Glutamic acid ameliorates estrogen deficiency–induced menopausal-like symptoms in ovariectomized mice

Han, Ning; Kim, Hee-Yun; Yang, Woong Mο; Jeong, Hyun‐Ja; Kim, Hyung-Min

doi:10.1016/j.nutres.2015.06.006

Cited by 13 publications

(8 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Deficiency of estrogen due to halted ovarian function is a pivotal role in the loss of bone mass in postmenopausal women [26]. Pathological factors for osteoporosis include imbalanced calcium (Ca) metabolism, decreased osteoblast activity, increased osteoclast function, and deficient estrogen production [27,28]. Generally, Ca has an important role in the human body, with various physiological functions.…”

Section: Introductionmentioning

confidence: 99%

Effect of Nano-Montmorillonite on Osteoblast Differentiation, Mineral Density, and Osteoclast Differentiation in Bone Formation

Kim

Lee

et al. 2020

Nanomaterials

View full text Add to dashboard Cite

Calcium-type montmorillonite, a phyllosilicate mineral, has diverse health benefits when introduced into the gastrointestinal tract or applied to the skin. However, the predominant use of this layered material has thus far been in traditional industries, despite its potential application in the pharmaceutical industry. We investigated the effects and mechanism of nano-montmorillonite (NM) on osteoblast and osteoclast differentiation in vivo and in vitro. We examined the osteogenic effects of NM with high calcium content (3.66 wt%) on alkaline phosphatase (ALP) activity, mineralization, bone microarchitecture, and expression level of osteoblast and osteoclast related genes in Ca-deficient ovariectomized (OVX) rats. Micro-computed tomography of OVX rats revealed that NM attenuated the low-Ca-associated changes in trabecular and cortical bone mineral density. It improved ALP activity and mineralization, as well as the expression of osteoblast and osteoclast differentiation associated genes. NM also activated the expression of runt-related transcription factor 2, osteocalcin, bone morphogenetic protein 2, and type 1 collagen via phosphorylated small mothers against decapentaplegic homolog 1/5/8 signaling. Further, NM repressed the expression of receptor activator for cathepsin K, nuclear factor kappa-B ligand and tartrate-resistant acid phosphatase. Therefore, NM inhibits osteoclastogenesis, stimulates osteoblastogenesis, and alleviates osteoporosis.

show abstract

Section: Introductionmentioning

confidence: 99%

Effect of Nano-Montmorillonite on Osteoblast Differentiation, Mineral Density, and Osteoclast Differentiation in Bone Formation

Kim

Lee

et al. 2020

Nanomaterials

View full text Add to dashboard Cite

show abstract

“…Increased osteoclast function, decreased osteoblast activity, imbalanced calcium ion (Ca 2+ ) metabolism, and the estrogen deficiency-mediated induction of inflammatory diseases may all be involved in the pathology of osteoporosis [6,7]. Dietary and nutritional factors have been identified as having a role in the incidence of osteoporosis and bone fractures.…”

Section: Introductionmentioning

confidence: 99%

“…Several studies have shown that addition of vitamin C to cultured osteoblast-like cells stimulates the initial deposition of a collagenous extracellular matrix [17,18], followed by the induction of specific genes associated with the osteoblast phenotype, such as alkaline phosphatase (ALP) [18,19] and osteocalcin [18,20], as well as osteopontin, osteonectin, and RUNX2 from undifferentiated mononuclear cells [21,22]. Generally, the ovariectomized (OVX) rat is thought to be a useful animal model for studying the effects of different osteoporosis treatments on the skeletal system [6,7]. Additionally, in OVX mice, vitamin C can prevent the loss of osteoblast differentiation markers (osteocalcin, RUNX2, and bone morphogenetic protein-2 [BMP-2]), attenuate bone loss, and stimulate bone formation [16].…”

Section: Introductionmentioning

confidence: 99%

Vitamin C Activates Osteoblastogenesis and Inhibits Osteoclastogenesis via Wnt/β-Catenin/ATF4 Signaling Pathways

et al. 2019

View full text Add to dashboard Cite

This study evaluated the effects of vitamin C on osteogenic differentiation and osteoclast formation, and the effects of vitamin C concentration on bone microstructure in ovariectomized (OVX) Wistar rats. Micro-computed tomography analysis revealed the recovery of bone mineral density and bone separation in OVX rats treated with vitamin C. Histomorphometrical analysis revealed improvements in the number of osteoblasts, osteoclasts, and osteocytes; the osteoblast and osteoclast surface per bone surface; and bone volume in vitamin C-treated OVX rats. The vitamin C-treated group additionally displayed an increase in the expression of osteoblast differentiation genes, including bone morphogenetic protein-2, small mothers against decapentaplegic 1/5/8, runt-related transcription factor 2, osteocalcin, and type I collagen. Vitamin C reduced the expression of osteoclast differentiation genes, such as receptor activator of nuclear factor kappa-B, receptor activator of nuclear factor kappa-B ligand, tartrate-resistant acid phosphatase, and cathepsin K. This study is the first to show that vitamin C can inhibit osteoporosis by promoting osteoblast formation and blocking osteoclastogenesis through the activation of wingless-type MMTV integration site family/β-catenin/activating transcription factor 4 signaling, which is achieved through the serine/threonine kinase and mitogen-activated protein kinase signaling pathways. Therefore, our results suggest that vitamin C improves bone regeneration.

show abstract

“…Oestrogen deficiency has been suggested to be the predominant cause of post-menopausal osteoporosis ( 1 ). Accompanied by the withdrawal of sex steroids in mammals, serum levels of the pituitary hormone follicle-stimulating hormone (FSH) are markedly increased ( 2 , 3 ).…”

Section: Introductionmentioning

confidence: 99%

FSH aggravates bone loss in ovariectomised rats with experimental periapical periodontitis

Qian

Guan

Bian

2016

Molecular Medicine Reports

View full text Add to dashboard Cite

Periapical bone loss is one of the prominent pathological and clinical features of periapical periodontitis. Previous studies have demonstrated that follicle-stimulating hormone (FSH) could directly affect skeletal remodelling by stimulating the formation and the function of osteoclasts in vitro and in vivo. However, the effect of FSH on periapical bone loss remained to be fully elucidated. In the current study, a rat model was established in order to verify the effect of FSH in experimental periapical lesions. It was identified that FSH aggravated the bone loss of periapical lesions. In addition, RANKL-, TRAP-, TNF-α- and IL-1β-positive cells were increased significantly in FSH-treated groups, which indicated that the function of FSH in bone loss may be mediated through the increasing activity of osteoclasts and the increased secretion of inflammatory cytokines. The results of the current study suggested that FSH, independent of oestrogen, may aggravate periapical bone loss by FSH receptors, which may serve an important role in the immune and inflammatory response of the host to root canal and periradicular infection during menopause.

show abstract

Glutamic acid ameliorates estrogen deficiency–induced menopausal-like symptoms in ovariectomized mice

Cited by 13 publications

References 64 publications

Effect of Nano-Montmorillonite on Osteoblast Differentiation, Mineral Density, and Osteoclast Differentiation in Bone Formation

Effect of Nano-Montmorillonite on Osteoblast Differentiation, Mineral Density, and Osteoclast Differentiation in Bone Formation

Vitamin C Activates Osteoblastogenesis and Inhibits Osteoclastogenesis via Wnt/β-Catenin/ATF4 Signaling Pathways

FSH aggravates bone loss in ovariectomised rats with experimental periapical periodontitis

Contact Info

Product

Resources

About