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1.
Braz. oral res. (Online) ; 31: e90, 2017. tab, graf
Article in English | LILACS | ID: biblio-952113

ABSTRACT

Abstract: The mechanism by which chronic periodontitis (CP) affects type 2 diabetes (T2DM) remains unclear. Therefore, the aim of this study is to evaluate the effects of periodontal therapy (PT) on the glycemic control and adipokines of patients with T2DM and CP with the purpose of elucidating the possible mechanisms by which CP influences T2DM. Forty-four patients with T2DM and CP were randomly divided into two groups according to whether they underwent PT. Periodontal status, blood glucose, and the levels of serum tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), adiponectin (APN), and fibroblast growth factor-21 (FGF-21) were measured at baseline and after 3 months. The results revealed that the probing depth (PD) and attachment loss (AL) were significantly improved, the serum levels of TNF-α and IL-6 were significantly decreased, and APN and FGF-21 exhibited substantial increases in the intervention group after 3 months (p < 0.05), whereas no significant changes were observed in the control group. The glycated hemoglobin (HbA1c) levels in both groups decreased significantly after 3 months compared with baseline (p < 0.05), but the intervention group exhibited a significantly greater change (p < 0.05). In conclusion, PT may relieve periodontal inflammation, which causes a reduction of insulin-antagonizing adipokines and an increase in insulin-sensitizing adipokines, thereby eliciting an improvement in glycemic control.


Subject(s)
Humans , Male , Female , Aged , Diabetes Mellitus, Type 2/prevention & control , Diabetes Mellitus, Type 2/blood , Adipokines/blood , Chronic Periodontitis/blood , Chronic Periodontitis/therapy , Reference Values , Time Factors , Blood Glucose/analysis , Glycated Hemoglobin/analysis , Periodontal Index , Interleukin-6/blood , Tumor Necrosis Factor-alpha/blood , Periodontal Attachment Loss , Diabetes Mellitus, Type 2/physiopathology , Chronic Periodontitis/physiopathology , Fibroblast Growth Factors/blood , Middle Aged
2.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 701-704, 2009.
Article in Chinese | WPRIM | ID: wpr-341154

ABSTRACT

This study investigated whether the curative effect of short-pulse gastric electrical stimulation (GES) on the vasopressin-induced dyspeptic symptoms was mediated by central opioid peptide-producing neurons. Five female beagle dogs implanted with 1 pair of electrodes in gastric serosa were used in a two-experiment study. In experiment one,the brain was scanned by positron emission tomography in 3 dogs with and without short-pulse GES,and the radioactivity in nuclei of solitary tract (NST) and hypothalamus was detected. Experiment two was composed of 4 sessions. In session one,the dogs were injected with vasopressin in the absence of short-pulse GES. With session two,the short-pulse GES was simultaneously given via the electrodes with the injection of vasopressin. In sessions three and four,naloxone and naloxone methiodide was administered respectively in the presence of short-pulse GES. Motion sickness-like symptoms were scored and compared among the different sessions. The results showed that the short-pulse GES significantly increased the radioactivity in NST and hypothalamic nuclei (P<0.05,vs control). The short-pulse GES could ameliorate the vasopressin-induced motion sickness-like symptoms in dogs. Naloxone,but not naloxone methiodide could attenuate the curative effects of short-pulse GES. It is concluded that NST and hypothalamic nuclei may participate in the mediation of the curative effects of short-pulse GES on dyspepsia-like symptoms. Central opioid peptide-containing neurons presumably mediate the therapeutic effect on dyspeptic symptoms of short-pulse GES.

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