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Nutrição, Inflamação e Desporto

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  • Diffusion of chemical substances through the interstitial fluid. A typical tissue is shown (schematically) in cross-section. The diffusion of oxygen from erythrocytes to cells in the tissue is shown as an example. Oxygen diffuses down a concentration gradient, from the erythrocytes, via the plasma and the interstitial fluid, into the cells, where its concentration is depleted as it is used in mitochondrial oxidation. CO2 diffuses back to the plasma in the same way. The interstitial fluid occupies the space between cells known as the extracellular space; this is not a true empty space, but in reality is occupied by glycoproteins and other molecules joining the cells. Nevertheless, it offers a path for diffusion of substances.
  • Maturation of mononuclear phagocytes and dendritic cells. Both dendritic cells and monocytes arise from a common precursor cell of the myeloid lineage in the bone marrow, and differentiation into monocytes or dendritic cells is driven by the cytokines monocyte colony-stimulating factor and Flt3 ligand, respectively (not shown). Dendritic cells further differentiate into subsets, the two major being conventional dendritic cells and plasmacytoid dendritic cells. Some dendritic cells may arise from monocytes in inflamed tissues. When blood monocytes are recruited into tissues, they become macrophages. Long-lived resident macrophages are present in all tissues of the body. At least two populations of blood monocytes exist (not shown), which are precursors, respectively, of macrophages that accumulate in response to infections and macrophages that are constitutively present in normal tissues. Macrophages in tissues become activated to perform antimicrobial and tissue repair functions in response to infections and tissue injury. Macrophages differentiate into specialized forms in particular tissues. CNS, central nervous system; DC, dendritic cell.
  • Maturation of mononuclear phagocytes and dendritic cells. Both dendritic cells and monocytes arise from a common precursor cell of the myeloid lineage in the bone marrow, and differentiation into monocytes or dendritic cells is driven by the cytokines monocyte colony-stimulating factor and Flt3 ligand, respectively (not shown). Dendritic cells further differentiate into subsets, the two major being conventional dendritic cells and plasmacytoid dendritic cells. Some dendritic cells may arise from monocytes in inflamed tissues. When blood monocytes are recruited into tissues, they become macrophages. Long-lived resident macrophages are present in all tissues of the body. At least two populations of blood monocytes exist (not shown), which are precursors, respectively, of macrophages that accumulate in response to infections and macrophages that are constitutively present in normal tissues. Macrophages in tissues become activated to perform antimicrobial and tissue repair functions in response to infections and tissue injury. Macrophages differentiate into specialized forms in particular tissues. CNS, central nervous system; DC, dendritic cell.
  • Maturation of mononuclear phagocytes and dendritic cells. Both dendritic cells and monocytes arise from a common precursor cell of the myeloid lineage in the bone marrow, and differentiation into monocytes or dendritic cells is driven by the cytokines monocyte colony-stimulating factor and Flt3 ligand, respectively (not shown). Dendritic cells further differentiate into subsets, the two major being conventional dendritic cells and plasmacytoid dendritic cells. Some dendritic cells may arise from monocytes in inflamed tissues. When blood monocytes are recruited into tissues, they become macrophages. Long-lived resident macrophages are present in all tissues of the body. At least two populations of blood monocytes exist (not shown), which are precursors, respectively, of macrophages that accumulate in response to infections and macrophages that are constitutively present in normal tissues. Macrophages in tissues become activated to perform antimicrobial and tissue repair functions in response to infections and tissue injury. Macrophages differentiate into specialized forms in particular tissues. CNS, central nervous system; DC, dendritic cell.
  • Prostaglandinas obtidas pela COX-1 na mucosa são responsáveis pela produção de muco Inibição aumenta risco de úlcerasCOX-1 leva à geração de TxA2 (agregação plaquetária)RIM: - PGE2 e PGI2 são importantes para o fluxo sanguíneo no rim - A vasodilatação compensatória em resposta à noradrenalina e/ou angiotensina II é mediada pela PGE2 - Inibir a COX-2 pode aumentar o risco de Hipertensão
  • Estudo em humanos (Exercício Excêntrico)
  • Mio D – factor de transcriçãoresponsávelpelaactivação das célulassatélite e subsequenteproliferação dos mioblastos
  • Estudo em animais
  • PGF2ALFA Aumenta síntese proteica do músculo esquelético
  • Mioblastos
  • Estudo com humanos
  • Estudo em animais
  • Osteoblasts and osteoclasts produce prostaglandin E2 (PGE2) during the initial stages of the bone healing process in a reaction catalysed by the enzyme cyclooxygenase (COX). COX-1 is expressed in normal bone as well as at the site of bone fracture. Inducible COX-2 is up-regulated especially during the initial stages of the bone repair process, and it produces higher amounts of PGs than COX-1. PG receptor types 2 and 4 (EP2 and EP4) mediate the effects of PGs on bone metabolism
  • Contents of o3 and o6 fatty acids in RBC, PLT, plasma PL, plasma CE and plasmaTG of the combined groups A and B at baseline (open bars)andafter8weekssupplementationwithALAandGLA(stripedbars).Datarepresentmean+SEMforninevegans.TheLCPo3/LCPo6ratio wasmultipliedby10.Thesupplementationregimenwas:4weeks2.01gALA(groupA)and1.17gGLA(groupB),followedby4weeks1.17gGLA þ 2.01g ALA (groups A and B).*Significantly different at P 5 0.05 by Student’s t - test.
  • Scatter plots of the inverse relation between concentrations of linoleic acid (LA) and docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and arachidonic acid (ARA) in red blood cell (RBC) phosphatidylcholine (PC) and ethanolamine phosphoglyceride (EPG). n = 105 Canadian women at 36 wk of gestation. The results were analyzed by using Pearson correlation analysis.
