The relationship of periodontal disease severity to serum and GCF substance P levels in diabetics

Objective: To compare circulating and gingival crevicular fluid (GCF) substance P concentrations in well- and poorly controlled type 2 diabetic patients with chronic periodontitis. METHOD AND MATERIALS: Forty-five serum and 90 GCF samples were collected from diabetic patients with periodontal disease, and the concentrations of substance P were quantified by radioimmunoassay. RESULTS: Serum substance P levels were higher in the poorly controlled diabetic group than in patients with good glycemic control (P = .01); within the poorly controlled group, patients with severe attachment levels had the highest circulating substance P levels (P = .02). Additionally, the diseased sites showed higher substance P levels than control sites (P = .0016). The GCF substance P concentrations in diseased sites correlated significantly with clinical findings such as Plaque Index (r = 0.51, P = .001) and bleeding on probing (r = 0.35, P = .029). CONCLUSION: Within the limits of this study, our preliminary findings indicate that periodontal inflammation may influence circulating and GCF substance P levels in poorly controlled diabetic subjects. (Quintessence Int 2012;43:587-596

The comparison of the intestinal adaptation effects of subcutaneous and oral insulin in a rats with short bowel syndrome

Aim: Insulin has been reported to have positive effects on intestinal adaptation after short bowel syndrome when applicated oral or subcutaneously. The purpose of this study is to compare the intestinal adaptation effects of subcutaneous and oral routes of insulin in rats with short bowel syndrome. Materials and Methods: The short bowel syndrome (SBS) was performed through 70-75% of small intestinal resection and an end-to-end anastomosis. The control group rats underwent SBS only. In the second group, oral insulin (1 U/ml) was administrated twice-daily. In the last group, the insulin was administrated subcutaneously (1 U/kg) as in the control group. All rats were killed on day 15. Outcome parameters were weight of small intestine, the crypt length, villous depth, the blood levels of vascular endothelial growth factor (VEGF), and granolocyt-monocyst colony-stimulating factor (GMCSF). Results: Intestinal weight was significantly more in oral insulin group and subcutaneous insulin group than in the control group (72.6 ± 4.3, 78.6 ± 4.8 and 59.7 ± 4.8) (P 0.05). VEGF values were not statistically significant between the groups (200.3 ± 41.6, 178.9 ± 30.7 and 184.3 ± 52.2) (P > 0.05). GMCSF was statistically higher in the control group than in other groups (3.34 ± 1.34, 1.56 ± 0.44 and 1.56 ± 0.44) (P < 0.05). Conclusion: Insulin has positive effects on intestinal adaptation in short bowel syndrome. Subcutaneous administration is slightly more effective than the oral route

Assessment of genotoxicity in rats treated with the antidiabetic agent, pioglitazone

Pioglitazone (PIO), a member of the thiazolidinedione class of antidiabetic agents, specifically targets insulin resistance. Drugs of this class act as ligands for the gamma subtype of the peroxisome proliferator-activated receptor. Although troglitazone, another drug in this class, displayed unacceptable hepatotoxicity, PIO was approved for human use by the U.S. Food and Drug Administration. To our knowledge, there are no published reports on the genotoxicity of PIO; however, the package insert indicates that it has minimal genotoxicity. In this study, we used the comet assay to investigate the DNA damage in the peripheral blood and liver cells of rats treated with PIO. Sixteen male Sprague-Dawley rats were randomly distributed into four groups, and dosed daily for 14 days by oral gavage with 0, 10, 20, and 40 mg/kg/day PIO. A dose-dependent increase in DNA damage, as assessed by % tail DNA, was observed in both hepatocytes and blood lymphocytes of the PIO-treated groups, with significant increases detected between the rats treated with all the doses of PIO and the control, and between the rats treated with different PIO doses (P < 0.005 to P < 0.0001). Treating nuclei from the exposed animals with an enzyme cocktail containing Fpg and Endonuclease III prior to performing the comet assay increased the level of DNA damage, which reflects oxidized purine and pyrimidine. Taken together, our data indicate that PIO is able to dose-dependently induce DNA damage in both the liver and blood lymphocytes of rats, which is partially due to the generation of oxidative lesions