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Published on: June 28, 2024
Effect of maternal periodontitis on GLUT4 and inflammatory pathway in adult offspring
Maria Sara de Lima Coutinho Mattera1, Fernando Yamamoto Chiba2, Flávia Lombardi Lopes3
1Multicenter Post-Graduate Program in Physiological Sciences (SBFis), Department of Basic Sciences, School of Dentistry, São Paulo State University (UNESP), Araçatuba, Brazil.
Insights
Maternal periodontal disease in rats resulted in low birth weight and insulin resistance in offspring. This was linked to increased inflammation and reduced GLUT4 expression, but not DNA methylation changes.
Area of Science:
- Reproductive biology and developmental origins of health and disease.
- Endocrinology and metabolic disorders.
- Immunology and inflammation.
Background:
- Maternal periodontal disease is linked to adverse offspring outcomes, including low birth weight (LBW) and insulin resistance (IR).
- Inflammatory pathways, such as TNF-α and NF-κB signaling, are implicated in reduced glucose transporter type 4 (GLUT4) expression.
- Epigenetic modifications, like DNA methylation, may also influence GLUT4 expression.
Purpose of the Study:
- To investigate insulin resistance (IR), inflammatory pathways, DNA methylation, and GLUT4 expression in adult offspring of rats with maternal periodontal disease.
- To determine the impact of maternal periodontal disease on the metabolic and molecular profiles of offspring.
Main Methods:
- Female Wistar rats with induced periodontal disease were mated with healthy males.
- Offspring were categorized into control (CN-o) and periodontal disease (PED-o) groups.
- Measurements included body weight, HOMA-IR index, protein levels and phosphorylation of inflammatory markers (TNF-α, NF-κBp65, IKKα/β, JNK, ERK 1/2), DNA methylation, and GLUT4 mRNA expression in gastrocnemius muscle.
Main Results:
- Offspring exposed to maternal periodontal disease (PED-o) exhibited LBW, IR, elevated TNF-α, and increased phosphorylation of IKKα/β, ERK 1/2, NF-κBp65, and NF-κBp50.
- A significant decrease in GLUT4 mRNA expression was observed in PED-o rats.
- No significant differences were found in JNK phosphorylation or DNA methylation within the evaluated regions of the Slc2a4 gene.
Conclusions:
- Maternal periodontal disease induces LBW, IR, and activates inflammatory pathways in adult offspring.
- The inflammatory cascade contributes to the observed decrease in GLUT4 expression in the gastrocnemius muscle.
- DNA methylation was not identified as a primary mechanism for altered GLUT4 expression in this model.
Background:
Maternal periodontal disease leads to low birth weight (LBW), insulin resistance (IR), increased TNF-α levels, and alterations in insulin signaling in adult offspring. TNF-α has been associated with the stimulation of IKKβ/NF-κB, 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-α and NF-κBp65 content in the gastrocnemius muscle (GM) by western blotting; IKKα/β, JNK, ERK 1/2, NF-κBp65, and NF-κBp50 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-α, IKKα/β, ERK 1/2, NF-κBp65, and NF-κBp50 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.
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