Saturated fatty acids enhance osteoclast survival

Oh, So-Ra; Sul, Ok-Joo; Kim, Youn-Young; Kim, Hye-Jin; Yu, Rina; Suh, Jae-Hee; Choi, Hye‐Seon

doi:10.1194/jlr.m800626-jlr200

Cited by 53 publications

(22 citation statements)

References 38 publications

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“…Consistently, saturated fatty acids have been shown to increase activation of NF-B and subsequent bone resorption via TLR4 in osteoclasts (38). In contrast, in the present study we observed that the inhibitory effect of GW9508 on NF-B transcriptional activity was GPR40-dependent similar to the GPR120-dependent anti-inflammatory effect of docosahexaenoic acid as demonstrated by Oh et al in macrophages (23).…”

Section: Journal Of Biological Chemistrysupporting

confidence: 82%

The Free Fatty Acid Receptor G Protein-coupled Receptor 40 (GPR40) Protects from Bone Loss through Inhibition of Osteoclast Differentiation*

Wauquier

Philippe

Léotoing

et al. 2013

Journal of Biological Chemistry

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Background: Long chain fatty acids have been shown to activate the membrane-bound receptor GPR40. Results: GPR40 agonist alters bone-resorbing cell differentiation through inhibition of the NF-B system. Conclusion: GPR40 exerts protective effects in vivo on bone tissue. Significance: GPR40 is a nutritional and therapeutic target opening up new avenues for clinical investigations in terms of metabolic and age-related bone disorders.

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Section: Journal Of Biological Chemistrysupporting

confidence: 82%

The Free Fatty Acid Receptor G Protein-coupled Receptor 40 (GPR40) Protects from Bone Loss through Inhibition of Osteoclast Differentiation*

Wauquier

Philippe

Léotoing

et al. 2013

Journal of Biological Chemistry

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“…Consistent with this idea, saturated FAs with a carbon chain length of 12 (laurate) or 16 (palmitate) reportedly activate TLR4 signaling in RAW264.7 macrophages in vitro 24,25) . The activation of TLR4 signaling by saturated FAs has also been reported in other cell types [26][27][28] . On the other hand, several reports have argued against the idea that TLRs are activated by saturated FFAs.…”

Section: Tlr4 Signaling Under Conditions Of Insulin Resistance and Pasupporting

confidence: 54%

Toll-Like Receptor, Lipotoxicity and Chronic inflammation: The Pathological Link Between Obesity and Cardiometabolic Disease

Eguchi

Manabe

2014

JAT

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The epidemic growth in the prevalence of obesity has made the impact of metabolic syndrome on cardiovascular events increasingly significant. Elevated visceral adiposity, the indispensable component of metabolic syndrome, is thought to play a primary role in the increasing incidence of cardiometabolic disorders. Importantly, obesity is not merely the simple expansion of adipose tissue mass; it also involves the activation of inflammatory processes within visceral adipose tissue. Adipose tissue inflammation on the one hand enhances the production of proinflammatory adipokines and on the other hand increases the release of free fatty acids via the activation of lipolysis. The adipokines and free fatty acids secreted from visceral fat then contribute to a cardiometabolic pathology. We herein summarize recent advances in our understanding of the mechanisms by which visceral obesity leads to the activation of inflammation in cardiovascular and metabolic tissues and promotes cardiometabolic disease. Our focus is on Toll-like receptor 4 signaling and free fatty acids as mediators of chronic inflammation in patients with metabolic syndrome and atherosclerosis.

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“…In contrast, another study has shown that SFA promoted osteoclast survival by preventing apoptosis. The stimulation of osteoclast survival in SFA-treated osteoclasts was induced via the Toll-like receptor 4 (TLR4) and NF-κB activation (27). These observations suggest that activation of NF-κB causes palmitate-induced apoptosis in osteoblasts and palmitate-induced survival in osteoclasts.…”

Section: Discussionmentioning

confidence: 70%

Bezafibrate prevents palmitate-induced apoptosis in osteoblastic MC3T3-E1 cells through the NF-κB signaling pathway

Zhong

Xiu²,

Wei³

et al. 2011

Int J Mol Med

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Abstract. Osteoporosis is a bone condition defined by low bone mass and increase of fracture risk due to imbalance between bone resorption by osteoclasts and bone formation by osteoblasts. Low bone mass is likely to be due to the alteration of the osteoclast and osteoblast lifespan through regulated apoptosis. Saturated fatty acid (SFA) intake is negatively associated with bone mineral density (BMD). Furthermore, SFA induces apoptosis in osteoblastic cell lines. Bezafibrate could increase bone mass in intact male rats principally through increasing periosteal bone formation. At present, it is unknown whether bezafibrate attenuates palmitate-induced apoptosis in MC3T3-E1 cells. In the present study, we found that palmitate stimulated the degradation of IκBα and NF-κB translocation, as well as up-regulation of NF-κB-mediated Fas expression in obsteoblastic MC3T3-E1 cells. Furthermore, the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) could restore palmitate-induced caspase-3 decrease and inhibit palmitate-induced cleaved caspase-3 increase. We observed that bezafibrate, a dual ligand for the peroxisome proliferatoractivated receptors α (PPARα) and PPARδ, significantly attenuated the palmitate-induced cytotoxicity as determined by the MTT assay and inhibited the palmitate-induced apoptosis as determined by a flow cytometry assay using Annexin V-FITC/PI and assessment of the activity of caspase-3. Pre-treatment of bezafibrate prevented palmitate-induced NF-κB activation. Therefore, these findings indicate that bezafibrate inbibits palmitate-induced apoptosis via the NF-κB signaling pathway. Our results point to bezafibrate as a new strategy to attenuate bone loss associated with high fat diet beyond its lipid-lowering actions.

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Saturated fatty acids enhance osteoclast survival

Cited by 53 publications

References 38 publications

The Free Fatty Acid Receptor G Protein-coupled Receptor 40 (GPR40) Protects from Bone Loss through Inhibition of Osteoclast Differentiation*

The Free Fatty Acid Receptor G Protein-coupled Receptor 40 (GPR40) Protects from Bone Loss through Inhibition of Osteoclast Differentiation*

Toll-Like Receptor, Lipotoxicity and Chronic inflammation: The Pathological Link Between Obesity and Cardiometabolic Disease

Bezafibrate prevents palmitate-induced apoptosis in osteoblastic MC3T3-E1 cells through the NF-κB signaling pathway

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