  • Proposed model for the mechanism of linoleic acid (LA)- mediated endothelial cell activation. LA treatment results in CYP 2C9 activation and production of superoxide radicals as well as depletion of glutathione in endothelial cells. The increased oxidative stress results in the activation of oxidative stress sensitive transcription factors such as NF-􏰆B and AP-1, leading to endothelial cell activation. Sulfa- phenazole, a specific inhibitor of CYP 2C9 suppresses the oxidative stress caused by LA treatment. The formation of leukotoxin and leu- kotoxindiol under physiological condition may help in the fatty acid detoxification process.
  • DifusionLibre y DifusionFacilitada (movimientoasistidoportransportadores) son formas de transportepasivo (a través de un gradiente de concentracion, o sea pasa de una region de mayor concentracionparauna region de menorconcentracion)
  • Glucose stimulation of insulin secretion in the pancreatic β-cell. Glucose enters the cell via the transporter GLUT2 (but see below) and is phosphorylated by glucokinase (GK) (hexokinase IV). These steps are similar to glucose utilization in the liver and allow the β-cell to “sense” the plasma glucose concentration. Generation of ATP from glucose utilization closes ATP- sensitive K+ channels in the cell membrane, stopping the outward flow of K+ ions that normally maintains the resting membrane potential (see Box 8.1, p. 215, for full description of this). This leads to membrane depolarization and opening of voltage-sensitive Ca2+ channels. Insulin is present in multiple secretory vesicles in the cell, as a crystalline complex in the center of the vesicle. An inward flux of Ca2+ ions causes exocytosis of the insulin-containing secretory vesicles, and hence insulin secretion. Glucose also stimulates synthesis of new insulin (Section 4.3.1). Although this scenario is true in rodent islets, there is some question over the presence of GLUT2 in human β-cells and it may be that GLUT1 and GLUT3 give the human β-cell sufficient glucose transport capacity (for discussion, see Schuit (1997)). The ATP-sensitive K+ channel has been much studied. It has two subunits. One is the K+ channel itself. This belongs to the family of inwardly-rectifying K+ channels (Kir, family 6 no. 2, hence Kir6.2). The other sub-unit modulates the activity of the channel and is the “receptor” for ATP (strictly, the complex Mg2+-ATP). But it is also the target for the drugs used to treat type 2 diabetes, the sulfonylureas (see later, Section 11.4.2). They bind, and cause channel closure, just as ATP does. Hence, this has become known as the sulfonylurea receptor, SUR. Again, there is a family of related proteins, and the one expressed in the β-cell is known as SUR1.
  • There is an intracellular pool of GLUT4 in membranous vesicles that can translocate to the cell membrane when insulin binds to its receptor. When the insulin signal is withdrawn, the GLUT4 proteins return to their intracellular pool.
  • OPG=Osteoprotegerin
  • Consequences of sleep restriction on immune and inflammatory changes and effects of recovery and sleep countermeasures. “After 8-h recovery sleep” indicates changes from similar time points measured following the sleep restriction intervention. “Sleep countermeasures” indicates the napping period during the day following the sleep restriction intervention. Abbreviations: C-reactive protein (CRP), interleukin-1 b (IL-1b); interleukin-6 (IL-6), interleukin-17 (IL-17); myeloperoxidase-modified low-density lipoprotein (Mox-LDL); peripheral blood mononuclear cell (PBMC); tumor necrosis factor-alpha (TNF-a).
  • Potential pathway(s) by which sleep restriction and insufficient recovery sleep lead to cardiovascular pathologies. Sleep restriction coupled to insufficient recovery sleep enhance the activity of the autonomic and stress systems. Vascular shear stress exacerbated by increased blood pressure leads to inflammation in the vascular wall potentially leading to the endothelial production of inflammatory mediators. The stress mediators cortisol/catecholamine can mobilize leukocyte in the blood circulation; among leukocyte subtype neutrophil degranulation can trigger an oxidative burst and the release of oxidative stress markers. Nap and its slow wave sleep (SWS) component can blunt the stress response e.g., reduce cortisol release with subsequent decreased leukocyte mobilization. Catecholamine can enhance the expression of nuclear factor-kappa B (NF-kB), an activator of pro-inflammatory gene expression, e.g., pro-inflammatory cytokines. All these physiopathological altered pathways following SR contribute to a chronic pro-inflammatory status ultimately leading to the development of cardiovascular pathologies. Abbreviations: C-reactive protein (CRP)
  • The gastrointestinal immune system. A, Schematic diagram of the cellular components of the mucosal immune system in the intestine. B, Photomicrograph of mucosal lymphoid tissue in the human intestine. Similar aggregates of lymphoid tissue are found throughout the gastrointestinal tract.
  • Mechanism of regulation of innate immune responses in the intestinal mucosa. Pattern recognition receptor expression and function in intestinal epithelial cells and lamina propria DCs minimize inflammatory responses to commensal bacteria in the lumen but promote responses to microbes that traverse the barrier and enter the lamina propria. Top, Pattern recognition receptors that recognize bacterial flagellin are compartmentalized in the cytosol (NLR) or basal membrane (TLR5) of intestinal epithelial cells but not on the apical/lumen membrane. Bottom,TLR4, which recognizes bacterial lipopolysaccharides, is expressed at low levels on intestinal epithelial cells and lamina propria DCs. TLR signaling does not induce inflammatory gene expression in lamina propria DCs because of more dominant effect of intracellular regulators of TLR signal transduction, such as TOLLIP and IRAK-M, compared with conventional DCs in other tissues.
  • Mechanisms of gliadin-induced zonulin release, increased intestinal permeability, and onset of autoimmunity. The production of specific gliadin-derived peptides by digestive enzymes causes CXCR3-mediated, MyD88-dependent zonulin release (2) and subsequent transactivation of EGFR by PAR2 leading to small intestine TJ disassembly (3). The increased intestinal permeability allows non-self antigens (including gliadin) to enter the lamina propria (4), where they are presented by HLA-DQ, -DR molecules (5). The presentation of one or more gliadin peptides leads to abrogation of oral tolerance (switch to Th1/Th17 response) and a marked increase in peripheral immune responses to gliadin. Furthermore, gliadin-loaded dendritic cells migrate from the small intestine to mesenteric and/or pancreatic lymph nodes (6) where they present gliadin-derived antigens. This presentation leads to migration of CD4−CD8− γδ and CD4−CD8+ αβ T cells to the target organ (gut and/or pancreas) where they cause inflammation (7). Implementation of a gluten-free diet or treatment with the zonulin inhibitor AT1001 (8) prevents the activation of the zonulin pathway and, therefore, of the autoimmune process targeting the gut or pancreatic β-cells.
