scholarly journals Voluntary running of defined distances alters bone microstructure in C57BL/6 mice fed a high-fat diet

2021 ◽  
Author(s):  
Lin Yan ◽  
Forrest H Nielsen ◽  
Sneha Sundaram ◽  
Jay Cao
Keyword(s):  
Bone Resorption ◽  
Bone Quality ◽  
High Fat Diet ◽  
Bone Microstructure ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
High Fat ◽  
Trabecular Thickness ◽  
Voluntary Running ◽  
Dose Dependent

Obesity increases the risk for pathological conditions such as bone loss. On the other hand, physical exercise reduces body adiposity. To test the hypothesis that physical activity improves bone quality, we evaluated voluntary running of defined distances on trabecular and cortical microstructure in mice fed a high-fat diet (HFD). Sedentary mice were fed the standard AIN93G diet or the HFD. Mice fed the HFD remained sedentary or were assigned to unrestricted running or 75%, 50%, and 25% of unrestricted running with an average running activity at 8.3, 6.3, 4.2, and 2.1 km per day, respectively. The bone structural differences found in sedentary mice were that HFD, compared the AIN93G diet, resulted in a lower bone volume fraction (BV/TV) and a higher structure model index (SMI) in vertebrae. Running had a greater effect on trabecular microstructure in femurs than in vertebrae; the decrease in SMI and an increase in trabecular thickness (Tb.Th) were in a dose-dependent manner. Running was positively correlated with BV/TV and Tb.Th and inversely correlated with SMI in femurs. The HFD increased plasma concentrations of tartrate-resistant acid phosphatase 5b, a marker of bone resorption, in sedentary mice; while running decreased it in a dose-dependent manner. The findings show that voluntary running improves bone quality in young adult mice fed an HFD. Novelty bullets • The high-fat diet alters bone microstructure by increasing bone resorption. • Quantitative voluntary running improves bone microstructure through its attenuation of bone resorption in mice fed a high-fat diet.

Voluntary running of defined distances reduces body adiposity and its associated inflammation in C57BL/6 mice fed a high-fat diet

2017 ◽  
Vol 42 (11) ◽  
pp. 1179-1184 ◽  
Author(s):  
Lin Yan ◽  
Sneha Sundaram ◽  
Forrest H. Nielsen
Keyword(s):  
High Fat Diet ◽  
Plasma Concentrations ◽  
Standard Diet ◽  
Dependent Manner ◽  
High Fat ◽  
Body Adiposity ◽  
Chemotactic Protein ◽  
Voluntary Running ◽  
Significant Difference ◽  
Dose Dependent

This study investigated the effect of voluntary running of defined distances on body adiposity in male C57BL/6 mice fed a high-fat diet. Mice were assigned to 6 groups and fed a standard AIN93G diet (sedentary) or a modified high-fat AIN93G diet (sedentary; unrestricted running; or 75%, 50%, or 25% of unrestricted running) for 12 weeks. The average running distance was 8.3, 6.3, 4.2, and 2.1 km/day for the unrestricted, 75%, 50%, and 25% of unrestricted runners, respectively. Body adiposity was 46% higher in sedentary mice when fed the high-fat diet instead of the standard diet. Running decreased adiposity in mice fed the high-fat diet in a dose-dependent manner but with no significant difference between sedentary mice and those running 2.1 km/day. In sedentary mice, the high-fat instead of the standard diet increased insulin resistance, hepatic triacylglycerides, and adipose and plasma concentrations of leptin and monocyte chemotactic protein-1 (MCP-1). Running reduced these variables in a dose-dependent manner. Adipose adiponectin was lowest in sedentary mice fed the high-fat diet; running raised adiponectin in both adipose tissue and plasma. Running 8.3 and 6.3 km/day had the greatest, but similar, effects on the aforementioned variables. Running 2.1 km/day did not affect these variables except, when compared with sedentariness, it significantly decreased MCP-1. The findings showed that running 6.3 kg/day was optimal for reducing adiposity and associated inflammation that was increased in mice by feeding a high-fat diet. The findings suggest that voluntary running of defined distances may counteract the obesogenic effects of a high-fat diet.

