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

Nenhuma Miniatura disponível
Citações na Scopus
3
Tipo de produção
article
Data de publicação
2013
DOI
Scopus
Web of Science
Título da Revista
ISSN da Revista
Título do Volume
Editora
VERLAG HANS HUBER
Autores
YAMADA, Monica
NORDE, Marina Maintinguer
BORGES, Maria Carolina
FUJII, Tatiane Mieko de Meneses
JACOB, Patricia Silva
ALONSO-VALE, Maria Isabel Cardoso
TORRES-LEAL, Francisco Leonardo
TIRAPEGUI, Julio
FOCK, Ricardo Ambrosio
Citação
INTERNATIONAL JOURNAL FOR VITAMIN AND NUTRITION RESEARCH, v.83, n.5, p.299-310, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
The 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.
Palavras-chave
obesity, insulin resistance, inflammation, fatty acids, white adipose tissue, high-fat diet, rats
URI
https://observatorio.fm.usp.br/handle/OPI/8780
Referências
  1. [Anonymous], 2010, GLOB STAT REP NONC D
  2. Arcari DP, 2009, OBESITY, V17, P2127, DOI 10.1038/oby.2009.158
  3. Atzmon G, 2002, HORM METAB RES, V34, P622, DOI 10.1055/s-2002-38250
  4. BONORA E, 1989, J CLIN ENDOCR METAB, V68, P374
  5. Borges MC, 2011, NUTRITION, V27, P399, DOI 10.1016/j.nut.2010.07.022
  6. Boura-Halfon S, 2009, AM J PHYSIOL-ENDOC M, V296, pE581, DOI 10.1152/ajpendo.90437.2008
  7. Buettner R, 2007, OBESITY, V15, P798, DOI 10.1038/oby.2007.608
  8. Calder PC, 2011, BRIT J NUTR, V106, pS1, DOI 10.1017/S0007114511005460
  9. Carvalho BM, 2012, DIABETOLOGIA, V55, P2823, DOI 10.1007/s00125-012-2648-4
  10. Catala-Niell A, 2008, CELL PHYSIOL BIOCHEM, V22, P327, DOI 10.1159/000149811
  11. Duntas H.L, 2009, HORM METAB RES, V41, P443
  12. Estrany ME, 2011, LIPIDS HEALTH DIS, V10, DOI 10.1186/1476-511X-10-52
  13. Fernandez ML, 2005, J NUTR, V135, P2075
  14. Gregersen S., 2012, J NUTR METAB
  15. Greiner T, 2011, TRENDS ENDOCRIN MET, V22, P117, DOI 10.1016/j.tem.2011.01.002
  16. Jobgen WJ, 2009, J NUTR, V139, P230, DOI 10.3945/jn.108.096362
  17. Kalupahana NS, 2011, OBESITY, V19, P245, DOI 10.1038/oby.2010.196
  18. Kim SJ, 2012, J NUTR BIOCHEM, V23, P113, DOI 10.1016/j.jnutbio.2010.10.012
  19. Klaus S, 2005, J NUTR, V135, P1854
  20. Kolb AF, 2013, MOL IMMUNOL, V54, P164, DOI 10.1016/j.molimm.2012.11.012
  21. Lam TKT, 2005, NAT NEUROSCI, V8, P579, DOI 10.1038/nn1456
  22. Liu WH, 2002, BIOCHEM BIOPH RES CO, V294, P347, DOI 10.1016/S0006-291X(02)00478-3
  23. MATTHEWS DR, 1985, DIABETOLOGIA, V28, P412, DOI 10.1007/BF00280883
  24. McDonald SD, 2011, NUTR RES, V31, P707, DOI 10.1016/j.nutres.2011.08.009
  25. Obici S, 2002, DIABETES, V51, P271
  26. Pang J, 2008, ARCH BIOCHEM BIOPHYS, V476, P178, DOI 10.1016/j.abb.2008.02.019
  27. REEVES PG, 1993, J NUTR, V123, P1939
  28. Reiterer G, 2004, J NUTR, V134, P1711
  29. Reyman M., 2013, INT J OBES LOND
  30. Rogero MM, 2008, CLIN NUTR, V27, P386, DOI 10.1016/j.clnu.2008.03.004
  31. Roth CL, 2012, HEPATOLOGY, V55, P1103, DOI 10.1002/hep.24737
  32. Safwat GM, 2009, NUTRITION, V25, P1157, DOI 10.1016/j.nut.2009.02.009
  33. Schaeffler A, 2009, IMMUNOLOGY, V126, P233, DOI 10.1111/j.1365-2567.2008.02892.x
  34. Schinner S, 2005, DIABETIC MED, V22, P674, DOI 10.1111/j.1464-5491.2005.01566.x
  35. Shen HY, 2008, J AM COLL NUTR, V27, P577
  36. Shirai N, 2005, ANAL BIOCHEM, V343, P48, DOI 10.1016/j.ab.2005.04.037
  37. Siriwardhana N, 2013, J NUTR BIOCHEM, V24, P613, DOI 10.1016/j.jnutbio.2012.12.013
  38. So M, 2011, LIPIDS HEALTH DIS, V10, DOI 10.1186/1476-511X-10-99
  39. Solinas G, 2010, FASEB J, V24, P2596, DOI 10.1096/fj.09-151340
  40. Swartz TD, 2010, PHYSIOL BEHAV, V99, P109, DOI 10.1016/j.physbeh.2009.10.016
  41. Vallim T, 2010, PROSTAG LEUKOTR ESS, V82, P211, DOI 10.1016/j.plefa.2010.02.016
  42. Woods SC, 2004, PHYSIOL BEHAV, V83, P573, DOI 10.1016/j.physbeh.2004.07.026

Coleções
Artigos e Materiais de Revistas Científicas - LIM/13
Artigos e Materiais de Revistas Científicas - ODS/03