Implication of fatty acids in the inhibitory effect of human adipocytes on osteoblastic differentiation

Lucas, Stéphanie; Clabaut, Aline; Ghali, Olfa; Haren, Nathalie; Hardouin, Pierre; Broux, Odile

doi:10.1016/j.bone.2013.04.010

Cited by 6 publications

(6 citation statements)

References 5 publications

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“…As mentioned before, like for other WAT, catecholamines or agonists of the β-adrenergic receptors stimulate fatty acid release from BMA both in vitro ( 121 , 127 , 128 ) and in vivo ( 114 ). Surprisingly, insulin addition does not seem necessary for human BM MSC adipogenesis and subsequent lipogenesis in vitro ( 109 , 127 , 129 ).…”

Section: Specific Properties Of Bma Versus Other Adipocytesmentioning

confidence: 83%

“…Results are conflicting for the resorbing cells since saturated fatty acids were reported either to reduce osteoclastogenesis ( 119 ) or to exert beneficial effects on mature osteoclasts by preventing their apoptosis ( 120 ). Though the amount of fatty acids released by BMA appears rather low in vitro ( 121 ), BMA could contribute to bone alterations through a detrimental fatty acid-mediated process referred as lipotoxicity. Moreover, a specific lipid pattern of BMA may be considered as a discriminative trait, which is rather puzzling considering that dietary fat intake usually impacts on the fatty acid composition of bone ( 122 ), adipose tissues, and blood ( 123 ).…”

Section: Specific Properties Of Bma Versus Other Adipocytesmentioning

confidence: 99%

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Bone Marrow Adipose Tissue: To Be or Not To Be a Typical Adipose Tissue?

2016

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Bone marrow adipose tissue (BMAT) emerges as a distinct fat depot whose importance has been proved in the bone–fat interaction. Indeed, it is well recognized that adipokines and free fatty acids released by adipocytes can directly or indirectly interfere with cells of bone remodeling or hematopoiesis. In pathological states, such as osteoporosis, each of adipose tissues – subcutaneous white adipose tissue (WAT), visceral WAT, brown adipose tissue (BAT), and BMAT – is differently associated with bone mineral density (BMD) variations. However, compared with the other fat depots, BMAT displays striking features that makes it a substantial actor in bone alterations. BMAT quantity is well associated with BMD loss in aging, menopause, and other metabolic conditions, such as anorexia nervosa. Consequently, BMAT is sensed as a relevant marker of a compromised bone integrity. However, analyses of BMAT development in metabolic diseases (obesity and diabetes) are scarce and should be, thus, more systematically addressed to better apprehend the bone modifications in that pathophysiological contexts. Moreover, bone marrow (BM) adipogenesis occurs throughout the whole life at different rates. Following an ordered spatiotemporal expansion, BMAT has turned to be a heterogeneous fat depot whose adipocytes diverge in their phenotype and their response to stimuli according to their location in bone and BM. In vitro, in vivo, and clinical studies point to a detrimental role of BM adipocytes (BMAs) throughout the release of paracrine factors that modulate osteoblast and/or osteoclast formation and function. However, the anatomical dissemination and the difficulties to access BMAs still hamper our understanding of the relative contribution of BMAT secretions compared with those of peripheral adipose tissues. A further characterization of the phenotype and the functional regulation of BMAs are ever more required. Based on currently available data and comparison with other fat tissues, this review addresses the originality of the BMAT with regard to its development, anatomy, metabolic properties, and response to physiological cues.

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Section: Specific Properties Of Bma Versus Other Adipocytesmentioning

confidence: 83%

Section: Specific Properties Of Bma Versus Other Adipocytesmentioning

confidence: 99%

Bone Marrow Adipose Tissue: To Be or Not To Be a Typical Adipose Tissue?

2016

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“…This is achieved in part through the expression and secretion of peptides derived from white adipose tissue, including leptin, adiponectin, omentin-1, vesfatin, and resistin, as well as via adipocytokines such as tumor necrosis factor alpha (TNFα), IL-6, and IL-1β [ 55 , 56 , 57 , 58 ]. Fatty acids [ 59 , 60 ], cholesterol [ 61 , 62 ], phospholipids [ 63 ], and several endogenous lipid metabolites, including prostaglandins [ 64 ] and oxysterols [ 65 ], are also reported to stimulate bone cell function and activity. The lineage commitment of BMSCs towards either an osteoblastic or adipogenic fate are closely related, and preferential engagement along one axis over the other contributes an essential role in regulating bone mass [ 54 ].…”

Section: Introductionmentioning

confidence: 99%

Sphingolipid-Induced Bone Regulation and Its Emerging Role in Dysfunction Due to Disease and Infection