scholarly journals PHARMACOLOGICAL SCREENING OF ANTI-OBESITY POTENTIAL OF ACORUS CALAMUS LINN. IN HIGH FAT CAFETERIA DIET FED OBESE RATS

2017 ◽  
Vol 10 (4) ◽  
pp. 384 ◽  
Author(s):  
Athesh K ◽  
Joshi G
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Serum Glucose ◽  
In Vivo Studies ◽  
Acorus Calamus ◽  
Dependent Manner ◽  
Fat Pad ◽  
High Fat ◽  
Dose Levels ◽  
Dose Dependent

Objective: To study the anti-obesity potential of aqueous rhizome extract of Acoruscalamus Linn. (AREAC)in high fat diet fed obese rats.Methods: Adult strain male Wistar rats used in this study were fed with High Fat Diet (HFD) for 60 days. For the treatment groups,AREAC was administered in a dose levels of100, 200 and 300 mg/kgbw, orally once a day along with HFD. Rats fed with normal pellet chow were served as normal control. The effect of AREAC on physical parameterssuch as body weight, organ weight, fat pad weights and various biochemical parameterslike serum glucose, insulin, leptin,lipid profile, liver markers, kidney markers and oxidative stress markers were analysed.In-vitro pancreatic lipase inhibition assay of AREAC was also studied.Results: Data of in-vivo studies revealedsignificant (p<0.05) reduction in percentage body weight gain, organ weights, fat pad weights and levels of serum glucose, insulin and leptin after treatment with AREAC in a dose dependent manner. Also, administration of AREAC significantly inhibited the increases in the concentrations of triglycerides, total cholesterol, LDL-cholesterol, VLDL-cholesterol, free-fatty acid and phospholipids in a dose dependent manner whereas, the level of HDL-cholesterol was found to be elevated on treatment. Moreover, on treatment with test drug,the elevated levels of serum liver and kidney markerssuch as AST, ALT, ALP, urea, creatinine were also brought back to near normalcy. Antioxidant status was found to be enhanced in liver tissues after treatment.In-vitro studies showed significant inhibition in the activity of pancreatic lipaseby AREAC.Conclusion: The data of the results obtained clearly depicted that AREAC was found to have pronounced anti-obesity activity particularly at the dose levels of 300 mg/kg bw.Key Words: Obesity, High Fat Diet, Leptin, AcoruscalamusLinn., Orlistat.  

scholarly journals Fermented Cordyceps militaris Extract Prevents Hepatosteatosis and Adipocyte Hypertrophy in High Fat Diet-Fed Mice

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1015 ◽  
Author(s):  
Nguyen Khoi Song Tran ◽  
Goon-Tae Kim ◽  
Si-Hyun Park ◽  
Dongyup Lee ◽  
Soon-Mi Shim ◽  
...  
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Lipid Droplets ◽  
Cordyceps Militaris ◽  
Acid Oxidation ◽  
Dependent Manner ◽  
Protective Effects ◽  
High Fat ◽  
Plasma Parameters ◽  
Dose Dependent

Nonalcoholic fatty liver diseases (NAFLD) is characterized by accumulation of lipid droplets in the liver. The objective of this study was to evaluate protective effects of fermented Cordyceps militaris extract by Pediococcus pentosaceus ON188 (ONE) against hepatosteatosis and obesity in mice fed a high-fat diet (HFD). Eight-week-old male C57BL/6J mice were fed HFD mixed with ONE for four weeks and its effects on hepatosteatosis and obesity were examined. Although ONE did not change food intake, it reduced body weights of mice at administration dose of 200 mg/kg/day. Activities of lactate dehydrogenase (LDH), aspartate transaminase (AST), and alanine transaminase (ALT) as plasma parameters were reduced by ONE in a dose-dependent manner. Hepatic lipid droplets and triglyceride (TG) levels were also reduced by ONE due to upregulation of fatty acid oxidizing genes such as carnithine palmitoyltransferase (CPT1) and peroxisomal proliferator activated receptor α(PPARα) mediated by induction of sphingosine kinase 2 (SPHK2). In epididymal fat tissue, sizes of adipocytes were significantly reduced by ONE in a dose-dependent manner. This is mainly due to suppression of lipogenesis and upregulation of adipocyte browning genes. Collectively, these results suggest that fermented ONE can activate fatty acid oxidation via SPHK2 in the liver. It can also suppress lipogenesis and activate browning in adipose tissue. Thus, ONE might have potential to be used for the development of functional foods against liver dysfunction and obesity.

