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Vol. 90. Núm. 2.
Páginas 161-168 (março - abril 2014)
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Vol. 90. Núm. 2.
Páginas 161-168 (março - abril 2014)
ARTIGO ORIGINAL
Open Access
A randomized triple-masked controlled trial on the effects of synbiotics on inflammation markers in overweight children
Ensaio clínico controlado randomizado triplo-cego dos efeitos de simbióticos sobre marcadores de inflamação em crianças com sobrepeso
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4397
Roya Kelishadia,b, Sanam Farajianb,
Autor para correspondência
farajian.sanam@gmail.com

Corresponding author.
, Morteza Safavib, Maryam Mirlohia,b, Mahin Hashemipoura,b
a Departamento de Pediatria, Centro de Pesquisa de Crescimento e Desenvolvimento Infantil, Isfahan University of Medical Sciences, Isfahan, Irã
b Escola de Nutrição e Ciência dos Alimentos, Isfahan University of Medical Sciences, Isfahan, Irã
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Informação do artigo
Abstract
Objective

the low degree of inflammation in obesity contributes to systemic metabolic dysfunction. Recent experimental studies proposed some effects of alteration in gut microbiota on inflammatory factors. This study aimed to assess the anti-inflammatory effects of a synbiotic supplement on inflammation markers in overweight and obese children and adolescents.

Methods

this randomized triple-masked controlled trial was conducted among 70 participants aged 6 to 18 years, with a body mass index (BMI) equal or higher than the 85th percentile. They were randomly assigned into two groups of equal number to receive synbiotic or placebo for eight weeks.

Results

fifty-six of 70 participants (80%) completed the study. Compared with the placebo group, the synbiotic group had significant decrease in mean values of tumor necrosis-α and interleukin-6, with significant increase in adiponectin; these changes were no longer significant after adjustment for BMI. There was no significant change in the mean values of high-sensitive C-reactive protein.

Conclusion

the present findings suggest the positive influence of synbiotic supplementation on inflammation factors, which are dependent to its effect on weight reduction in overweight and obese children.

Keywords:
Synbiotic
Children and adolescents
Obesity
Inflammation
Trial
Resumo
Objetivo

o baixo grau de inflamação na obesidade contribui para disfunção metabólica sistêmica. Estudos experimentais recentes propuseram alguns efeitos de alteração na microbiota intestinal sobre fatores inflamatórios. O objetivo deste estudo foi avaliar os efeitos anti-inflamatórios de um suplemento simbiótico sobre marcadores de inflamação em crianças e adolescentes com sobrepeso e obesos.

Métodos

este ensaio clínico controlado randomizado triplo-cego foi conduzido entre 70 participantes com idade entre seis e 18 anos, com índice de massa corporal (IMC) igual ou acima do 85° percentil. Eles foram aleatoriamente divididos em dois grupos de igual número de participantes para receber simbiótico ou placebo por oito semanas.

Resultados

no todo, 56 de 70 participantes (80%) concluíram o estudo. Em comparação ao grupo placebo, o grupo simbiótico teve redução significativa nos valores médios de necrose tumoral-α e interleucina-6, com aumento significativo na adiponectina; essas alterações não eram mais expressivas após o ajuste do IMC. Não houve alteração impor- tante nos valores médios da proteína C-reativa altamente sensível.

Conclusão

nossas conclusões sugerem a influência positiva da suplementação simbióti- ca sobre fatores inflamatórios, dependente de seu efeito sobre a redução de peso em crianças com sobrepeso e obesas.

