Adiponectin increases bone mass by suppressing osteoclast and activating osteoblast

Oshima, Kazuya; Nampei, Akihide; Matsuda, Morihiro; Iwaki, Masanori; Fukuhara, Atsunori; Hashimoto, Jun; Yoshikawa, Hideki; Shimomura, Iichiro

doi:10.1016/j.bone.2006.01.119

Cited by 79 publications

(128 citation statements)

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“…Injecting leptin intracerebroventricularly leads to bone loss, whereas leptin knockout mice show higher bone mass (Elefteriou et al 2004). Contrary to leptin, adiponectin promotes osteoblast differentiation and inhibits osteoclast formation (Oshima et al 2006). Our data suggested that IL6 gene knockout may reduce adipocyte differentiation and accumulation, enhance the expression of adiponectin while inhibiting the expression of leptin, thus preventing bone loss induced by the high-fat diet.…”

Section: Discussionmentioning

confidence: 63%

Interleukin-6 gene knockout antagonizes high-fat-induced trabecular bone loss

Wang¹,

Tian²,

Kun

et al. 2016

Journal of Molecular Endocrinology

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The purpose of the study was to determine the roles of interleukin-6 (IL6) in fat and bone communication. Male wild-type (WT) mice and IL6 knockout (IL6 −/− ) mice were fed with either regular diet (RD) or high-fat diet (HFD) for 12 weeks. Bone mass and bone microstructure were evaluated by micro-computed tomography. Gene expression related to lipid and bone metabolisms was assayed with real-time quantitative polymerase chain reaction. Bone marrow cells from both genotypes were induced to differentiate into osteoblasts or osteoclasts, and treated with palmitic acid (PA). HFD increased the body weight and fat pad weight, and impaired lipid metabolism in both WT and IL6 −/− mice. The dysregulation of lipid metabolism was more serious in IL6 −/− mice. Trabecular bone volume fraction, trabecular bone number and trabecular bone thickness were significantly downregulated in WT mice after HFD than those in the RD (P < 0.05). However, these bone microstructural parameters were increased by 53%, 34% and 40%, respectively, in IL6 −/− mice than those in WT mice on the HFD (P < 0.05). IL6 −/− osteoblasts displayed higher alkaline phosphatase (ALP) activity and higher mRNA levels of Runx2 and Colla1 than those in WT osteoblasts both in the control and PA treatment group (P < 0.05). IL6 −/− mice showed significantly lower mRNA levels of PPARγ and leptin and higher mRNA levels of adiponectin in comparison with WT mice on HFD. In conclusion, these findings suggested that IL6 gene deficiency antagonized HFD-induced bone loss. IL6 might bridge lipid and bone metabolisms and could be a new potential therapeutic target for lipid metabolism disturbance-related bone loss.

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Section: Discussionmentioning

confidence: 63%

Interleukin-6 gene knockout antagonizes high-fat-induced trabecular bone loss

Wang¹,

Tian²,

Kun

et al. 2016

Journal of Molecular Endocrinology

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“…Research has shown that receptors for adiponectin are present on osteoblasts and may influence proliferation, differentiation, and the mineralization effects of these bone-remodeling cells (46,47). However, this association is not consistent (48).…”

Section: Discussionmentioning

confidence: 93%

Long-Term Supplementation of Green Tea Extract Does Not Modify Adiposity or Bone Mineral Density in a Randomized Trial of Overweight and Obese Postmenopausal Women

Dostal

Arikawa

Espejo

et al. 2016

The Journal of Nutrition

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“…While Shinoda et al48 found no abnormalities regarding bone mass and turnover in Ad-/Ad- mice, Williams et al49 as well as Oshima et al 50 found an increased bone density. Conversely, adiponectin overexpressing mice had increased bone mass, parameters of bone resorption and bone erosion were not affected 51.…”

Section: Discussionmentioning

confidence: 96%