Lenalidomide and Bortezomib Inhibit Osteoclast Differentiation and Activation in Multiple Myeloma: Clinical Implications.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3485-3485 ◽  
Author(s):  
Iris Breitkreutz ◽  
Sonia Vallet ◽  
Marc S. Raab ◽  
Yu-Tzu Tai ◽  
Noopur Raje ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Resorption ◽  
Mononuclear Cells ◽  
Osteoclast Differentiation ◽  
Flow Cytometric Analysis ◽  
Tartrate Resistant Acid Phosphatase ◽  
Normal Donor ◽  
Dependent Manner ◽  
Osteolytic Bone Disease ◽  
Dose Dependent

Abstract Osteolytic bone disease in Multiple Myeloma (MM) is caused by enhanced osteoclast (OCL) activation and inhibition of osteoblast function. The proteasome inhibitor bortezomib (PS341, Velcade) has potent anti-myeloma activity with impressive clinical responses. A recent study indicated that bortezomib has inhibitory effects on OCL (ASH 2005, Abstract #2488). Lenalidomide (CC-5013, Revlimid) is an immunomodulatory derivative of thalidomide that has shown promising anti-MM effects in patients with relapsed or refractory MM (Richardson et. al, Blood Jul 06). Significantly, a phase I clinical trial showed that lenalidomide and bortezomib could achieve responses in the majority of patients with MM, refractory to either agent alone (ASH 2005, Abstract #365). However, the effect of lenalidomide on human OCL lineage is unknown. Here we investigated the effect of lenalidomide and bortezomib on human OCL. Peripheral blood mononuclear cells (PBMC) from MM patients (n=11) and healthy donors (n=5) were stimulated with receptor activator of NFk-B ligand (RANKL) (50ng/ml) and M-CSF (25ng/ml) for two weeks to induce OCL formation, in the presence or absence of lenalidomide or bortezomib. OCL were identified by flow cytometric analysis using anti-aVb3 integrin. Lenalidomide and bortezomib inhibited OCL differentiation in a dose-dependent manner (n=13, median control: 70.9% at 0 μM; 63% at lenalidomide 2μM and 45% at 10μM; 35% at bortezomib 2nM and 11% at 5nM). TRAP staining (tartrate-resistant acid phosphatase) was performed to identify OCL and confirm OCL activity. Lenalidomide, as well as bortezomib inhibited OCL in a dose-dependent manner, as evidenced by a marked decrease in TRAP+ cells. To assess bone resorption activity, OCL were cultured with dentine discs, in the presence or absence of lenalidomide and bortezomib, followed by light microscopic analysis and additional measurement of soluble collagen I fragments from the supernatant. Both lenalidomide and bortezomib inhibited bone resorption in a dose-dependent manner. We next asked whether mature OCL were affected. OCL were induced by cytokine stimulation for 3 weeks and treated for 72h, followed by flow cytometry. Neither lenalidomide nor bortezomib altered total number of aVb3 integrin-expressing mature OCL (n=6). In addition, OCL culture supernatants were collected, and two major MM growth and survival factors produced by OCL, B-cell activation factor (BAFF) and a proliferation-inducing ligand (APRIL), were measured by specific ELISA. Both lenalidomide and bortezomib strongly inhibited secretion of BAFF and APRIL. Finally, we determined whether lenalidomide and bortezomib inhibited expression of transcriptional factors important for OCL differentiation and survival. Cell lysates of CD14-expressing monocytic cells from normal donor PBMCs were subject to immunoblotting. Importantly, lenalidomide inhibited OCL differentiation by downregulation of PU.1 expression. These results therefore indicate, that lenalidomide and bortezomib inhibit OCL differentiation, thereby directly preventing the development of new osteolytic lesions. Moreover, BAFF and APRIL secretion by OCL is downregulated, thereby inhibiting MM cell survival in the bone marrow microenvironment.

scholarly journals DIHYDROTESTOSTERONE DOWNREGULATES BONE RESORPTION ACTIVITY OF OSTEOCLASTS IN DOSE DEPENDENT MANNER: AN IN VITRO MODEL USING RAW 264.7 CELLS

