scholarly journals Physical Exercise Improves Glycemic and Inflammatory Profile and Attenuates Progression of Periodontitis in Diabetic Rats (HFD/STZ)

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1702 ◽  
Author(s):  
Eric Andrade ◽  
Viviam Silva ◽  
Natália Moura ◽  
Renata Foureaux ◽  
Débora Orlando ◽  
...  
Keyword(s):  
Bone Loss ◽  
Physical Exercise ◽  
Alveolar Bone ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Diabetic Rats ◽  
Alveolar Bone Loss ◽  
Low Density ◽  
Tnf Α ◽  
Inflammatory Profile

The authors aimed to evaluate the effects of physical exercise on the metabolism and progression of periodontal disease (PD), induced by ligature in diabetic rats induced by high fat diet and streptozotocin (HFD/STZ). Diabetes Mellitus (DM) was induced by four weeks of a hyperlipidic diet associated with a single low-dose of streptozotocin (35 mg/kg/animal). The exercise groups swam for 60 min/day for eight weeks (five times/week). In the last two weeks of exercise, a ligature was placed around the right and left mandibular first molars. The authors determined alveolar bone loss by morphometry. Blood biochemical profile and serum levels of IL-10 and TNF-α were evaluated by colorimetric and enzyme-linked immunosorbent assays (ELISA), respectively. The diabetic animals subjected to exercise showed decreased alveolar bone loss, lower glycemia, triacylglycerols and glycosylated hemoglobin levels than the controls. Total cholesterol and its fractions (High density lipoprotein—HDL-c, Low density lipoprotein—LDL-c and Very low density lipoprotein—VLDL-c) remained similar among the groups. Animals with PD showed higher levels of TNF-α and lower levels of IL-10, when compared to animals without PD. In diabetic animals with PD, physical exercise decreased TNF-α levels and increased IL-10 levels as well as the IL10/TNF-α ratio. In conclusion, eight weeks of physical exercise improved glycemic control and systemic inflammatory profile, and attenuated alveolar bone loss in rats with DM and PD.

scholarly journals Regulation of very-low-density-lipoprotein lipid secretion in hepatocyte cultures derived from diabetic animals

1989 ◽  
Vol 262 (1) ◽  
pp. 313-319 ◽  
Author(s):  
J M Duerden ◽  
S M Bartlett ◽  
G F Gibbons
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
Whole Body ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Short Period ◽  
Streptozotocin Diabetic Rats ◽  
Cholesterol Secretion

Hepatocytes were derived from 2-3-day streptozotocin-diabetic rats and maintained in culture for up to 3 days. Compared with similar cultures from normal animals, these hepatocytes secreted less very-low-density-lipoprotein (VLDL) triacylglycerol, but the decrease in the secretion of VLDL non-esterified and esterified cholesterol was not so pronounced. This resulted in the secretion of relatively cholesterol-rich VLDL particles by the diabetic hepatocytes. Addition of insulin for a relatively short period (24 h) further decreased the low rates of VLDL triacylglycerol secretion from the diabetic hepatocytes. The secretion of VLDL esterified and non-esterified cholesterol also declined. These changes occurred irrespective of whether or not exogenous fatty acids were present in the culture medium. Little or no inhibitory effect of insulin was observed after longer-term (24-48 h) exposure to the hormone. Both dexamethasone and a mixture of lipogenic precursors (lactate plus pyruvate) stimulated VLDL triacylglycerol and cholesterol secretion, but not to the levels observed in hepatocytes from normal animals. The low rate of hepatic VLDL secretion in diabetes contrasts with the increase in whole-body VLDL production rate. This suggests that the intestine is a major source of plasma VLDL in insulin-deficient diabetes.

scholarly journals Evaluation of hydrated extract of phaseolus Vulgaris L. (bean plant) on hypoglycemia and hypolipidemic in streptozotocin-induced diabetic albino Wistar rats

2019 ◽  
Vol 10 (4) ◽  
pp. 3704-3710
Author(s):  
Helisha Ruth Obonyo ◽  
Senthemarai Selvi V
Keyword(s):  
Phaseolus Vulgaris ◽  
Blood Serum ◽  
Common Bean ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Diabetic Rats ◽  
Low Density ◽  
Phaseolus Vulgaris L ◽  
Reference Drug ◽  
The Impact

