Journal of dental research, 2014-06, Vol.93 (6), p.596-601
2014
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- Autor(en) / Beteiligte
- Titel
- Obesity-associated Gingival Vascular Inflammation and Insulin Resistance
- Ist Teil von
- Journal of dental research, 2014-06, Vol.93 (6), p.596-601
- Ort / Verlag
- Los Angeles, CA: SAGE Publications
- Erscheinungsjahr
- 2014
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Obesity is a risk factor for periodontitis, but the pathogenic mechanism involved is unclear. We studied the effects of insulin in periodontal tissues during the state of obesity-induced insulin resistance. Gingival samples were collected from fatty (ZF) and lean (ZL, control) Zucker rats. Endothelial nitric oxide synthase (eNOS) expression was decreased, and activities of protein kinase C (PKC) α, ß2, δ, and ϵ isoforms were significantly increased in the gingiva from ZF rats compared with those from ZL rats. Expression of oxidative stress markers (mRNA) and the p65 subunit of NF-κB was significantly increased in ZF rats. Immunohistochemistry revealed that NF-κB activation was also increased in the gingival endothelial cells from transgenic mice overexpressing NF-κB-dependent enhanced green fluorescent protein (GFP) and on a high-fat vs. normal chow diet. Analysis of the gingiva showed that insulin-induced phosphorylation of IRS-1, Akt, and eNOS was significantly decreased in ZF rats, but Erk1/2 activation was not affected. General PKC inhibitor and an anti-oxidant normalized the action of insulin on Akt and eNOS activation in the gingiva from ZF rats. This provided the first documentation of obesity-induced insulin resistance in the gingiva. Analysis of our data suggested that PKC activation and oxidative stress may selectively inhibit insulin-induced Akt and eNOS activation, causing endothelial dysfunction and inflammation.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0022-0345eISSN: 1544-0591DOI: 10.1177/0022034514532102Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4023466
- Format
- –
- Schlagworte
- AKT protein, Alveolar Bone Loss - etiology, Alveolar Bone Loss - metabolism, Animals, Biotechnology, Cytokines, Dentistry, Diabetes, Endothelial cells, Endothelial Cells - chemistry, Endothelium, Vascular - chemistry, Extracellular signal-regulated kinase, Gingiva, Gingivitis - etiology, Gingivitis - metabolism, Glucose, Green fluorescent protein, Gum disease, High fat diet, Immunoglobulins, Immunohistochemistry, Inflammation, Insulin, Insulin receptor substrate 1, Insulin Receptor Substrate Proteins - analysis, Insulin resistance, Insulin Resistance - physiology, Isoforms, Kinases, Male, Mice, Mice, Transgenic, mRNA, NF-κB protein, Nitric Oxide Synthase Type III - analysis, Nitric-oxide synthase, Obesity, Obesity - complications, Oncogene Protein v-akt - analysis, Oxidative stress, Oxidative Stress - physiology, Periodontitis, Phosphorylation, Protein kinase C, Protein Kinase C beta - analysis, Protein Kinase C-alpha - analysis, Protein Kinase C-delta - analysis, Protein Kinase C-epsilon - analysis, Proteins, Rats, Rats, Zucker, Research Reports, Risk factors, Rodents, Studies, Transcription Factor RelA - analysis, Transgenic mice, Vasculitis - etiology, Vasculitis - metabolism