Palavras-chave:
Simbiótico
Crianças e adolescentes
Obesidade
Inflamação
Ensaio clínico
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Referências
[1]
E. Scarpellini, J. Tack.
Obesity and metabolic syndrome: aninflammatory condition.
Dig Dis., 30 (2012), pp. 148-153
[2]
G.S. Hotamisligil.
Endoplasmic reticulum stress and inflammation in obesity and type 2 diabetes.
Novartis Found Symp., 286 (2007), pp. 86-94
[3]
G.S. Hotamisligil, E. Erbay.
Nutrient sensing and inflammation inmetabolic diseases.
Nat Rev Immunol., 8 (2008), pp. 923-934
[4]
P.D. Cani, M. Osto, L. Geurts, A. Everard.
Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity.
Gut Microbes., 3 (2012), pp. 279-288
[5]
F. Bäckhed, J.K. Manchester, C.F. Semenkovich, J.I. Gordon.
Mechanisms underlying the resistance to diet-induced obesity ingerm-free mice.
Proc Natl Acad Sci U S A., 104 (2007), pp. 979-984
[6]
R.E. Ley, F. Bäckhed, P. Turnbaugh, C.A. Lozupone, R.D. Knight, J.I. Gordon.
Obesity alters gut microbial ecology.
Proc Natl Acad Sci USA., 102 (2005), pp. 11070-11075
[7]
F. Bäckhed, H. Ding, T. Wang, L.V. Hooper, G.Y. Koh, A. Nagy, et al.
The gut microbiota as an environmental factor that regulates fat storage.
Proc Natl Acad Sci USA., 101 (2004), pp. 15718-15723
[8]
P.D. Cani, J. Amar, M.A. Iglesias, M. Poggi, C. Knauf, D. Bastelica, et al.
Metabolic endotoxemia initiates obesity and insulin resistance.
Diabetes., 56 (2007), pp. 1761-1772
[9]
P.D. Cani, R. Bibiloni, C. Knauf, A. Waget, A.M. Neyrinck, N.M. Delzenne, et al.
Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice.
Diabetes., 57 (2008), pp. 1470-1481
[10]
M. Safavi, S. Farajian, R. Kelishadi, M. Mirlohi, M. Hashemipour.
The effects of synbiotic supplementation on some cardiometabolic risk factors in overweight and obese children: a randomized triple-masked controlled trial.
Int J Food Sci Nutr., 64 (2013), pp. 687-693
[11]
R.J. Kuczmarski, C.L. Ogden, S.S. Guo, L.M. Grummer-Strawn, K.M. Flegal, Z. Mei, et al.
2000 CDC growth charts for theUnited States: methods and development.
Vital Health Stat 11., 246 (2002), pp. 1-190
[12]
R. Kelishadi, G. Ardalan, R. Gheiratmand, R. Majdzadeh, M. Hosseini, M.M. Gouya, et al.
Thinness, overweight and obesity in anational sample of Iranian children and adolescents: CASPIAN Study.
Child Care Health Dev., 34 (2008), pp. 44-54
[13]
M.Z. Strowski, B. Wiedenmann.
Probiotic carbohydrates reduce intestinal permeability and inflammation in metabolic diseases.
Gut., 58 (2009), pp. 1044-1045
[14]
T.H. Frazier, J.K. DiBaise, C.J. McClain.
Gut microbiota, intestinal permeability, obesity-induced inflammation, and liver injury.
JPEN J Parenter Enteral Nutr., 35 (2011), pp. 14S-20S
[15]
K.C. Johnson-Henry, K.A. Donato, G. Shen-Tu, M. Gordanpour, P.M. Sherman.
Lactobacillus rhamnosus strain GG prevents enterohemorrhagic Escherichia coli O157:H7-induced changes in epithelial barrier function.
Infect Immun., 76 (2008), pp. 1340-1348
[16]
N. Parassol, M. Freitas, K. Thoreux, G. Dalmasso, R. Bourdet-Sicard, P. Rampal.
Lactobacillus casei DN-114 001 inhibits the increase inparacellular permeability of enteropathogenic Escherichia coli-infected T84 cells.
Res Microbiol., 156 (2005), pp. 256-262