2017 ◽  
Vol 9 (10) ◽  
pp. 86
Author(s):  
Hnin Ei Thu ◽  
Zahid Hussain ◽  
Isa Naina Mohamed ◽  
Ahmad Nazrun Shuid
Keyword(s):  
Bone Resorption ◽  
Cathepsin K ◽  
Raw 264.7 Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Raw 264.7 ◽  
Dependent Manner ◽  
Sod Activity ◽  
Osteoclastic Differentiation ◽  
Dose Dependent

Objective: Numerous studies have evidenced the bone regulatory potential of dihydrotestosterone in androgen-deficient osteoporosis. The present study was thus aimed to explore the translational mechanism of dihydrotestosterone to down-regulate the bone resorption activity of osteoclasts using RAW 264.7 cells as in vitro model.Methods: Prior to analyze the efficacy of dihydrotestosterone (5α-DHT) to alleviate osteoclastic differentiation, their cell viability and cell proliferative ability was assessed using lactate dehydrogenase (LDH) and MTS assays. The osteoclastic differentiation capacity of dihydrotestosterone was evaluated by measuring TRAP activity and the expression of bone resorption-related proteins such as matrix metallopeptidase-9 (MMP-9), cathepsin-K, tartrate-resistant acid phosphatase (TRAP) and NFATc1. Moreover, the effects of dihydrotestosterone were also evaluated on superoxide (free radicals) generation and superoxide dismutase (SOD) activity in RANKL-induced osteoclasts.Results: Dihydrotestosterone showed no toxicity towards RAW 264.7 cells and significantly enhanced their proliferation and growth rates in a dose-dependent fashion. It was also observed that dihydrotestosterone exhibits a remarkable inhibitory effect on differentiation, maturation and activation of osteoclasts. The marked inhibition of differentiation and activation of osteoclasts caused by 5α-DHT was due to down-regulation of the expression of MMP-9, cathepsin-K, TRAP, NFATc1, generation of superoxide and up-regulation of SOD activity in the RAW 264.7 cells.Conclusion: Resulting data provided substantially in vitroevidence for the pronounced anti-osteoclastogenetic activity of dihydrotestosterone and its therapeutic value in treating osteoporosis and other bone-erosive disorders. 

scholarly journals Pluchea indica (L.) Less. Tea Ameliorates Hyperglycemia, Dyslipidemia, and Obesity in High Fat Diet-Fed Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Kittipot Sirichaiwetchakoon ◽  
Gordon Matthew Lowe ◽  
Sajeera Kupittayanant ◽  
Seekaow Churproong ◽  
Griangsak Eumkeb
Keyword(s):  
High Fat Diet ◽  
Complete Blood Count ◽  
Total Phenolic ◽  
Oral Glucose ◽  
Dependent Manner ◽  
High Fat ◽  
Caffeoylquinic Acid ◽  
Dicaffeoylquinic Acid ◽  
Significant Difference ◽  
Dose Dependent

Pluchea indica (L.) Less. (P. indica) tea has been used for a health-promoting drink, especially in Southeast Asia. The effect of P. indica tea (PIT) on amelioration of hyperglycemia; dyslipidemia that was total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), and triglyceride (TG); and obesity in high fat diet-induced (HFD) mice was investigated. Oral glucose tolerance test (OGTT) displayed that PIT at 400 and 600 mg/kg orally ameliorated hyperglycemia with a dose-dependent manner compared to the untreated group. Moreover, PIT at these dosages exhibited significantly lower TC, LDL-C, TG, and perigonadal fat weight in HFD treated mice compared to HFD mice (P<0.05) with a dose-dependent manner. In contrast, HDL-C was higher than in the HFD group, but not a significant difference (P>0.05). The PIT chemical analysis results demonstrated that PIT contained total phenolic content (TPC), total flavonoid content (TFC), 4-O-caffeoylquinic acid (4-CQ), 5-O-caffeoylquinic acid (5-CQ), 3,4-O-dicaffeoylquinic acid (3,4-CQ), 3,5-O-dicaffeoylquinic acid (3,5-CQ), 4,5-O-dicaffeoylquinic acid (4,5-CQ), beta-caryophyllene, and gamma-gurjunene that may play an important role in inhibiting hyperlipidemia and hyperglycemia. Also, histological analysis expressed that the mean area and amount of perigonadal fat adipocytes of PIT treated groups were significantly lower and higher than the HFD group (P<0.05), respectively. The toxicity test of PIT at 600 mg/kg/day in mice showed that serum creatinine, alanine transaminase (ALT), alkaline phosphatase (ALP), and complete blood count (CBC) levels of HFD and PIT treated groups were not significantly different compared to the normal control diet group (NCD) (P>0.05). These results suggest that PIT does not become toxic to the kidney, liver, and blood. In conclusion, PIT has the potential to develop into healthy food supplement or medicine for the prevention and treatment of hyperglycemic, hyperlipidemic, and obese patients.

