Nutrient-Adjusted High-Fat Diet is Associated with Absence of Periepididymal Adipose Tissue Inflammation: Is there a Link with Adequate Micronutrient Levels?

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorYAMADA, Monica
dc.contributor.authorNORDE, Marina Maintinguer
dc.contributor.authorBORGES, Maria Carolina
dc.contributor.authorFUJII, Tatiane Mieko de Meneses
dc.contributor.authorJACOB, Patricia Silva
dc.contributor.authorFONSECA-ALANIZ, Miriam Helena
dc.contributor.authorALONSO-VALE, Maria Isabel Cardoso
dc.contributor.authorTORRES-LEAL, Francisco Leonardo
dc.contributor.authorTIRAPEGUI, Julio
dc.contributor.authorFOCK, Ricardo Ambrosio
dc.contributor.authorBORELLI, Primavera
dc.contributor.authorCURI, Rui
dc.contributor.authorROGERO, Marcelo Macedo
dc.date.accessioned2015-02-06T19:55:59Z
dc.date.available2015-02-06T19:55:59Z
dc.date.issued2013
dc.description.abstractThe aim of this study was to investigate the real impact of dietary lipids on metabolic and inflammatory response in rat white adipose tissue. Male healthy Wistar rats were fed ad libitum with a control diet (CON, n = 12) or with an adjusted high-fat diet (HFD, n = 12) for 12 weeks. Oral glucose and insulin tolerance tests were performed during the last week of the protocol. Plasma fatty acid, lipid profile, body adiposity, and carcass chemical composition were analyzed. Plasma concentration of leptin, adiponectin, C-reactive protein (CRP), TNF-alpha, IL-6, and monocyte chemotactic protein (MCP-1) was measured. Periepididymal adipose tissue was employed to evaluate TNF-a, MCP-1, and adiponectin gene expression as well as NF-kappa B pathway and AKT proteins. Isocaloric intake of the adjusted HFD did not induce hyperphagia, but promoted an increase in periepididymal (HFD = 2.94 +/- 0.77 vs. CON = 1.99 +/- 0.26 g/100 g body weight, p = 0.01) and retroperitoneal adiposity (FLFD = 3.11 +/- 0.81 vs. CON = 2.08 +/- 0.39 g/100 g body weight, p = 0.01) and total body lipid content (HFD = 105.3 +/- 20.8 vs. CON = 80.5 +/- 7.6 g carcass, p = 0.03). Compared with control rats, HFD rats developed glucose intolerance (p = 0.01), dyslipidemia (p = 0.02) and exhibited higher C-reactive protein levels in response to the HFD (HFD = 1002 168 vs. CON = 611 260 ng/mL, p = 0.01). The adjusted HFD did not affect adipokine gene expression or proteins involved in inflammatory signaling, but decreased AKT phosphorylation after insulin stimulation in periepididymal adipose tissue (p = 0.01). In this study, nutrient-adjusted HFD did not induce periepididymal adipose tissue inflammation in rats, suggesting that the composition of HFD differently modulates inflammation in rats, and adequate micronutrient levels may also influence inflammatory pathways.
dc.description.indexMEDLINE
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2009/54395 -0, 2010/14164-7]
dc.identifier.citationINTERNATIONAL JOURNAL FOR VITAMIN AND NUTRITION RESEARCH, v.83, n.5, p.299-310, 2013
dc.identifier.doi10.1024/0300-9831/a000172
dc.identifier.eissn1664-2821
dc.identifier.issn0300-9831
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/8780
dc.language.isoeng
dc.publisherVERLAG HANS HUBER
dc.relation.ispartofInternational Journal for Vitamin and Nutrition Research
dc.rightsrestrictedAccess
dc.rights.holderCopyright VERLAG HANS HUBER
dc.subjectobesity
dc.subjectinsulin resistance
dc.subjectinflammation
dc.subjectfatty acids
dc.subjectwhite adipose tissue
dc.subjecthigh-fat diet
dc.subjectrats
dc.subject.otherinsulin-resistance
dc.subject.otherisocaloric intake
dc.subject.otherskeletal-muscle
dc.subject.otherenergy-balance
dc.subject.otherobese rats
dc.subject.otherkappa-b
dc.subject.otherglucose
dc.subject.otherdeficiency
dc.subject.otherrodents
dc.subject.otherplasma
dc.subject.wosNutrition & Dietetics
dc.titleNutrient-Adjusted High-Fat Diet is Associated with Absence of Periepididymal Adipose Tissue Inflammation: Is there a Link with Adequate Micronutrient Levels?
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalYAMADA, Monica:Univ Sao Paulo, Sch Publ Hlth, Dept Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalNORDE, Marina Maintinguer:Univ Sao Paulo, Sch Publ Hlth, Dept Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalBORGES, Maria Carolina:Univ Sao Paulo, Sch Publ Hlth, Dept Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalFUJII, Tatiane Mieko de Meneses:Univ Sao Paulo, Sch Publ Hlth, Dept Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalJACOB, Patricia Silva:Univ Sao Paulo, Sch Publ Hlth, Dept Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalALONSO-VALE, Maria Isabel Cardoso:Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalTORRES-LEAL, Francisco Leonardo:Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalTIRAPEGUI, Julio:Univ Sao Paulo, Fac Pharmaceut Sci, Dept Food & Expt Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalFOCK, Ricardo Ambrosio:Univ Sao Paulo, Fac Pharmaceut Sci, Dept Clin & Toxicol Anal, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalBORELLI, Primavera:Univ Sao Paulo, Fac Pharmaceut Sci, Dept Clin & Toxicol Anal, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalCURI, Rui:Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-01246904 Sao Paulo, Brazil
hcfmusp.author.externalROGERO, Marcelo Macedo:Univ Sao Paulo, Sch Publ Hlth, Dept Nutr, BR-01246904 Sao Paulo, Brazil
hcfmusp.citation.scopus3
hcfmusp.contributor.author-fmusphcMIRIAM HELENA FONSECA ALANIZ
hcfmusp.description.beginpage299
hcfmusp.description.endpage310
hcfmusp.description.issue5
hcfmusp.description.volume83
hcfmusp.origemWOS
hcfmusp.origem.scopus2-s2.0-84910632216
hcfmusp.origem.wosWOS:000343186200005
hcfmusp.publisher.cityBERN 9
hcfmusp.publisher.countrySWITZERLAND
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