance. The primary mechanisms by which adiponectin enhance insulin sensitivity appears to be through increased fatty acid oxidation and inhibition of hepatic glucose production. Adiponectin levels are increased by thiazoledinedione treatment, and this effect might be important for the enhanced insulin sensitivity induced by thiazolidinediones. In contrast, adiponectin levels are reduced by pro-inflammatory cytokines especially tumour necrosis factor-alpha. In summary, adiponectin in addition to possible anti-inflammatory and anti-atherogenic effects appears to be an insulin enhancer, with potential as a new pharmacologic treatment modality of the metabolic syndrome and type 2 diabetes.

                Author and article information

                Role: Academic Editor
                Mar Drugs
                Mar Drugs
                Marine Drugs
                12 November 2015
                November 2015
                : 13
                : 11
                : 6838-6865
                [1 ]Department of Chemistry & QOPNA, University of Aveiro, Aveiro 3810-193, Portugal; E-Mails: anaseca@ 123456uac.pt (A.M.L.S.); diana@ 123456ua.pt (D.C.G.A.P.); artur.silva@ 123456ua.pt (A.M.S.S.)
                [2 ]Department of Diagnostic and Therapeutic Technologies, School of Health Sciences, Polytechnic Institute of Bragança, Bragança 5300-121, Portugal; E-Mail: oliviapereira@ 123456ipb.pt
                [3 ]Department of Technological Science and Development, University of Azores, Ponta Delgada 9501-801, Portugal
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: susanacardoso@ 123456ua.pt ; Tel.: +351-234-370-360; Fax: +351-234-370-084.
                © 2015 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 license ( http://creativecommons.org/licenses/by/4.0/).



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