The current research was intended to comprehend hypoglycemic and anti-lipidaemic exercises of hydrated common bean (phaseolus Vulgaris L.) seed extracts on streptozotocin-induced diabetic albino rats. At a set portion fluctuate of 100, 200,300 mg/kg body weight of common bean extracts was orally directed as one portion for every day to polygenic disorder rats for a measure of thirty days. The impact of P.vulgaris L. on hypoglycemic, glycosylated hemoprotein (HbA1c) and blood serum lipid profile (Total cholesterin), Triglyceride (TG), very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), High-density lipoprotein (HDL)) in plasma were estimated in the regular and diabetic induced rat. The outcomes demonstrated that quick glucose,serum TC, TG, LDL, VLDL, levels were significantly (p<0.05) attenuate, while blood serum HDL, the level was extensively (p<0.05) upgraded inside the diabetic rats. The inconclusive amount of pace of 300 mg/kg is more reasonable than that of a hundred mg/kg. Our examination so shows that Phaseolus vulgaris L has a powerful adversary to diabetic and anti-lipidaemic impacts on streptozotocin-induced diabetic rats, and results were comparable to reference drug glibenclamide.

scholarly journals Telmisartan Prevents Alveolar Bone Loss by Decreasing the Expression of Osteoclasts Markers in Hypertensive Rats With Periodontal Disease

2020 ◽  
Vol 11 ◽  
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi de Sousa ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Bone Loss ◽  
Bone Formation ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Renin Angiotensin System ◽  
Alveolar Bone Loss ◽  
Hypertensive Rats ◽  
Bone Formation Markers ◽  
Tnf Α

Periodontal disease (PD) is a prevalent inflammatory disease with the most severe consequence being the loss of the alveolar bone and teeth. We therefore aimed to evaluate the effects of telmisartan (TELM), an angiotensin II type 1 receptor (Agtr1) antagonist, on the PD-induced alveolar bone loss, in Wistar (W) and Spontaneous Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk, and 10 mg/kg TELM was concomitantly administered for 15 days. The hemimandibles were subjected to microtomography, ELISA was used for detecting tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), CXCL3, and CCL2, while qRT-PCR was used for analyzing expression of components of renin-angiotensin system (RAS) (Agt, Ace, Agt1r, Agt2r, Ace2, and Masr), and bone markers (Runx2, Osx, Catnb, Alp, Col1a1, Opn, Ocn, Bsp, Bmp2, Trap, Rank, Rankl, CtsK, Mmp-2, Mmp-9, and osteoclast-associated receptor (Oscar)). The SHR + PD group showed greater alveolar bone loss than the W + PD group, what was significantly inhibited by treatment with TELM, especially in the SHR group. Additionally, TELM reduced the production of TNF-α, IL-1β, and CXCL3 in the SHR group. The expression of Agt increased in the groups with PD, while Agtr2 reduced, and TELM reduced the expression of Agtr1 and increased the expression of Agtr2, in W and SHRs. PD did not induce major changes in the expression of bone formation markers, except for the expression of Alp, which decreased in the PD groups. The bone resorption markers expression, Mmp9, Ctsk, and Vtn, was higher in the SHR + PD group, compared to the respective control and W + PD group. However, TELM attenuated these changes and increased the expression of Runx2 and Alp. Our study suggested that TELM has a protective effect on the progression of PD, especially in hypertensive animals, as evaluated by the resorption of the lower alveolar bone. This can be partly explained by the modulation in the expression of Angiotensin II receptors (AT1R and AT2R), reduced production of inflammatory mediators, the reduced expression of resorption markers, and the increased expression of the bone formation markers.

scholarly journals Effect of inhaled corticosteroid on TNF-α production and alveolar bone loss in Wistar rats

2011 ◽  
Vol 56 (11) ◽  
pp. 1398-1403 ◽  
Author(s):  
Luciana Dondonis Daudt ◽  
Juliano Cavagni ◽  
Eduardo José Gaio ◽  
Andressa Souza ◽  
Iraci Lucena da Silva Torres ◽  
...  
Keyword(s):  
Bone Loss ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Inhaled Corticosteroid ◽  
Tnf Α

Involvement of Cot/Tp12 in Bone Loss during Periodontitis

2010 ◽  
Vol 89 (2) ◽  
pp. 192-197 ◽  
Author(s):  
T. Ohnishi ◽  
A. Okamoto ◽  
K. Kakimoto ◽  
K. Bandow ◽  
N. Chiba ◽  
...  
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Periodontal Tissue ◽  
Rankl Expression ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Experimental Periodontitis ◽  
Deficient Mice

