Pro-inflammatory Cytokines and Osteocytes

Zhou, Miao; Li, Shuyi; Pathak, Janak L.

doi:10.1007/s11914-019-00507-z

Cited by 60 publications

(52 citation statements)

References 77 publications

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“…Moreover, it remains to be elucidated if the effects on obesity-related variables induced by blueberries consumption are long- Higuera-Hernández et al Journal of functional foods xxx (xxxx) xxx-xxx term. Moreover, it is possible that additional biochemical elements related to inflammation and glucose metabolism, including cytokines, might be under the influence of blueberry supplementation (Gonzalez, Garrie, & Turner, 2018;Kern, Mittenbühler, Vesting, Ostermann, Wunderlich, & Wunderlich, 2018;Zhou, Li, & Pathak, 2019). Future studies should address whether contents of TNFα and IL6 in obese subjects respond to blueberry intake in diet.…”

Section: Female Anthropometric Biochemical and Ad Measurements In Prmentioning

confidence: 99%

Blueberry intake included in hypocaloric diet decreases weight, glucose, cholesterol, triglycerides and adenosine levels in obese subjects

Higuera-Hernández

Reyes-Cuapio

Gutiérrez-Mendoza

et al. 2019

Journal of Functional Foods

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Obesity is a disease characterized by an excessive accumulation of fat in the body and it has been linked the enhancement of inflammation-related endogenous molecules, such as adenosine (AD). Since blueberries may induce anti-obesity effects, we tested the hypothesis that blueberries consumption contained in hypocaloric diet would decrease weight, BMI as well as glucose, cholesterol, triglycerides and AD levels in obese subjects. The baseline conditions of obesity-related variables were collected for all subjects prior the implementation of blueberries intake. Later, participants received a hypocaloric diet that included the consumption of blueberries (50 g/ day) during 30 days. We found that male obese subjects that consumed blueberries showed a decrease in weight, glucose, cholesterol, triglycerides and AD whereas female obese subjects that ate blueberries in hypocaloric diet showed no differences in weight, BMI, glucose and triglycerides but displayed a diminution in cholesterol and AD levels. Data suggest that intake of blueberries seems to decrease some of the obese-linked parameters in male or female subjects. Importantly, blueberry consumption decreased the inflammation-related compound AD in both sexes.

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Section: Female Anthropometric Biochemical and Ad Measurements In Prmentioning

confidence: 99%

Blueberry intake included in hypocaloric diet decreases weight, glucose, cholesterol, triglycerides and adenosine levels in obese subjects

Higuera-Hernández

Reyes-Cuapio

Gutiérrez-Mendoza

et al. 2019

Journal of Functional Foods

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“…Osteocyte-specific release of growth factors and signaling molecules is disturbed during long-term unloading, such as occurs in astronauts during space traveling and long-term bed rest ( 11 ). Similarly, inflammatory conditions caused by various inflammatory diseases also affect osteocyte function and signaling ( 41 , 42 ). Various genetic abnormality-associated rare bone diseases are related to disrupted osteocyte functions.…”

Section: Introductionmentioning

confidence: 99%

“…The osteocyte is the main source of sclerostin, a negative regulator of Wnt/β-catenin signaling. Mechanical loading reduces, while proinflammatory cytokines enhance sclerostin production in osteocytes ( 31 , 41 ). Sclerostin deficiency in various rare genetic bone diseases, such as sclerosteosis and van Buchem disease, causes osteopetrosis, a high bone mass phenotype ( 36 ).…”