AZD6244 (ARRY-142886), a Potent and Selective MEK1/2 Inhibitor Blocks the ERK1/2 Signaling Pathway, Inhibits Osteoclast Differentiation and Activation in Multiple Myeloma: Clinical Implications.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3467-3467 ◽  
Author(s):  
Iris Breitkreutz ◽  
Sonia Vallet ◽  
Marc S. Raab ◽  
Xianfeng Li ◽  
Noopur Raje ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Resorption ◽  
Mononuclear Cells ◽  
Mapk Pathway ◽  
Osteoclast Differentiation ◽  
Flow Cytometric Analysis ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
Flow Cytometric ◽  
Dose Dependent

Abstract Multiple myeloma (MM)-associated bone disease is caused by upregulation of osteoclast (OCL) activity and constitutive inhibition of osteoblast function. The extracellular signal-regulated kinase 1/2 (ERK1/2) MAP kinase pathway contributes to cytokine-induced OCL differentiation and maturation. We hypothesized that inhibition of ERK1/2 could prevent OCL differentiation and downregulate OCL function. Here we investigate the effects of AZD6244, which blocks the ERK1/2 MAPK pathway via direct inhibition of MEK1/2, on OCL in MM. Peripheral blood mononuclear cells (PBMC) from healthy donors (n=3) and MM patients (n=11) were harvested and stimulated with RANKL (50ng/ml) and M-CSF (25ng/ml) for 2 weeks to induce OCL formation, in the presence or absence of AZD6244. OCL characteristics were measured by flow cytometric analysis of anti-alphaVbeta3 integrin expression. AZD6244 inhibited OCL differentiation in a dose-dependent manner (n=11, median control: 77.4% at 0 uM; 77% at 0.02 uM; 54% at 0.2 uM; 53% at 2 uM; 38% at 5 uM; 29% at 10 uM). TRAP staining (tartrate-resistant acid phosphatase) was performed to identify OCL and to confirm activity. Importantly, AZD6244 inhibited OCL in a dose-dependent manner, as evidenced by a marked loss of TRAP+ cells. To assess bone resorption activity, OCL were cultured with dentine discs in the presence or absence of AZD6244, followed by the measurement of soluble collagen I fragments in the supernatant. AZD6244 inhibited bone resorption in a dose-dependent manner. We next asked whether AZD6244 affects mature OCL. Mature OCL were induced by cytokine stimulation for 2 weeks and then AZD6244 was added for 3 days, followed by flow cytometric analysis. AZD6244 had no effect on total number of alphaVbeta3 integrin-expressing mature OCL (n=6). Two major myeloma growth and survival factors produced by OCL, B-cell activation factor (BAFF) and a proliferation-inducing ligand (APRIL), were measured in OCL culture supernatants by ELISA. AZD6244 significantly inhibited secretion of BAFF and APRIL. In addition, macrophage inflammatory protein (MIP-1alpha), an important OCL differentiation factor and MM survival factor, was inhibited. These results indicate that AZD6244 inhibits OCL differentiation induced by M-CSF and RANKL, leading to reduced bone resorption activity. Moreover, AZD6244 downregulates MIP-1alpha and BAFF, APRIL secretion by OCL, which could inhibit MM cell survival in the bone marrow microenvironment. We have also demonstrated that AZD6244 inhibits proliferation and survival of human MM cell lines, either sensitive or resistant to conventional chemotherapy, as well as freshly isolated patient MM cells (Abstract #553572 and #553605, ASH 2006). In conclusion, the present study provides a preclinical rationale for the evaluation of AZD6244 (ARRY-142886) as a potential new therapy for patients with MM.