  • PNA - aglutinina de amendoimSBA – aglutinina de soja PHA - Fitohemaglutinina Feijão (Phaseolus vulgaris)
  • PNA - aglutinina de amendoimSBA – aglutinina de sojaPHA - FitohemaglutininaFeijão (Phaseolusvulgaris)
  • Transcript

    • 1. INFLAMAÇÃO NO DESPORTONutrição no Exercício Físico e Desporto Pedro Carrera Bastos, 2013
    • 2. INFLAMAÇÃO AGUDA Perda deCalor Vermelhidão Inchaço Dor função Delves PJ, Roitt, IM. N Engl J Med. 2000 Jul 6;343(1):37-49.
    • 3. Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases, 2013
    • 4. Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases, 2013
    • 5. Bioactive Food as Dietary Interventions for Arthritis and Related Inflammatory Diseases, 2013
    • 6. Exercise 24 hours after exercise 1 day to 2 weeks after exercise During exercise After exercise Recovery 24 hours · leukocyte mechanical damage to muscle after exerciseinfiltration Exercise · proliferation of satellite cells 1 day to 2 weeks after exercise tissue · inflammation · acquisition of protective effectDuring exercise After exercise Recoverymechanical damage to muscle · leukocyte infiltration · proliferation of satellite cells blood circulationtissue · inflammation · acquisition of protective effect priming adhesion molecules PMN monocytesblood circulation CK endothelial cells Mb adhesion molecules primingPMN monocytes cytokines Mb CK CK macrophages chemoattractants cytokines endothelial cells Mb growth factors ROS phagocytosiscytokines Mb enzymes CK macrophages chemoattractants phagocytosis cytokines growth damaged muscle tissue muscle tissue factors regenerated muscle fibres fragments fragments satellite cells muscle fibres ROS phagocytosis enzymes Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process (PMN, polymorphonuclear leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species) phagocytosis damaged muscle tissue muscle tissue regeneratedmuscle fibres fragments fragments satellite cells muscle fibres Peake J, Nosaka K, Suzuki K. Exerc Immunol Rev. 2005;11:64-85 Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process
    • 7. FIGURE 2. Diagrammatic representation of the movement of leukocytesthrough the endothelium and the subsequent generation of inflammatorymediators. Calder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
    • 8. De Caterina R. N Engl J Med 2011
    • 9. AINES De Caterina R. N Engl J Med 2011
    • 10. Coxibs De Caterina R. N Engl J Med 2011
    • 11. COX-1 COX-2 Coxibs AINES “ Side pocket” NSAID binding space Intracellular membrane F S F Br CHCO 2H SO 2CH3 Bulky grouping CH3 COX-1 inhibitor COX-2 inhibitor Flurbiprofen DuP697Fig ure 18.2. Serhan CN, Ward PA, Gilroy DW, editors. Fundamentals of Inflammation. Cambridge Univ Pr; 2010: 234-243.
    • 12. Paulsen G, Mikkelsen UR, Raastad T, Peake JM. Exerc Immunol Rev. 2012;18:42-97
    • 13. Lesão c/ contracçõesexcêntricas em Coelhos 2xdia Durante 6 dias
    • 14. Lesão c/ contracçõesexcêntricas em Coelhos 2xdia Durante 6 dias
    • 15. Lesão c/ contracçõesexcêntricas em Coelhos 2xdia Durante 6 dias
    • 16.  Células em cultura durante 96 horas Inibição selectiva da COX-2 diminui proliferação de células satélite Inibição de COX-1 e COX-2 reduz diferenciação e fusão de células satélite Muscle Nerve 30: 497–500, 2004
    • 17. Mio D – factor de transcrição responsávelpela activação das células satélite esubsequente proliferação dos mioblastos Gharaibeh B, et al. Birth Defects Res C Embryo Today. 2012 Mar;96(1):82-94.
    • 18. J Appl Physiol 103: 425–431, 2007 14 atletas Corrida de 36 Km Indometacina (100 mg) vs Placebo Ingestão: durante 4 dias antes da corrida até à data da última biópsia RESULTADOS:
    • 19. J Appl Physiol 103: 425–431, 2007 Células Satélite23
    • 20. J Appl Physiol 103: 425–431, 2007 Células Satélite24
    • 21. J Appl Physiol 103: 425–431, 2007 Células Satélite25
    • 22. Células satélite J Appl Physiol 107: 1600–1611, 2009200 contrações excêntricas26NSAID numa perna (antes, durante e até 4,5 h depois) e a outra como controlo
    • 23. Schoenfeld BJ. J Strength Cond Res. 2012 May;26(5):1441-53.
    • 24. Am J Physiol Cell Physiol 287: C475–C483, 2004Lesão induzida pelo frio Inibidor de COX-2
    • 25. INIBIDOR DA COX-2 EM RATOS APÓS ESTÍMULO MUSCULAR: Reduziu Inflamação Atenuou o crescimento das miofibrilhas Reduziu a activação e proliferação das células satélite
    • 26. Shen W. Am J Pathol 2005; 167:1105–1117
    • 27. J. Clin. Endocrinol. Metab. 2001 86: 5067-5070ACETAM IBUPROF PLACEBO
    • 28. Inibidor da COX-2
    • 29. Am J Physiol Endocrinol Metab 2002; 282: E551–E556 24 adultos masculinos RCT com Placebo 10-14 series de 10 rep excéntricas RM DIMINUIÇÃO (24h): Fractional synthesis rate Sem efeitos na dor comparado com placebo
    • 30. Am J Physiol Endocrinol Metab 2002; 282: E551–E556 Fractional Synthesis Rate34
    • 31. 35 Am J Physiol Regul Integr Comp Physiol 296: R1132–R1139, 2009.
