Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring
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Citações na Scopus
13
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Autores
MATTERA, Maria Sara de Lima Coutinho
CHIBA, Fernando Yamamoto
LOPES, Flavia Lombardi
TSOSURA, Thais Veronica Saori
BRITO, Victor Gustavo Balera
OLIVEIRA, Sandra Helena Penha de
PEREIRA, Renato Felipe
MARANI, Fernando
SANTOS, Rodrigo Martins dos
Citação
JOURNAL OF PERIODONTOLOGY, v.90, n.8, p.884-893, 2019
Resumo
Background Maternal periodontal disease leads to low birth weight (LBW), insulin resistance (IR), increased TNF-alpha levels, and alterations in insulin signaling in adult offspring. TNF-alpha has been associated with the stimulation of IKK beta/NF-kappa B, resulting in the decreased expression of GLUT4. Another mechanism that may be involved in decreasing GLUT4 expression is DNA methylation. This study aimed to evaluate in the adult offspring of rats with periodontal disease: IR, inflammatory pathways, DNA methylation, and expression of GLUT4. Methods Female Wistar rats were distributed into control and experimental periodontal disease groups. Seven days after induction of periodontal disease, both groups were mated with healthy male rats. After weaning, male offspring were distributed into control offspring (CN-o) and periodontal disease offspring (PED-o) groups. Body weights were measured from 0-75 days of age. At day 75, the following were measured in the offspring: IR (HOMA-IR index); TNF-alpha and NF-kappa Bp65 content in the gastrocnemius muscle (GM) by western blotting; IKK alpha/beta, JNK, ERK 1/2, NF-kappa Bp65, and NF-kappa Bp50 phosphorylation status in the GM by western blotting; DNA methylation by restriction digest and real-time PCR(qAMP); and expression of GLUT4 mRNA in the GM by real-time PCR. Results LBW, IR, increases in TNF-alpha, IKK alpha/beta, ERK 1/2, NF-kappa Bp65, and NF-kappa Bp50 decreased expression of GLUT4 mRNA were observed in the PED-o rats. No differences were identified in JNK phosphorylation status and DNA methylation in the evaluated regions of the GLUT4-encoding gene Slc2a4. Conclusion Maternal periodontal disease causes LBW, IR, activation of inflammatory pathways, and decreased GLUT4 expression in the GM of adult offspring.
Palavras-chave
diabetes mellitus, DNA methylation, glucose transporter type 4, low birth weight, periodontal diseases, tumor necrosis factor-alpha
Referências
- Backdahl L, 2009, INT J BIOCHEM CELL B, V41, P176, DOI 10.1016/j.biocel.2008.08.023
- Bansal Mansi, 2013, Rev Obstet Gynecol, V6, P135
- Barker DJP, 1997, CLIN OBSTET GYNECOL, V40, P853, DOI 10.1097/00003081-199712000-00019
- BARKER DJP, 1995, BRIT MED J, V311, P171, DOI 10.1136/bmj.311.6998.171
- Baylin Stephen B, 2005, Nat Clin Pract Oncol, V2 Suppl 1, pS4, DOI 10.1038/ncponc0354
- Boersma B, 1997, ENDOCR REV, V18, P646, DOI 10.1210/er.18.5.646
- Bonora E, 2000, DIABETES CARE, V23, P57, DOI 10.2337/diacare.23.1.57