[17]
C.E. McNaught, N.P. Woodcock, A.D. Anderson, J. MacFie.
A prospective randomised trial of probiotics in critically ill patients.
Clin Nutr., 24 (2005), pp. 211-219
[18]
B. Klarin, M. Wullt, I. Palmquist, G. Molin, A. Larsson, B. Jeppsson.
Lactobacillus plantarum 299 v reduces colonisation of Clostridium difficile in critically ill patients treated with antibiotics.
Acta Anaesthesiol Scand., 52 (2008), pp. 1096-1102
[19]
P.D. Cani, S. Possemiers, T. Van de Wiele, Y. Guiot, A. Everard, O. Rottier, et al.
Changes in gut microbiota control inflammation in obese mice through a mechanism involving GLP-2-driven improvement of gut permeability.
Gut., 58 (2009), pp. 1091-1103
[20]
N.M. Delzenne, A.M. Neyrinck, P.D. Cani.
Modulation of the gutmicrobiota by nutrients with prebiotic properties: consequences for host health in the context of obesity and metabolic syndrome.
Microb Cell Fact., 10 (2011), pp. S10
[21]
A. Hakansson, G. Molin.
Gut microbiota and inflammation.
Nutrients., 3 (2011), pp. 637-682
[22]
D.M. Tsukumo, M.A. Carvalho-Filho, J.B. Carvalheira, P.O. Prada, S.M. Hirabara, A.A. Schenka, et al.
Loss-of-function mutation inToll-like receptor 4 prevents diet-induced obesity and insulin resistance.
Diabetes., 56 (2007), pp. 1986-1998
[23]
Y.H. Hong, Y. Nishimura, D. Hishikawa, H. Tsuzuki, MiyaharaH, C. Gotoh, et al.
Acetate and propionate short chainfatty acids stimulate adipogenesis via GPCR43.
Endocrinology., 146 (2005), pp. 5092-5099
[24]
P.D. Cani, N.M. Delzenne.
The role of the gut microbiota inenergy metabolism and metabolic disease.
Curr Pharm Des., 15 (2009), pp. 1546-1558
[25]
F. Item, D. Konrad.
Visceral fat and metabolic inflammation: theportal theory revisited.
[26]
B. Kleessen, L. Hartmann, M. Blaut.
Fructans in the diet cause alterations of intestinal mucosal architecture, released mucins and mucosa-associated bifidobacteria in gnotobiotic rats.
Br J Nutr., 89 (2003), pp. 597-606
[27]
A.L. Bartholome, D.M. Albin, D.H. Baker, J.J. Holst, K.A. Tappenden.
Supplementation of total parenteral nutrition with butyrate acutely increases structural aspects of intestinal adaptation after an 80% jejunoileal resection in neonatal piglets.
JPEN J Parenter Enteral Nutr., 28 (2004), pp. 210-222
[28]
K.A. Tappenden, L.A. Drozdowski, A.B. Thomson, M.I. McBurney.
Short-chain fatty acid-supplemented total parenteral nutritionalters intestinal structure, glucose transporter 2 (GLUT2) mRNA and protein, and proglucagon mRNA abundance in normal rats.
Am J Clin Nutr., 68 (1998), pp. 118-125
[29]
C. Reinhardt, C.S. Reigstad, F. Bäckhed.
Intestinal microbiotaduring infancy and its implications for obesity.
J Pediatr Gastroenterol Nutr., 48 (2009), pp. 249-256
[30]
P. Hugenholtz, B.M. Goebel, N.R. Pace.
Impact of culture- independent studies on the emerging phylogenetic view of bacterial diversity.
J Bacteriol., 180 (1998), pp. 4765-4774

Como citar este artigo: Kelishadi R, Farajian S, Safavi M, Mirlohi M, Hashemipour M. A randomized triple-masked controlled trial on the effects of synbiotics on inflammation markers in overweight children. J Pediatr (Rio J). 2014;90:161-8.

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