Glucagon‐like peptide 2 decreases osteoclasts by stimulating apoptosis dependent on nitric oxide synthase

Lü, Yi; Lu, Dongdong; Hu, Yu

doi:10.1111/cpr.12443

Cited by 11 publications

(9 citation statements)

References 41 publications

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“…Glucagon-like peptide 2 (GLP2), a molecule regulating energy metabolism, is a beneficial factor in glucose metabolism in mice with high-fat diet-induced obesity. It prevents osteoporosis by inhibiting osteoclast proliferation and promoting apoptosis ( 136 ). Osteoclasts cultured on the bone slices transport glucose almost twice as fast as the osteoclasts away from bone to ensure a sufficient energy supply for bone resorption.…”

Section: The Coupling Of Systemic Energy Metabolism Disorder With Osteoclast Energy Metabolismmentioning

confidence: 99%

The Role of Osteoclast Energy Metabolism in the Occurrence and Development of Osteoporosis

Lin

Zhu

2021

Front. Endocrinol.

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In recent decades, the mechanism underlying bone metabolic disorders based on energy metabolism has been heavily researched. Bone resorption by osteoclasts plays an important role in the occurrence and development of osteoporosis. However, the mechanism underlying the osteoclast energy metabolism disorder that interferes with bone homeostasis has not been determined. Bone resorption by osteoclasts is a process that consumes large amounts of adenosine triphosphate (ATP) produced by glycolysis and oxidative phosphorylation. In addition to glucose, fatty acids and amino acids can also be used as substrates to produce energy through oxidative phosphorylation. In this review, we summarize and analyze the energy-based phenotypic changes, epigenetic regulation, and coupling with systemic energy metabolism of osteoclasts during the development and progression of osteoporosis. At the same time, we propose a hypothesis, the compensatory recovery mechanism (involving the balance between osteoclast survival and functional activation), which may provide a new approach for the treatment of osteoporosis.

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Section: The Coupling Of Systemic Energy Metabolism Disorder With Osteoclast Energy Metabolismmentioning

confidence: 99%

The Role of Osteoclast Energy Metabolism in the Occurrence and Development of Osteoporosis

Lin

Zhu

2021

Front. Endocrinol.

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“…This data suggests that GLP-2 plays a role in maintenance in myenteric neurons including nNOS neurons. GLP-2 enhances the expression of iNOS through stimulating the activity of TGFβ-Smad2/3 signaling in osteoclasts in vitro , which may contribute to the inhibition of the proliferation of osteoclasts and which may provide potential therapeutic targets for the treatment of osteoporosis ( Lu et al, 2018 ).…”

Section: Glucagon-like Peptidementioning

confidence: 99%

The Role of Gasotransmitters in Gut Peptide Actions

et al. 2021

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Although gasotransmitters nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S) receive a bad connotation; in low concentrations these play a major governing role in local and systemic blood flow, stomach acid release, smooth muscles relaxations, anti-inflammatory behavior, protective effect and more. Many of these physiological processes are upstream regulated by gut peptides, for instance gastrin, cholecystokinin, secretin, motilin, ghrelin, glucagon-like peptide 1 and 2. The relationship between gasotransmitters and gut hormones is poorly understood. In this review, we discuss the role of NO, CO and H2S on gut peptide release and functioning, and whether manipulation by gasotransmitter substrates or specific blockers leads to physiological alterations.

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“…3,4 Patients with osteoporosis, diabetes and Paget's disease suffer from accelerated bone destruction and pathological bone loss. 8,9 Increased number or function of osteoclasts cause bone absorption to prevail over formation, leading to not only bone microstructural deterioration and increased bone frailty, but also biomaterial implants failure. 8,9 Increased number or function of osteoclasts cause bone absorption to prevail over formation, leading to not only bone microstructural deterioration and increased bone frailty, but also biomaterial implants failure.…”

Section: Introductionmentioning

confidence: 99%

“…[5][6][7] Osteoclasts are multinucleated giant cells exactly verified to degrade bone solely and essential for maintaining mineral homeostasis. 8,9 Increased number or function of osteoclasts cause bone absorption to prevail over formation, leading to not only bone microstructural deterioration and increased bone frailty, but also biomaterial implants failure. [10][11][12] Hydroxyapatite (HA), an inorganic component in bone tissues, provides most of bone mechanical properties (eg strength and stiffness).…”

Section: Introductionmentioning

confidence: 99%

Fluorine‐contained hydroxyapatite suppresses bone resorption through inhibiting osteoclasts differentiation and function in vitro and in vivo

et al. 2019

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Objectives: Fluorine, an organic trace element, has been shown to unfavourably effect osteoclasts function at a low dose. Use of hydroxyapatite (HA) has been effective in exploring its roles in promoting bone repair. In this study, we used HA modified with fluorine to investigate whether it could influence osteoclastic activity in vitro and ovariectomy-induced osteoclasts hyperfunction in vivo. Materials and methods: Fluorohydroxyapatite (FHA) was obtained and characterized by scanning electron microscope (SEM). Osteoclasts proliferation and apoptosis treated with FHA were assessed by MTT and TUNEL assay. SEM, F-actin, TRAP activity and bone resorption experiment were performed to determine the influence of FHA on osteoclasts differentiation and function. Moreover, HA and FHA were implanted into ovariectomized osteoporotic and sham surgery rats. Histology and Micro-CT were examined for further verification. Results: Fluorine released from FHA slowly and sustainably. FHA hampered osteoclasts proliferation, promoted osteoclasts apoptosis, suppressed osteoclasts differentiation and function. Experiments in vivo validated that FHA participation brought about an inhibitory effect on osteoclasts hyperfunction and less bone absorption. Conclusion:The results indicated that FHA served as an efficient regulator to attenuate osteoclasts formation and function and was proposed as a candidature for bone tissue engineering applications.

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Glucagon‐like peptide 2 decreases osteoclasts by stimulating apoptosis dependent on nitric oxide synthase

Abstract: GLP2 induces apoptosis via TGFβ-Smad2/3 signalling, which contributes to the inhibition of the proliferation of osteoclasts and which may provide potential therapeutic targets for the treatment of osteoporosis.

Cited by 11 publications

References 41 publications

The Role of Osteoclast Energy Metabolism in the Occurrence and Development of Osteoporosis

The Role of Osteoclast Energy Metabolism in the Occurrence and Development of Osteoporosis

The Role of Gasotransmitters in Gut Peptide Actions

Fluorine‐contained hydroxyapatite suppresses bone resorption through inhibiting osteoclasts differentiation and function in vitro and in vivo

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