- Calkins K, 2011, CURR PROB PEDIATR AD, V41, P158, DOI 10.1016/j.cppeds.2011.01.001
- Carvalho CRO, 1996, ENDOCRINOLOGY, V137, P151, DOI 10.1210/en.137.1.151
- Cianfarani S, 1999, ARCH DIS CHILD, V81, pF71, DOI 10.1136/fn.81.1.F71
- Davenport ES, 2002, J DENT RES, V81, P313, DOI 10.1177/154405910208100505
- de Alvaro C, 2004, J BIOL CHEM, V279, P17070, DOI 10.1074/jbc.M312021200
- Mattera MSDC, 2016, LIFE SCI, V148, P194, DOI 10.1016/j.lfs.2016.02.010
- DeFronzo RA, 2009, DIABETES CARE, V32, pS157, DOI 10.2337/dc09-S302
- Dhanasekaran DN, 2008, ONCOGENE, V27, P6245, DOI 10.1038/onc.2008.301
- Furuya DT, 2013, MOL CELL ENDOCRINOL, V370, P87, DOI 10.1016/j.mce.2013.01.019
- Gandhimadhi D, 2010, J Indian Soc Periodontol, V14, P114, DOI 10.4103/0972-124X.70832
- Godfrey K M, 2001, Public Health Nutr, V4, P611
- Guimaraes AN, 2012, J CLIN PERIODONTOL, V39, P1024, DOI 10.1111/jcpe.12000
- Haerian-Ardakani A, 2013, IRAN J REPROD MED, V11, P625
- HALES CN, 1991, BMJ-BRIT MED J, V303, P1019, DOI 10.1136/bmj.303.6809.1019
- Hales CN, 2001, BRIT MED BULL, V60, P5, DOI 10.1093/bmb/60.1.5
- Hofman PL, 1997, J CLIN ENDOCR METAB, V82, P402, DOI 10.1210/jc.82.2.402
- Ide M, 2013, J CLIN PERIODONTOL, V40, pS181, DOI [10.1111/jcpe.12063, 10.1902/jop.2013.134009]
- Kaneto H, 2005, J MOL MED-JMM, V83, P429, DOI 10.1007/s00109-005-0640-x
- Lasheen NN, 2015, PHYSL REP, V3, P1
- Liu CX, 2016, CYTOKINE, V86, P100, DOI 10.1016/j.cyto.2016.06.028
- Liu HW, 2013, J NUTR BIOCHEM, V24, P1859, DOI 10.1016/j.jnutbio.2013.05.002
- Madianos PN, 2013, J PERIODONTOL, V84, pS170, DOI [10.1902/jop.2013.1340015, 10.1111/jcpe.12082]
- Mannem S, 2011, CONTEMP CLIN DENT, V2, P88, DOI 10.4103/0976-237X.83067
- Moore LD, 2013, NEUROPSYCHOPHARMACOL, V38, P23, DOI 10.1038/npp.2012.112
- Morrison JL, 2010, PEDIATR NEPHROL, V25, P669, DOI 10.1007/s00467-009-1407-3
- Nakano H, 2004, TRENDS IMMUNOL, V25, P402, DOI 10.1016/j.it.2004.05.007
- Oakes Christopher C., 2009, V507, P271, DOI 10.1007/978-1-59745-522-0_20
- Oeckinghaus A, 2009, CSH PERSPECT BIOL, V1, DOI 10.1101/cshperspect.a000034
- Offenbacher S, 2005, J PERIODONTOL, V76, P2133, DOI 10.1902/jop.2005.76.11-S.2133
- Plomgaard P, 2005, DIABETES, V54, P2939, DOI 10.2337/diabetes.54.10.2939
- Pozo E, 2016, HISTOL HISTOPATHOL, V31, P231, DOI 10.14670/HH-11-671
- Raychaudhuri N, 2008, J BIOL CHEM, V283, P13611, DOI 10.1074/jbc.M800128200
- Rodini CO, 2008, J MOL HISTOL, V39, P275, DOI 10.1007/s10735-008-9163-4
- Schwabe RF, 2006, AM J PHYSIOL-GASTR L, V290, pG583, DOI 10.1152/ajpgi.00422.2005
- Shirakashi DJ, 2013, J PERIODONTOL, V84, P407, DOI 10.1902/jop.2012.110372
- Shoelson SE, 2006, J CLIN INVEST, V116, P1793, DOI 10.1172/JCI29069
- Silva JLT, 2005, MOL CELL ENDOCRINOL, V240, P82, DOI 10.1016/j.mce.2005.05.006
- Siqueira FM, 2007, J PERIODONTOL, V78, P2266, DOI 10.1902/jop.2007.070196
- Thompson RF, 2010, J BIOL CHEM, V285, P15111, DOI 10.1074/jbc.M109.095133
- Vaag AA, 2012, DIABETOLOGIA, V55, P2085, DOI 10.1007/s00125-012-2589-y
- Zeng Y, 2013, MOL MED REP, V7, P306, DOI 10.3892/mmr.2012.1134