Periodontitis causes resorption of alveolar bone, in which RANKL induces osteoclastogenesis. The binding of lipopolysaccharide to Toll-like receptors causes phosphorylation of Cot/Tp12 to activate the MAPK cascade. Previous in vitro studies showed that Cot/Tp12 was essential for the induction of RANKL expression by lipopolysaccharide. In this study, we examined whether Cot/Tp12 deficiency reduced the progression of alveolar bone loss and osteoclastogenesis during experimental periodontitis. We found that the extent of alveolar bone loss and osteoclastogenesis induced by ligature-induced periodontitis was decreased in Cot/Tp12-deficient mice. In addition, reduction of RANKL expression was observed in periodontal tissues of Cot/Tp12-deficient mice with experimental periodontitis. Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-α mRNA expression in gingiva of mice with experimental periodontitis. Our observations suggested that Cot/Tp12 is essential for the progression of alveolar bone loss and osteoclastogenesis in periodontal tissue during experimental periodontitis mediated through increased RANKL expression.

Enhanced accumulation of cholesterol ester in macrophages from diabetic rats incubated with oxidized low-density lipoprotein

1994 ◽  
Vol 55 (6) ◽  
pp. 660-665
Author(s):  
Jun Matsui ◽  
Tomio Onuma ◽  
Masahiro Tsutsui ◽  
Michitaka Shimura ◽  
Toru Kikuchi ◽  
...  
Keyword(s):  
Cholesterol Ester ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Diabetic Rats ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein

Effect of an Aldose Reductase Inhibitor on Alveolar Bone Loss Associated with Periodontitis in Diabetic Rats

2010 ◽  
Vol 122 (3) ◽  
pp. 138-144 ◽  
Author(s):  
Peter F. Kador ◽  
Tomofumi Hamada ◽  
Richard A. Reinhardt ◽  
Karen Blessing
Keyword(s):  
Bone Loss ◽  
Aldose Reductase ◽  
Reductase Inhibitor ◽  
Alveolar Bone ◽  
Diabetic Rats ◽  
Alveolar Bone Loss ◽  
Aldose Reductase Inhibitor

scholarly journals Local and Systemic Responses in Matrix Metalloproteinase 8-Deficient Mice during Porphyromonas gingivalis-Induced Periodontitis

2008 ◽  
Vol 77 (2) ◽  
pp. 850-859 ◽  
Author(s):  
Heidi Kuula ◽  
Tuula Salo ◽  
Emma Pirilä ◽  
Anita M. Tuomainen ◽  
Matti Jauhiainen ◽  
...  
Keyword(s):  
Bone Loss ◽  
Matrix Metalloproteinase ◽  
Porphyromonas Gingivalis ◽  
Alveolar Bone ◽  
Inflammatory Responses ◽  
Density Lipoprotein ◽  
Alveolar Bone Loss ◽  
Type I ◽  
Site Specific ◽  
Vldl Particle

ABSTRACT Periodontitis is a bacterium-induced chronic inflammation that destroys tissues that attach teeth to jaw bone. Pathologically excessive matrix metalloproteinase 8 (MMP-8) is among the key players in periodontal destruction by initiating type I collagen degradation. We studied MMP-8 in Porphyromonas gingivalis-induced periodontitis by using MMP-8-deficient (MMP8 −/− ) and wild-type (WT) mice. Alveolar bone loss, inflammatory mediator expression, serum immunoglobulin, and lipoprotein responses were investigated to clarify the role of MMP-8 in periodontitis and systemic inflammatory responses. P. gingivalis infection induced accelerated site-specific alveolar bone loss in both MMP8 −/− and WT mice relative to uninfected mice. The most extensive bone degradation took place in the P. gingivalis-infected MMP8 −/− group. Surprisingly, MMP-8 significantly attenuated (P < 0.05) P. gingivalis-induced site-specific alveolar bone loss. Increased alveolar bone loss in P. gingivalis-infected MMP8 −/− and WT mice was associated with increase in gingival neutrophil elastase production. Serum lipoprotein analysis demonstrated changes in the distribution of high-density lipoprotein (HDL) and very-low-density lipoprotein (VLDL) particles; unlike the WT mice, the MMP8 −/− mice underwent a shift toward a smaller HDL/VLDL particle sizes. P. gingivalis infection increased the HDL/VLDL particle size in the MMP8 −/− mice, which is an indicator of lipoprotein responses during systemic inflammation. Serum total lipopolysaccharide activity and the immunoglobulin G-class antibody level in response to P. gingivalis were significantly elevated in both infected mice groups. Thus, MMP-8 appears to act in a protective manner inhibiting the development of bacterium-induced periodontal tissue destruction, possibly through the processing anti-inflammatory cytokines and chemokines. Bacterium-induced periodontitis, especially in MMP8 −/− mice, is associated with systemic inflammatory and lipoprotein changes that are likely involved in early atherosclerosis.