    • 32. Exercise 24 hours after exercise 1 day to 2 weeks after exercise During exercise After exercise Recovery 24 hours · leukocyte mechanical damage to muscle after exerciseinfiltration Exercise · proliferation of satellite cells 1 day to 2 weeks after exercise tissue · inflammation · acquisition of protective effectDuring exercise After exercise Recoverymechanical damage to muscle · leukocyte infiltration · proliferation of satellite cells blood circulationtissue · inflammation · acquisition of protective effect priming adhesion molecules PMN monocytesblood circulation CK endothelial cells Mb adhesion molecules primingPMN monocytes cytokines Mb CK CK macrophages chemoattractants cytokines endothelial cells Mb growth factors ROS phagocytosiscytokines Mb enzymes CK macrophages chemoattractants phagocytosis cytokines growth damaged muscle tissue muscle tissue factors regenerated muscle fibres fragments fragments satellite cells muscle fibres ROS phagocytosis enzymes Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process (PMN, polymorphonuclear leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species) phagocytosis damaged muscle tissue muscle tissue regeneratedmuscle fibres fragments fragments satellite cells muscle fibres Peake J, Nosaka K, Suzuki K. Exerc Immunol Rev. 2005;11:64-85 Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process
    • 33. Exercise 24 hours after exercise 1 day to 2 weeks after exercise During exercise After exercise Recovery 24 hours · leukocyte mechanical damage to muscle after exerciseinfiltration Exercise · proliferation of satellite cells 1 day to 2 weeks after exercise tissue · inflammation · acquisition of protective effectDuring exercise After exercise Recoverymechanical damage to muscle · leukocyte infiltration · proliferation of satellite cells blood circulationtissue · inflammation · acquisition of protective effect priming adhesion molecules PMN monocytesblood circulation CK endothelial cells Mb adhesion molecules primingPMN monocytes cytokines Mb CK CK macrophages chemoattractants cytokines endothelial cells Mb growth factors ROS phagocytosiscytokines Mb enzymes CK macrophages chemoattractants phagocytosis cytokines growth damaged muscle tissue muscle tissue factors regenerated muscle fibres fragments fragments satellite cells muscle fibres ROS phagocytosis enzymes Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process (PMN, polymorphonuclear leucocyte; Mb, myoglobin; CK, creatine kinase; ROS, reactive oxygen species) phagocytosis damaged muscle tissue muscle tissue regeneratedmuscle fibres fragments fragments satellite cells muscle fibres Peake J, Nosaka K, Suzuki K. Exerc Immunol Rev. 2005;11:64-85 Figure 1 Exercise-induced muscle damage and subsequent muscle inflammation and regeneration process
    • 34. Basic & Clinical Pharmacology & Toxicology 2007; 102: 10–14
    • 35. Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33 Serhan CN. Annu. Rev. Immunol. 2007. 25:101–37 Roubenoff R. Nutr Rev. 2007 Dec;65(12 Pt 2):S208-12 Tidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187Inflamação Aguda Regeneração Inflamação Crónica Lesão e Dor Crónica Catabolismo muscular e ósseo Síndrome de Morte Súbita Doenças Metabólicas39 e Neurodegenativas
    • 36. Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33 Serhan CN. Annu. Rev. Immunol. 2007. 25:101–37 Roubenoff R. Nutr Rev. 2007 Dec;65(12 Pt 2):S208-12 Tidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187Inflamação Aguda AA Regeneração Inflamação Crónica Lesão e Dor Crónica Catabolismo muscular e ósseo Síndrome de Morte Súbita Doenças Metabólicas40 e Neurodegenativas
    • 37. Chen LC, Ashcroft DM. Pharmacoepidemiol Drug Saf. 2007 Jul;16(7):762-72
    • 38. De Caterina R. N Engl J Med 2011
    • 39. Lipooxigenases Ciclooxigenases LTA4 TXA2 LTB4 PGE2 LTC4 Ácido Araquidónico PGF2α LTD4 20:4 n-6 PGD2 LTE4 PGI2 12-HETE LTA5 TXA3 LTB5 Ácido Eicosapentaenóico PGE3 LTC5 (EPA) PGF3 α LTD5 20:5 n-3 PGD3 LTE5 PGI3 Bastos P. An Nutr Esp Func 2007; 7(36): 17-24
    • 40. EPA/DHA E AACalder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S.
    • 41. Time course relativo à incorporação de EPA e DHA INCORPORAÇÃO DE EPA Y DHA NOS em fosfolipídios de membrana de células mononucleares FOSFOLÍPIDOS DE CÉLULAS MONONUCLEARES DHA in mononuclear cell PL (%)EPA in mononuclear cell PL (%) 4 4 3 3 2 1 2 0 1 0 4 8 12 20 0 4 8 12 20 Time (weeks) Time (weeks) Indivíduos saudáveis: 2,1 g EPA + 1,1 g DHA/dia/12 semanas Eur. J. Clin. Invest. 30, 260-274, 2000
    • 42. DHACalder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
    • 43. DHACalder PC. Am J Clin Nutr 2006;83(suppl):1505S–19S)
    • 44. RESOLUÇÃO DA INFLAMAÇÃO Gilroy DW. 2010
    • 45. SeráadequadoBloquear? Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
    • 46. Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
    • 47. RESOLUÇÃO DA INFLAMAÇÃO Lipoxinas Serhan CN. Am J Pathol. 2010 Oct;177(4):1576-91
    • 48. Serhan CN, Chiang N. British Journal of Pharmacology (2008) 153, S200–S215.
    • 49. Serhan CN, Chiang N. British Journal of Pharmacology (2008) 153, S200–S215.
