Please use this identifier to cite or link to this item: https://repositorio.udes.edu.co/handle/001/3260
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dc.contributor.authorLópez López, Josespa
dc.contributor.authorLópez Jaramillo, Patriciospa
dc.contributor.authorCamacho López, Paul Anthonyspa
dc.contributor.authorGómez Arbeláez, Diegospa
dc.contributor.authorCohen, Daniel Dylanspa
dc.date.accessioned2019-07-03T16:40:15Zspa
dc.date.available2019-07-03T16:40:15Zspa
dc.date.issued2015spa
dc.identifier.isbn0962-9351spa
dc.identifier.issn1466-1861spa
dc.identifier.urihttp://repositorio.udes.edu.co/handle/001/3260spa
dc.description9 p.spa
dc.description.abstractHypertension affects one billion individuals worldwide and is considered the leading cause of cardiovascular death, stroke, and myocardial infarction. This increase in the burden of hypertension and cardiovascular diseases (CVD) is principally driven by lifestyle changes such as increased hypercaloric diets and reduced physical activity producing an increase of obesity, insulin resistance, and low-grade inflammation. Visceral adipocytes are the principal source of proinflammatory cytokines and systemic inflammation participates in several steps in the development of CVD. However, maternal and infant malnutrition also persists as a major public health issue in low- to middle-income regions such as Latin America (LA). We propose that the increased rates of cardiovascular and metabolic diseases in these countries could be the result of the discrepancy between a restricted nutritional environment during fetal development and early life, and a nutritionally abundant environment during adulthood. Maternal undernutrition, which may manifest in lower birth weight offspring, appears to accentuate the relative risk of chronic disease at lower levels of adiposity. Therefore, LA populations may be more vulnerable to the pathogenic consequences of obesity than individuals with similar lifestyles in high-income countries, which may be mediated by higher levels of proinflammatory markers and lower levels of muscle mass and strength observed in low birth weight individuals.eng
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.relation.ispartofMediators of Inflammationeng
dc.rightsDerechos Reservados - Universidad de Santander, 2015spa
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/spa
dc.sourcehttps://www.hindawi.com/journals/mi/2015/710613/eng
dc.titleThe Link between Fetal Programming, Inflammation, Muscular Strength, and Blood Pressureeng
dc.typeArtículo de revistaspa
dc.identifier.doi10.1155/2015/710613spa
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.rights.creativecommonsAtribución-NoComercial 4.0 Internacional (CC BY-NC 4.0)spa
dc.subject.proposalFetal Programmingeng
dc.subject.proposalInflammationeng
dc.subject.proposalMuscular strengtheng
dc.subject.proposalBlood Pressureeng
dc.type.coarhttp://purl.org/coar/resource_type/c_6501spa
dc.type.driverinfo:eu-repo/semantics/articlespa
dc.type.versioninfo:eu-repo/semantics/publishedVersionspa
dc.type.contentTextspa
dc.type.redcolhttp://purl.org/redcol/resource_type/ARTspa
oaire.accessrightshttp://purl.org/coar/access_right/c_abf2spa
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85spa
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