To invesitgate the protein expression for leptin receptor in skeletal muscle in periodontitis and obese rat models, with the aim of exploring the effect of experimental periodontitis on adipokines receptors in insulin-targeting tissues and underlying mechanisms of skeletal muscle insulin resistance.

Forty natal SD male rats were randomly divided into four groups, respectively: obese rats with periodontitis (OB+ CP group), obese rats without periodontitis (OB group), normal rats with periodontitis (CP group) and normal rats without periodontitis (C group). Obese rat model was established by subcutaneous injection of sodium glutamate. Experimental periodontitis was induced by ligation and inoculation of periodontal pathogens. Immunohistochemical analysis of leptin receptor expression in skeletal muscle of four groups was employed.

In the skeletal muscle, the protein for leptin receptor in the C group and CP group were popular and strong positive, and there was no statistically significant difference between the groups (P > 0.05). The protein expressions in the OB + CP group and OB group were decreased. Fewer protein expression was detected in the OB + CP group when compared with OB group (P < 0.05). A synergistic interaction between obesity and periodontitis was evident to the expression for the leptin receptor (P < 0.05). Local infection induced by experimental periodontitis can barely down-regulate the protein expression for leptin receptor in the skeletal muscle. However, periodontitis can significantly down-regulate the protein expressions with the presence of obesity.

To investigate the effects of chronic periodontitis on kidney function of OLETF rats.

30 spontaneous type 2 diabetes mellitus (T2DM) OLETF rats aged 4 weeks were selected as the experimental objects, and 20 LETO rats with normal sugar tolerance of the same species and the same week age were selected as the control group. When the rats arrived the glucose tolerance damage stage at the age of 36 weeks, 26 OLETF rats (O group) were divided into diabetes mellitus combined periodontitis group (O CP(+) group) and diabetic group (O CP(-) group) randomly, and 20 LETO rats (L group) were randomly divided into periodontitis group (L CP(+) group) and normal group (L CP(-) group). Then the chronic periodontis models were established on the rats in the O CP(+) group and L CP(+) group, by silk thread ligation combined with coated bacteria. All the rats were executed at the 56 weeks age, when the models were established for 20 weeks. The serum was collected and analyzed by automatic biochemical machine to measure the biochemical indicators of renal function, including the following 4 indexes: serum albumin (ALB), total protein (TP), urea and creatinine (CR).

The levels of serum TP and ALB decreased significantly in O group than in L group (P＜0.01), as the same result when compared O CP(+) group with O CP(-) group (P＜0.01), however, there was no significant difference when compared L CP(+) group to L CP(-) group. Serum CR was significantly higher in O group than in L group (t = 9.099, P = 0.005), the same as that in O CP(+) group when compared with O CP(-) group (t = 4.443, P＜0.001), while there was no significant difference when compared L CP(+) group to L CP(-) group. Serum urea levels in O group was significantly higher than in L group (t = 5.684, P = 0.024), While there was no significant difference between O CP(+) group and O CP(-) group (t = 1.484, P = 0.160), the same as that between L CP(+) group and L CP(-) group (t =0.075, P = 0.932).

It shows that chronic periodontitis may not cause changes in kidney function in normal rats. However, in the case of T2DM, chronic periodontitis may increase the existing kidney damage. It indicates that T2DM and chronic periodontitis may have interactions in the development of diabetic kidney disease.