    • 50. Serhan, CN. Annu. Rev. Immunol. 2007. 25:101–37
    • 51. Serhan CN, Chiang N. Rheum Dis Clin N Am 30 (2004) 69–95
    • 52. DOSES BAIXAS DE ASPIRINAChiang N et al. Aspirin triggers antiinflammatory 15-epi-lipoxin A4 and inhibits thromboxane in a randomized human trial. PNAS 2004. 101; 42
    • 53. De Caterina R. N Engl J Med 2011
    • 54. Barnes PJ, Karin M. N Engl J Med. 1997 Apr 10;336(15):1066-71.
    • 55. NF-kB e Lesão MuscularTidball JG, Villalta SA. Am J Physiol Regul Integr Comp Physiol 2010; 298: R1173–R1187
    • 56. EPA & DHACalder PC. Biochimie. 2009 Feb 3. [Epub ahead of print]
    • 57. ÓMEGA-3 E INFLAMAÇÃO 17 meta-análises de RCTs testando os efeitos de Ómega-3 na AR 3-4 meses: redução da dor articular, minutos de rigidez matutina, número de articulações com dor e menor uso de AINES Goldberg RJ, Katz J. Pain 129 (2007)
    • 58. EPA & DHA por cada 100g peixeFedacko. n−3 PUFAs—From dietary supplements to medicines. Pathophysiology 14 (2007) 127–132
    • 59. CONCENTRAÇÕES DE MERCÚRIO Concentração Peixe Mercúrio (ppm) Peixe-espada 0,97 Arenque 0,35 Atum 0,12 Bacalhau 0,11 Salmão 0,01 Adaptado: FDA (EUA) 66
    • 60. BETA-OXIDAÇÃOACTIVIDADE LIMITADA ACTIVIDAD E LIMITADA
    • 61. VEGANS TÊM NÍVEIS BAIXOS DE AA E DHAFokkema et al. Polyunsaturated fatty acid status of Dutch vegans and omnivores. Prostaglandins, Leukotrienes and Essential FattyAcids (2000)
    • 62. 9 vegans saudáveis suplementados com: A: 2.01 g ALA (4 ml óleo de linhaça) B: 1.17 g GLA (6 ml óleo borragem) A+B
    • 63. Blasbalg TL, et al. Am J Clin Nutr. 2011
    • 64. Blasbalg TL, et al. Am J Clin Nutr. 2011
    • 65. LA diminui DHA na membrana dos eritrócitos N= 105 Mulheres (Canadá) Grávidas (com 36semanas de LA diminui gestação) EPA na membrana dos eritrócitos Friesen RW, Innis SM. Am J Clin Nutr. 2010 Jan;91(1):23-31.
    • 66. RÁCIO ÓMEGA 6/ÓMEGA 3 DE ALGUNS ALIMENTOS Alimento Rácio ω6/ω3 Ovo convencional 19,4 Ovo de Creta 1,3 Carne (músculo) bovina 5,19 alimentada com cereais Carne (músculo) bovina 2,2 alimentada a pasto Simopoulos AP. J Nutr. 2001 Nov;131(11 Suppl):3065S-73S. Review Cordain L et al. European Journal of Clinical Nutrition 2002; 56:181 – 191.
    • 67. Journal of the American College of Nutrition, Vol. 22, No. 6, 502–510 (2003)
    • 68. Journal of the American College of Nutrition, Vol. 22, No. 6, 502–510 (2003)
    • 69. Exercício  Número de Neutrófilos circulantes Físico Fagocitose dos Migração para resíduos celulares local da lesão Libertação de lisoenzimas e radicais de oxigénioApós o exercício excêntrico são observados maiores  nos neutrófilos do que após o exercício concêntrico CANNON JG. ORENCOLE SF. FIELDING RA. et al. Am J Physiol, 259(6 Pt 2): R1214-9, 1990. SMITH JK. GRISHAM MB. GRANGER DN. KORTHUIS RJ. Am J Physiol, 256(3 Pt 2): H789-93, 1989.
    • 70. VITAMINA CHowatson G, van Someren KA. Sports Med. 2008;38(6):483-503.
    • 71. VITAMINA EHowatson G, van Someren KA. Sports Med. 2008;38(6):483-503.
    • 72. VITAMINAS C + EHowatson G, van Someren KA. Sports Med. 2008;38(6):483-503.
    • 73. 16 MULHERES 14 HOMENS• Idade: 21-24 anos• Sessão de 7 séries de 20 Agachamentos c/ 3 min de intervalo entre séries• Solução Placebo vs Solução c/ BCAA 15 min antes da sessão• Dose: 92 mg/Kg (Mulheres); 77 mg/Kg (Homens)• Cross-over Shimomura Y, et al. J Nutr. 2006 Feb;136(2):529S-532S.
    • 74. • 15 ciclistas Sexo Masculino• Bebida c/ CHO vs CHO + P (4/1): 1,8 ml/Kg a cada 15 min• Bebida c/ CHO vs CHO + P (4/1): 10 ml/Kg após exercício• Bebida c/ CHO: 26 g CHO por 355 ml de água• Bebida CHO + P (4/1): [26 g CHO + 6,5 g P] por 355 ml de água Saunders MJ, Kane MD, Todd MK. Med Sci Sports Exerc. 2004 Jul;36(7):1233-8.
    • 75. Saunders MJ, Kane MD, Todd MK. Med Sci Sports Exerc. 2004 Jul;36(7):1233-8.
    • 76. Saunders MJ, Kane MD, Todd MK. Med Sci Sports Exerc. 2004 Jul;36(7):1233-8.