Section: Introductionmentioning

confidence: 99%

The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

2020

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Osteocytes are the most abundant (~95%) cells in bone with the longest half-life (~25 years) in humans. In the past osteocytes have been regarded as vestigial cells in bone, since they are buried inside the tough bone matrix. However, during the last 30 years it has become clear that osteocytes are as important as bone forming osteoblasts and bone resorbing osteoclasts in maintaining bone homeostasis. The osteocyte cell body and dendritic processes reside in bone in a complex lacuno-canalicular system, which allows the direct networking of osteocytes to their neighboring osteocytes, osteoblasts, osteoclasts, bone marrow, blood vessels, and nerves. Mechanosensing of osteocytes translates the applied mechanical force on bone to cellular signaling and regulation of bone adaptation. The osteocyte lacuno-canalicular system is highly efficient in transferring external mechanical force on bone to the osteocyte cell body and dendritic processes via displacement of fluid in the lacuno-canalicular space. Osteocyte mechanotransduction regulates the formation and function of the osteoblasts and osteoclasts to maintain bone homeostasis. Osteocytes produce a variety of proteins and signaling molecules such as sclerostin, cathepsin K, Wnts, DKK1, DMP1, IGF1, and RANKL/OPG to regulate osteoblast and osteoclast activity. Various genetic abnormality-associated rare bone diseases are related to disrupted osteocyte functions, including sclerosteosis, van Buchem disease, hypophosphatemic rickets, and WNT1 and plastin3 mutation-related disorders. Meticulous studies during the last 15 years on disrupted osteocyte function in rare bone diseases guided for the development of various novel therapeutic agents to treat bone diseases. Studies on genetic, molecular, and cellular mechanisms of sclerosteosis and van Buchem disease revealed a role for sclerostin in bone homeostasis, which led to the development of the sclerostin antibody to treat osteoporosis and other bone degenerative diseases. The mechanism of many other rare bone diseases and the role of the osteocyte in the development of such conditions still needs to be investigated. In this review, we mainly discuss the knowledge obtained during the last 30 years on the role of the osteocyte in rare bone diseases. We speculate about future research directions to develop novel therapeutic drugs targeting osteocyte functions to treat both common and rare bone diseases.

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“…In particular, chronic inflammatory diseases alter osteocyte function and cause osteocyte apoptosis, and may thus interfere with glucocorticoid-induced effects. (31) The use of a healthy young population of males only, however, does also limit the applicability of our findings to daily practice. Another limitation is that this study combines two equally designed placebocontrolled, double-blind, dose-response intervention trials that were not designed to study sclerostin or bone turnover markers as outcome variables, neither powered for this purpose.…”

Section: Discussionmentioning

confidence: 85%

Short‐Term Glucocorticoid Treatment Reduces Circulating Sclerostin Concentrations in Healthy Young Men: A Randomized, Placebo‐Controlled, Double‐Blind Study

et al. 2020

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Glucocorticoid use is the most common cause of osteoporosis in young individuals. In the current study, we investigated the effects of glucocorticoid treatment on circulating sclerostin concentrations and serum bone turnover markers in healthy young men. We performed additional measurements in two combined randomized, placebo‐controlled, double‐blind, dose–response intervention studies: 64 healthy men (age: 22 ± 2 years; BMI: 22.1 ± 1.7 kg/m2) were allocated to receive placebo (n = 16), prednisolone 7.5 mg once daily (n = 24), or prednisolone 30 mg once daily (n = 24) for 2 weeks using block randomization. Primary outcome variables were serum sclerostin and serum bone turnover markers (CTx and P1NP), before and after the intervention. Baseline characteristics and variables did not differ between intervention groups. Compared with placebo, prednisolone high‐dose decreased serum sclerostin concentrations (−8.5 [−28.0 to 7.3] versus 1.5 [−6.5 to 20.0] pg/mL, p = 0.048), decreased P1NP concentrations (−28.0 [−39.3 to −18.3] versus –1.5 [−15.3 to 11.3] μg/L, p < 0.001) and increased CTx concentrations (108.0 [55.0 to 177.0] versus 64.0 [−24.3 to 120.0] ng/L, p = 0.038). Compared with placebo, prednisolone low‐dose did not alter sclerostin concentrations (p = 0.5) or CTx concentrations (p = 0.7), but tended to decrease P1NP concentrations (−9.0 [−24.0 to −1.3] versus –1.5 [−15.3 to 11.3] μg/L, p = 0.095). At baseline concentrations of sclerostin were positively correlated with concentrations of CTx (Spearman's rank correlation coefficient ρ = +0.409, p = 0.001), but not with P1NP. No significant correlations were observed between changes in outcome variables during the interventions. Short‐term high‐dose, but not low‐dose, prednisolone treatment reduces serum sclerostin concentrations in healthy young men. Whether this reflects a counter regulatory mechanism to compensate glucocorticoid‐induced negative effects through other mechanisms remains to be elucidated. © 2020 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

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Pro-inflammatory Cytokines and Osteocytes

Cited by 60 publications

References 77 publications

Blueberry intake included in hypocaloric diet decreases weight, glucose, cholesterol, triglycerides and adenosine levels in obese subjects

Blueberry intake included in hypocaloric diet decreases weight, glucose, cholesterol, triglycerides and adenosine levels in obese subjects

The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

Short‐Term Glucocorticoid Treatment Reduces Circulating Sclerostin Concentrations in Healthy Young Men: A Randomized, Placebo‐Controlled, Double‐Blind Study

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