Seal,

Hughes,

Wei

et al. 2024

IJMS

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The human skeleton is a metabolically active system that is constantly regenerating via the tightly regulated and highly coordinated processes of bone resorption and formation. Emerging evidence reveals fascinating new insights into the role of sphingolipids, including sphingomyelin, sphingosine, ceramide, and sphingosine-1-phosphate, in bone homeostasis. Sphingolipids are a major class of highly bioactive lipids able to activate distinct protein targets including, lipases, phosphatases, and kinases, thereby conferring distinct cellular functions beyond energy metabolism. Lipids are known to contribute to the progression of chronic inflammation, and notably, an increase in bone marrow adiposity parallel to elevated bone loss is observed in most pathological bone conditions, including aging, rheumatoid arthritis, osteoarthritis, and osteomyelitis. Of the numerous classes of lipids that form, sphingolipids are considered among the most deleterious. This review highlights the important primary role of sphingolipids in bone homeostasis and how dysregulation of these bioactive metabolites appears central to many chronic bone-related diseases. Further, their contribution to the invasion, virulence, and colonization of both viral and bacterial host cell infections is also discussed. Many unmet clinical needs remain, and data to date suggest the future use of sphingolipid-targeted therapy to regulate bone dysfunction due to a variety of diseases or infection are highly promising. However, deciphering the biochemical and molecular mechanisms of this diverse and extremely complex sphingolipidome, both in terms of bone health and disease, is considered the next frontier in the field.

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“…Although there are numerous studies dealing with the impact of different fatty acids on osteoblastogenesis in primary human ( Elbaz et al, 2010 ; Gunaratnam et al, 2013 ; Kim et al, 2008 ; Maurin et al, 2002 ) and rat ( Yeh et al, 2013 ; Yeh et al, 2014 ) osteoblasts, the exact impact of fatty acids on osteogenic differentiation is still unclear. While a number of studies ( Gunaratnam et al, 2013 ; Kim et al, 2008 ; Lucas et al, 2013 ; Wang et al, 2013 ) indicate an inhibition of cell proliferation and differentiation, as well as an induction of apoptosis by palmitate, others ( Yeh et al, 2014 ) were not able to provide evidence for the influence of palmitate on these functions. Indirect co-culture studies with osteoblasts and fatty acid producing adipocytes, as well as the usage of an adipocyte-conditioned medium (from adipocyte monocultures) in osteoblast-monocultures, reveals that adipocytes are able to induce adipogenic differentiation of osteoblasts ( Clabaut et al, 2010 ) and to reduce osteoblast functioning ( Wang et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

“…In co-cultures of osteoblasts and differentiating pre-adipocytes, the negative impact of fatty acids, such as palmitate biosynthesized from the adipocytes, could be circumvented by an inhibition of acetyl CoA carboxylase and fatty acid synthase in the adipocytes ( Elbaz et al, 2010 ), stimulation of the palmitate degradation ( Yeh et al, 2014 ), as well as specific inhibitors of autophagy or apoptosis ( Gunaratnam et al, 2013 ). All co-cultivation studies, and studies investigating the impact of palmitate on adipogenesis and osteogenesis as mentioned above, are based on cultivation and incubation times respectively between 20 and 72 h ( Clabaut et al, 2010 ; Gunaratnam et al, 2013 ; Hickson-Bick et al, 2002 ; Kim et al, 2008 ; Lucas et al, 2013 ; Maurin et al, 2002 ; Wang et al, 2013 ; Yeh et al, 2014 , 2014). In summary, these studies suggest a reduction of osteoblast function during short-term incubation of the cell cultures by palmitate.…”

Section: Introductionmentioning

confidence: 99%

Effect of long term palmitate treatment on osteogenic differentiation of human mesenchymal stromal cells - Impact of albumin

et al. 2020

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The long-term effects of palmitate (PA) on osteogenic differentiation capacity of human mesenchymal stromal cells (hMSCs) were investigated by cultivating the cells in osteogenic differentiation medium (O-w/o) and osteogenic medium containing PA (O-BSA-PA) for 21 days. Osteogenic medium containing BSA (O-BSA) was used as a control. By means of rt-qPCR, successful osteogenic differentiation was observed in the O-w/o regarding the levels of osteogenic and cell-communication related genes ( OCN , Col1 , BMP2 , ITGA1 , ITGB1 , Cx43 , sp1 ) in contrast to expression levels observed in cells incubated within basal medium. However, in the O-BSA, these genes were found to have decreased significantly. In cases of Cx43 and sp1 , PA significantly reinforced the reductive effect of BSA alone. O-BSA notably decreased glucose and pyruvate consumption, whereas glutamine consumption significantly increased. In comparison to O-BSA addition of PA significantly reduced glycolysis and glutaminolysis. ToF-SIMS analysis confirmed increased incorporation of supplemented deuterated PA into the cell membranes, while the overall PA-concentration remained unchanged compared to cells incubated in the O-BSA and O-w/o. Therefore, the effects on gene expression and the metabolism did not result from the membrane alterations, but may have risen from inter- and intracellular effects brought on by BSA and PA.

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Implication of fatty acids in the inhibitory effect of human adipocytes on osteoblastic differentiation

Cited by 6 publications

References 5 publications

Bone Marrow Adipose Tissue: To Be or Not To Be a Typical Adipose Tissue?

Bone Marrow Adipose Tissue: To Be or Not To Be a Typical Adipose Tissue?

Sphingolipid-Induced Bone Regulation and Its Emerging Role in Dysfunction Due to Disease and Infection

Effect of long term palmitate treatment on osteogenic differentiation of human mesenchymal stromal cells - Impact of albumin

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