    • 77.  N: 387 recrutas  Duração: 54 dias  Metodologia: Imediatamente após o treino:  Grupo Prot: 8 grs de HC + 10 grs de P + 3 g de L  Grupo HC: 8 grs de HC + 0 grs de P + 3 g de L  Grupo Placebo: 0 grs de HC + 0 grs de P + 0 g de LFlakoll PJ, et al.. J Appl Physiol. 2004 Mar;96(3):951-6
    • 78. Alterações 34º dia vs início Alterações último dia vs inícioFlakoll PJ, et al.. J Appl Physiol. 2004 Mar;96(3):951-6
    • 79. NF-KB E DOENÇAS DA CIVILIZAÇÃO • DCV • Hipertensão • Síndrome Metabólica • Sarcopenia • Osteoporose • Depressão • Cancro Ahn KS, Aggarwal BB. Ann N Y Acad Sci. 2005 Nov;1056:218-33
    • 80. Informação para o resto do organismoStraub, R.H. et al., 2010. Journal of Internal Medicine
    • 81. GASTO ENERGÉTICOStraub, R.H. et al., 2010. Journal of Internal Medicine
    • 82. SISTEMA IMUNOLÓGICO Consumo de 2000 kJ/dia: 477,6 Kcal/dia  Activação≈ 25-30%  En repouso: 1600 kJ  381 Kcal/dia70%: glucose e glutamina Straub, R.H. et al., 2010. Journal of Internal Medicine
    • 83. GLUTS
    • 84. IR
    • 85. IR
    • 86. IR
    • 87. IR
    • 88. GLICEMIA E INSULINEMIALast AR, Wilson SA. Low-Carbohydrate Diet. Am Fam Physician 2006;73:1942-8
    • 89. INFLAMAÇÃO E OSSO Substratos importantes na Inflamação: Cálcio e Fósforo Aportados pelo osso se estiver próximo do local de Inflamação TNF-a IL-6 IL-1-b PTH Straub, R.H. et al., 2010. Journal of Internal Medicine, 267(6), pp.543-560.
    • 90. Biologics: Targets & Therapy 2008:2(4) 663–669
    • 91. LIGANDOS DOS TLRS
    • 92. Bactérias Gram Bactérias Positivas Gram Negativas Vírus Takeda K, Akira S. Int Immunol. 2005 Jan;17(1):1-14.
    • 93. CitoquinasInflamatórias
    • 94. Resposta Inflamatória Recrutamento de células imunológicas Calor “Calor” “Enrojecimiento” Rubor “Hinchazon” Inchaço “dor” DorPodolsky. Inflammatory Bowel Disease. N Engl J Med. 2002 Aug 8;347(6):417-29
    • 95. VIAS ENTRADA LPS NA CIRCULAÇÃO Caesar R, et al. Journal of Internal Medicine 2010
    • 96. Viswanathan VK, Hodges K, Hecht G. Nat Rev Microbiol. 2009 Feb;7(2):110-9
    • 97. VIAS ENTRADA LPS NA CIRCULAÇÃO Caesar R, et al. Journal of Internal Medicine 2010
    • 98. X3 +90 g Gordura e/ou
    • 99. NataSumo deLaranja
    • 100. NataGlucoseSumo deLaranja
    • 101. Glucose Nata Sumo de Laranja
    • 102. 24 PorcosEx vivo mucosal to serosal endotoxin LPS no plasmatransport permeability (Papp) Mani V, Hollis JH, Gabler NK. Nutr Metab (Lond). 2013 Jan 10;10(1):6. [Epub ahead of print]
    • 103. 24 PorcosEx vivo mucosal to serosal endotoxin LPS no plasmatransport permeability (Papp) Mani V, Hollis JH, Gabler NK. Nutr Metab (Lond). 2013 Jan 10;10(1):6. [Epub ahead of print]
    • 104. Alimentos ocidentais:
    • 105. Sumo de LaranjaSumo de Laranja
    • 106. TRANSPORTE TRANS E PARA CELULAR  3mm de epitélio  Moléculas <100 Da passam por difusão: Na+ ou Cl-  Se aumenta a permeabilidade passam moléculas de >100-150 Da  Outras barreiras: muco, peristaltismo, junções estreitas, enzimas, secreções ácidas, IgA, etcThe Institute for Functional Medicine. CLINICAL NUTRITION. A Functional Approach. Second Edition. 2004
    • 107. CAUSAS DA HIPERPERMEABILIDADE INTESTINAL
    • 108. DIETA RICA EM GORDURA Y ANTIBIÓTICOS Cani PD, et al. Diabetes 2008;57(6):1470–81.
    • 109. DIETA RICA EM GORDURA Y ANTIBIÓTICOS Cani PD, et al. Diabetes 2008;57(6):1470–81.
    • 110. FÁRMACOS  AINES  AntiácidosCordain L, et al. Br J Nutr. 2000 Mar;83(3):207-17
    • 111. CAUSAS DIETÉTICASPimentos Álcool Jensen-Jarolim E, et al. J Nutr. 1998 Mar;128(3):577-81 Tsukura Y, et al. Biol Pharm Bull. 2007 Oct;30(10):1982-6 Purohit V, et al. Alcohol. 2008 Aug;42(5):349-61
    • 112. DISBIOSE / SIBO Bacterias Intestinales Linfocitos TCordain L, et al. Br J Nutr. 2000 Mar;83(3):207-17
    • 113. Visser J et al. Tight Junctions, Intestinal Permeability, and Autoimmunity. Ann. N.Y. Acad. Sci. 1165: 195–205 (2009).
    • 114. Cani PD, et al. Diabetologia 2007
    • 115. Lind HC. JAMA. 2004;292(7):852-858
    • 116. Lind HC. JAMA. 2004;292(7):852-858
    • 117. GOLD STANDARD: LACTULOSE BREATH TEST Bures J, et al. WJG. 2010 vol. 16 (24) pp. 2978-90
    • 118. CEREAIS PROLAMINAS GLÚTEN GLUTENINASKagnoff MF. Celiac disease: pathogenesis of a model immunogenetic disease. J Clin Invest. 2007 Jan;117(1):41-9
    • 119. PROLAMINASHordeina – CevadaSecalina - CenteioGliadina – Trigo Drago S, et al. Scand J Gastroenterol. 2006 Apr;41(4):408-19. Lammers KM, et al. Gastroenterology. 2008 Jul;135(1):194-204.e3.