scholarly journals Resolution phase agonists &bone remodeling

2016 ◽  
Author(s):  
Ευάγγελος Παπαθανασίου
Keyword(s):  
Bone Loss ◽  
Alveolar Bone ◽  
Peritoneal Macrophages ◽  
Alveolar Bone Loss ◽  
Cytokine Signaling ◽  
Periodontal Inflammation ◽  
Oral Inoculation ◽  
Tnf Α ◽  
Socs Proteins ◽  
Anti Inflammatory

Periodontitis is the 6th most prevalent disease in the world and the primary cause for tooth loss in adults. The host immune response plays a key role in bacteria-induced alveolar bone resorption. Endogenous control of the magnitude and duration of inflammatory signaling is considered an important determinant of the extent of periodontal pathology. Suppressor of cytokine signaling (SOCS) proteins are inhibitors of cytokine signaling pathways and may play a role in controlling periodontal inflammation. SOCS proteins are also considered crucial intracellular mediators of the anti-inflammatory actions of lipid mediator agonists including resolvins such as RvE1. We hypothesized that SOCS-3 regulates inflammatory cytokine signaling and alveolar bone loss in experimental periodontitis and that the anti-inflammatory actions of RvE1 are SOCS-3 dependent. Periodontal bone loss was induced in myeloid-specific SOCS-3-knockout (KO) and SOCS-3-wild-type (WT) C57Bl6-B.129 mice by oral inoculation with 1×109 colony-forming units (CFU) P. gingivalis A7436 using an oral gavage model for periodontitis. Sham controls for both types of mice received vehicle without bacteria. The mice were euthanized 6 weeks after the last oral inoculation. Morphometric, histomorphometric, and µCT analyses were performed to assess alveolar bone loss. Peritoneal macrophages were elicited with 4% thioglycolate broth and isolated from myeloid SOCS-3-KO and SOCS-3-WT mice by differential centrifugation. Macrophages were cultured at a concentration of 1.5×106 cells/ml in 6-well plates. After 2 hours, non-adherent cells were discarded and the remaining adherent cells were treated with either culture medium alone (control) or with 100 ng/ml P. gingivalis A7436 LPS or with culture medium and 100nM RvE1 or with 100 ng/ml P. gingivalis A7436 LPS and RvE1 100nM (n≥3 wells per group). Supernatants and cells were collected after 12 hours. Cytokine levels were assessed using Luminex multiplex bead immunoassay and RNA was extracted by Trizol and processed for qRT-PCR. Increased bone loss was demonstrated in P. gingivalis-infected SOCS-3- KO mice compared to P. gingivalis-infected WT mice by direct morphological measurements, µCT analyses and quantitative histology. Loss of SOCS-3 function resulted in increased number of alveolar bone osteoclasts and increased RANKL expression after P. gingivalis infection. SOCS-3 deficiency in myeloid cells also promoted a higher P. gingivalis LPS-induced inflammatory response by inducing a higher secretion of IL-1β, IL-6, TNF-α and KC (IL-8) by peritoneal macrophages from SOCS-3-KO mice. 100nM RvE1 resulted in a significant decrease in P. gingivalis LPS-induced secretion of IL-6, TNF-α and IL-8 by increasing mRNA expression of SOCS-3 and ERV1 in macrophages from SOCS-3-WT mice compared to macrophages from myeloid SOCS-3-KO ones. Our data implicate SOCS-3 as a critical negative regulator of alveolar bone loss in experimental periodontitis and P. gingivalis LPS-induced inflammatory response. SOCS-3 regulates the anti-inflammatory actions of RvE1 on P. gingivalis LPS-induced inflammatory cytokines in macrophages. Understanding further the role of SOCS proteins in regulating periodontal inflammation may provide novel pathways of host susceptibility to periodontitis and new therapeutic targets for modulating the immune response to achieve successful resolution of periodontal inflammation.

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