The oral focal inflammation may cause deleterious systemic manifestations in the body human, including diabetes mellitus (DM). This fact is relevant because some surgical procedures in patients with non-controlled diabetic involve serious risk to health. The pulp's disease (LP) is a local inflammation and it increases amounts of inflammatory cytokines such as TNF-a and IL-6, known to induce cellular resistance to insulin. The inflammation associated with insulin deficiency causes physiological changes like immunosuppression, reducing osteoblasts numbers and consequent impairment of tissue repair in the patient. However, It is still unknown the correlation between DM and LP. Aware that the inflammatory cytokines TNF-and IL-6 can cause changes in insulin signal, it becomes necessary to investigate the possibility of a local inflammatory process, as the LP "per se", to cause insulin resistance in non-diabetic people. The aim of this study is to evaluate in rats with LP: 1) plasmatic concentration of glucose, insulin, cholesterol and triglycerides; 2) insulin sensitivity; 3) tyrosine phosphorylation status of pp185 (IRS1/IRS2) in white adipose tissue, skeletal muscle gastrocnemius and liver. In this study will be used 30 Wistar's rats (2 months-old) divided into two groups: a) control rats without the LP; b) LP induced in rats with right upper molars employing drill fitted with carbon steel ball in the end with 0.1 mm. After 30 days of induction of LP, the animals will be anesthetized for the experiments. (AU)
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(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ASTOLPHI, RAFAEL DIAS;
CURBETE, MARIANE MACHADO;
COLOMBO, NATALIA HELENA;
SHIRAKASHI, DAISY JAQUELINE;
CHIBA, FERNANDO YAMAMOTO;
CARRARA PRIETO, ANNELISE KATRINE;
ANGELO CINTRA, LUCIANO TAVARES;
MOGAMI BOMFIM, SUELY REGINA;
SUMIDA, DORIS HISSAKO.
Periapical Lesions Decrease Insulin Signal and Cause Insulin Resistance.
JOURNAL OF ENDODONTICS,
Web of Science Citations: 18.
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