    • 120. J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.Autistas con dieta sin gluten
    • 121. LECTINAS1. Sjolander A et all. Int Arch Allergy Appl Immunol 1984; 75, 230–236.2. Greer F, et al. Digestion 1985; 32, 42–46.3. Pellegrina CD et al. Toxicol Appl Pharmacol 2005;207:170-78
    • 122. LECTINAS QUE PODEM LIGAR-SE A CÉLULAS INTESTINAIS Gérmen de Trigo: 300 – 350 mg/kg WGA (1) Farinha de trigo integral: 30-50 mg/kg WGA (2) Farinha de trigo refinado: 4.4 mg/kg WGA (2) Feijão: 1,000-10,000 mg/kg PHA (3) Soja: 200 – 2,000 mg/kg SBA (3) Tomate: <10 mg/kg TL (3) Amendoim: 110 mg/kg PNA (1) 1. Vincenzi S, et al. J Agric Food Chem. 2002 Oct 23;50(22):6266-70. 2. Matucci A et al. Food Control 2004;15: 391-95 3. Peumans WJ, Van Damme EJM. Trends Food Sci Technol 1996;7:132-39
    • 123. Adaptado de Cordain L, 2009 (con autorização) Vilosidades LÚMEN WGA/PHA Enterócitos Tight Junction Integridade Hiperpermeabilidade1. Sjolander A et al. The effect of concanavalin A and wheat germ agglutinin on the ultrastructureand permeability of rat intestine. Int Arch Allergy Appl Immunol 1984; 75, 230–236.2. Greer F & Pusztai A (1985) Toxicity of kidney bean (Phaseolus vulgaris) in rats: changes in intestinalpermeability. Digestion32, 42–46.3. Pellegrina CD et al. Plant lectins as carriers for oral drugs: Is wheat germ agglutinin a suitablecandidate? Toxicol Appl Pharmacol 2005;207:170-78
    • 124. SAPONINAS Leguminosas  Glicosídeos Esteróides (Glicoalcalóides) ou Glicosídeos Triterpenóides  Função Principal: Proteger aSolanáceas planta do ataque de insectos e de microrganismos  Em mamíferos aumenta permeabilidade intestinal e causa hemólise de eritrócitos Francis G et al. Brit J Nutr 2002;88:587-605
    • 125. Adaptado de Cordain L, 2009 (com permissão) BATATA INGLESA O PIOR!! Total saponinas: α-solanina + α-chaconina (mg/kg) Casca de Batata 1. Casca Frita 1450 Frita 2. Batata Frita com Casca 720 3. Chips (EUA) 180 4. Batata Assada Congelada 123 5. Casca de batata congelada 121 6. Batata Assada 113 7. Farinha de Batata desidratada 75 8. Batata Cozida sem casca 42 9. Batata com casca enlatada 34 10. Batata Frita Congelada 31 11. Batata Frita (McDonald’s) 8 12. Puré de Batata Congelado 5 13. Batata sem casca enlatada 2Smith DB, Roddick JG, Jones JL. Trends in Food Sci Technol 1996;7:126-131.
    • 126. Adaptado de Cordain L, 2009 (con autorização) α-Tomatina (mg/kg) TOMATE 1. Tomates verdes pequenos 548 2. Tomates verdes médios 169 3. Tomates verdes em escabeche (Marca A) 71.5 4. Tomates verdes não maduros escabeche 28 O pior!! 5. Tomates verdes em escabeche (Marca B) 28 6. Molho tomate verde 27.5 7. Tomate vermelho secado ao sol 21 8. Verde grande não maduro 16 9. Verde grande não maduro tipo 210 10. Tomate cherry sungold 11 11. Tomate verde frito 11 12. Tomate verde no microondas 11 13. Tomate cherry amarelo 9.7 14. Ketchup 8.6 15. Molho tomate vermelho 5.7 16. Tomate cherry pera amarelo 4.5 17. Sumo de tomate 2.8 18. Tomate cherry vermelho 2.7 19. Caldo concentrado de tomate 2.2 20. Tomate cherry pera vermelho 1.3 21. Tomate amarelo médio 1.3 22. Tomate amarelo grande 1.1 23. Tomate estufado em lata 1.1 24. Tomate maduro vermelho para carne 0.9 25. Tomate green zebra 0.6 26. Roma 0.4 27. Tomate vermelho maduro normal 0.3 Friedman M, Levin CE. J Agric Food Chem 1995;43:1507-1511
    • 127. Adaptado de Cordain L, 2009 (com permissão) SOJA Total de Saponinas da Soja (mg/kg)O PIOR!! 1. Isolado de Proteína de Soja 10600 2. Feijão de Soja 4040 4. Farinha de Soja 3310 5. Tempeh 1530 6. Tofu 590 7. Leite de Soja 470 Tempeh Tofu Ju J, Lee S, Hendrich S, Murphy PA. J Agric Food Chem 2002;50:2587-94
    • 128. Adaptado de Cordain L, 2009 LEGUMINOSAS (mg/kg)1. Feijão haricot 41002. Fríjoles (P. vulgaris) 38003. Feijão Vermelho (P. vulgaris) 35004. Judías negras 34005. Fava (Vicia faba) 31006. Grão 23007. Ervilha 18008. Rebenmtos de Feijão 11009. Lentilhas 110010. Chícharo 110011. Feijão Manteiga 100012. Feijão cozido em lata 110013. Feijão verde (P. vulgaris) 100014. Amendoim <100 Shi J. J Med Food. 2004 Spring;7(1):67-78 Price KR, et al. J Sci Food Agric 1986;37:1185-91 Sparg SG, et al. J Ethnopharmacol. 2004 Oct;94(2-3):219-43
    • 129. Adaptado de Cordain L, 2009 (com permissão) OUTROS ALIMENTOS Total saponinas: (mg/kg) 1. Rebentos de Alfalfa 8000 2. Amaranto 7900 3. Quinoa 5930 4. Extracto de Quillaja 100Quinoa Amaranto Alfalfa Oda K, et al. Biol Chem. 2000 Jan;381(1):67-74
    • 130. Adaptado de Cordain L, 2009 (com permissão) COMO AS SAPONINAS CAUSAM HIPERPERMEABILIDADE INTESTINAL Saponina ColesterolSaponinas ligam-se a moléculas de colesterol na membrana pela afinidade do componente Aglicónico pelo esterol de membrana Keukens EA et al. Biochim Biophys Acta 1995;1240: 216-228.