scholarly journals Identification of short-chain pyroglutamyl peptides in Japanese salted fermented soy paste (miso) and their anti-obesity effect

2020 ◽  
Vol 12 ◽  
Author(s):  
Saki Shirako ◽  
Yumi Kojima ◽  
Takeo Hasegawa ◽  
Toshikazu Yoshikawa ◽  
Yasuki Matsumura ◽  
...  
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Water Extract ◽  
Short Chain ◽  
Dependent Manner ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Peptide Fraction ◽  
Liquid Chromatography Tandem Mass ◽  
Dose Dependent

Miso, a paste of salted fermented soybean, is a seasoning used extensively in traditional Japanese cuisine. Herein, pyroglutamyl peptides present in miso were identified by a liquid chromatography-tandem mass spectrometry (LC-MS/MS), detecting precursor ions, which generated immonium ion of pyroglutamyl residue. By using this method, 13 pyroglutamyl peptides were identified in four types of miso. Administration of the water extract prepared from 0.6 g soybean miso/kg body weight/day significantly suppressed high fat diet-induced weight gain. A similar effect was exerted by the hydrophobic pyroglutamyl peptide fraction, including pyroglutamyl proline (pEP), pEV, pEI, and pEL. Administration of a mixture of synthetic pEP, pEV, pEI, and pEL in a ratio to that in miso or pEL alone also suppressed the weight gain in a dose dependent manner. These results suggest that the short-chain hydrophobic pyroglutamyl peptides present in miso are effective in suppressing high fat diet-induced obesity.

scholarly journals Decitabine Inhibits Bone Resorption in Periodontitis by Upregulating Anti-Inflammatory Cytokines and Suppressing Osteoclastogenesis

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 199
Author(s):  
Urara Tanaka ◽  
Shunichi Kajioka ◽  
Livia S. Finoti ◽  
Daniela B. Palioto ◽  
Denis F. Kinane ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Resorption ◽  
Bone Loss ◽  
Inflammatory Cytokines ◽  
Osteoclast Differentiation ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
Bone Homeostasis ◽  
Osteoblastic Cell Line ◽  
Anti Inflammatory

DNA methylation controls several inflammatory genes affecting bone homeostasis. Hitherto, inhibition of DNA methylation in vivo in the context of periodontitis and osteoclastogenesis has not been attempted. Ligature-induced periodontitis in C57BL/6J mice was induced by placing ligature for five days with Decitabine (5-aza-2′-deoxycytidine) (1 mg/kg/day) or vehicle treatment. We evaluated bone resorption, osteoclast differentiation by tartrate-resistant acid phosphatase (TRAP) and mRNA expression of anti-inflammatory molecules using cluster differentiation 14 positive (CD14+) monocytes from human peripheral blood. Our data showed that decitabine inhibited bone loss and osteoclast differentiation experimental periodontitis, and suppressed osteoclast CD14+ human monocytes; and conversely, that it increased bone mineralization in osteoblastic cell line MC3T3-E1 in a concentration-dependent manner. In addition to increasing IL10 (interleukin-10), TGFB (transforming growth factor beta-1) in CD14+ monocytes, decitabine upregulated KLF2 (Krüppel-like factor-2) expression. Overexpression of KLF2 protein enhanced the transcription of IL10 and TGFB. On the contrary, site-directed mutagenesis of KLF2 binding site in IL10 and TFGB abrogated luciferase activity in HEK293T cells. Decitabine reduces bone loss in a mouse model of periodontitis by inhibiting osteoclastogenesis through the upregulation of anti-inflammatory cytokines via KLF2 dependent mechanisms. DNA methyltransferase inhibitors merit further investigation as a possible novel therapy for periodontitis.

High-fat diet and caffeine interact to modulate bone microstructure and biomechanics in mice

Life Sciences ◽  
2021 ◽  
pp. 119450
Author(s):  
Fernanda Batista de Souza ◽  
Rômulo Dias Novaes ◽  
Cynthia Fernandes Ferreira Santos ◽  
Franciele Angelo de Deus ◽  
Felipe Couto Santos ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Bone Microstructure ◽  
High Fat
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