    • 131. SAPONINAS QUE DEMONSTRARAM AUMENTAR PERMEABILIDADE INTESTINALSaponina Alimento Referênciaα-Tomatina Tomate Johnson IT et al. J Nutr 1986;116:2270-77α-Solanina, Keukens EA et al. Biochimica et Biopysica Actaα-chaconina Batata Inglesa 1995;1240:216-228Saponina daSoja Soja Alvarez JR et al. Pediatr Res 1982;16:728-31.Saponina da Extracto deQuillaja Quillaja Chao AC et al. J Pharm Sci 1998;87:1395-99.Saponina daQuinoa Quinoa Gee JM et al. J Sci Food Agric 1993;63:201-09Saponina da Rebentos deAlfalfa Alfalfa Story JA et al. Am J Clin Nutr 1984;39:917-29 To
    • 132. Adaptado de Cordain L, 2009 (com permissão) (SAPONINA + LECTINA) tem efeito sinérgico sobre permeabilidade intestinal:Saponina Lectina AlimentoSaponina da Soja SBA Soja Tofu Alvarez JR et al. Pediatr Res 1982;16:728-31.
    • 133. Adaptado de Cordain L, 2009 (com autorização) PHA o WGA Lumen intestinal EGF Receptor EGF Receptor Para LinfaHormi K et al. Cell Tissue Res 1994;278:439-50Rebbaa A et al. J Neurochem 1996;67:2265-2272 Para CirculaçãoLochner N, et al. Pharm Res. 2003 May;20(5):833-9.
    • 134. Cordain L. Potential Therapeutic Characteristics of Pre-agricultural Diets in the Prevention and Treatment of Multiple Sclerosis. Direct MS (Multiple Sclerosis) of Canada Conference. Calgary, Canada, Outubro de 2007 B/A B/A WGA Bacteria/Péptidos dietéticosLectina B/A WGA Lumen intestinal Receptor EGF Receptor EGF Para Linfa B/A WGA Para Activa Células T Circulação
    • 135. ESTIMULANTES TLRS EM VERDURAS E FRUTAS PROCESSADAS MINIMAMENTE Inicialmente só em algumas carnes e lácteos Analisados: cenoura ralada, cebola cortada, maçã em rodelas, folhas verdes de salada, espinafres, grelos e rebentos de leguminosas Armazenados a 5ºCErridge, C., 2011. Stimulants of Toll-like receptor (TLR)-2 and TLR-4 are abundant in certain minimally-processed vegetables. Food and Chemical Toxicology, 49(6), pp.1464-1467.
    • 136. ESTIMULANTES DE TLRS TLR4 TLR2 Agrião em salada  Agrião Vegetais verdes em  Agrião em salada saladas  Vegetais verdes em Espinafres saladas Cenoura ralada  Espinafres Cebola cortada +++  Cenoura ralada Rebentos de feijão +++  Cebola cortada +++  Rebentos de feijão +++ Erridge, C., 2011. Stimulants of Toll-like receptor (TLR)-2 and TLR-4 are abundant in certain minimally-processed vegetables. Food and Chemical Toxicology, 49(6), pp.1464-1467.
    • 137. QUANTIDADE  Concentrações mais altas que as que estão no intestino delgado  LPS: 100 ng/ml vs 11 g/g  BLP: 1000 ng/ml vs 18 g/gErridge, C., 2011. Diet, commensals and the intestine as sources of pathogen-associated molecular patterns in atherosclerosis, type 2 diabetes and non-alcoholic fatty liver disease. Atherosclerosis, 216(1), pp.1-6.
    • 138. MESMO QUANDO SÃO FERVIDOS DURANTE 10 MIN
    • 139. MAS NÃO EM VERDURAS NÃO PROCESSADAS E DESCASCADAS  Cenoura  Cebola  Batata  Brócolo  Pimento  Abóbora  Grão Erridge, C., 2011. Stimulants of Toll-like receptor (TLR)-2 and TLR-4 are abundant in certain minimally-processed vegetables. Food and Chemical Toxicology, 49(6), pp.1464-1467.
    • 140. EFEITO ARMAZENAMENTO A 5ºCErridge, C., 2011. Stimulants of Toll-like receptor (TLR)-2 and TLR-4 are abundant in certain minimally-processed vegetables. Food and Chemical Toxicology, 49(6), pp.1464-1467.
    • 141. SUFICIENTE PARA ACTIVAR SIST IMUNOLÓGICO? Se humanos absorvessem 0.1% de LPS  5 mg/kg de LPS oral seria suficiente  Possível dieta ocidentalErridge, C., 2011. Diet, commensals and the intestine as sources of pathogen-associated molecular patterns in atherosclerosis, type 2 diabetes and non-alcoholic fatty liver disease. Atherosclerosis, 216(1), pp.1-6.
    • 142. ÓMEGA-3 E INFLAMAÇÃO  Inibição TLR4  Inibição TLR2  Inibe transcrição NFk-B através de PPARWendel M and Heller PAR. Lipoproteins in inflammation and sepsis. II. Clinical aspects. Intensive Care Med (2007) 33:25–35
    • 143. CURCUMINAhttp://www.curcuminresearch.org
    • 144. http://www.curcuminresearch.org
    • 145. http://www.curcuminresearch.org
    • 146. OBRIGADOpedro.bastos@nutriscience.pt www.nutriscience.pt

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