Obesity-Induced Changes in Bone Marrow Homeostasis

Beňová, Andrea; Tencerová, Michaela

doi:10.3389/fendo.2020.00294

Cited by 71 publications

(44 citation statements)

References 199 publications

(165 reference statements)

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“…Obesity also mediates changes in bone-marrow, where immune cells are originated. This stem cell differentiation impairment affects systemic inflammatory pathways [ 38 ].…”

Section: Obesity Inflammation and Oxidative Stressmentioning

confidence: 99%

Iron Metabolism in Obesity and Metabolic Syndrome

González-Domínguez

Visiedo-Garcia

Domínguez-Riscart

et al. 2020

IJMS

131

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Obesity is an excessive adipose tissue accumulation that may have detrimental effects on health. Particularly, childhood obesity has become one of the main public health problems in the 21st century, since its prevalence has widely increased in recent years. Childhood obesity is intimately related to the development of several comorbidities such as nonalcoholic fatty liver disease, dyslipidemia, type 2 diabetes mellitus, non-congenital cardiovascular disease, chronic inflammation and anemia, among others. Within this tangled interplay between these comorbidities and associated pathological conditions, obesity has been closely linked to important perturbations in iron metabolism. Iron is the second most abundant metal on Earth, but its bioavailability is hampered by its ability to form highly insoluble oxides, with iron deficiency being the most common nutritional disorder. Although every living organism requires iron, it may also cause toxic oxygen damage by generating oxygen free radicals through the Fenton reaction. Thus, iron homeostasis and metabolism must be tightly regulated in humans at every level (i.e., absorption, storage, transport, recycling). Dysregulation of any step involved in iron metabolism may lead to iron deficiencies and, eventually, to the anemic state related to obesity. In this review article, we summarize the existent evidence on the role of the most recently described components of iron metabolism and their alterations in obesity.

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“…Obesity also mediates changes in bone-marrow, where immune cells are originated. This stem cell differentiation impairment affects systemic inflammatory pathways [ 38 ].…”

Section: Obesity Inflammation and Oxidative Stressmentioning

confidence: 99%

Iron Metabolism in Obesity and Metabolic Syndrome

González-Domínguez

Visiedo-Garcia

Domínguez-Riscart

et al. 2020

IJMS

131

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“…Further work is needed to reproduce these findings, considering important factors such as age and gender, and better define whether the metabolic benefits of UVR 16 are related to changes in cDC proportions in iBAT, if functional links between MEP, vascularisation and whitening of BAT exist, and how findings here in mice are relevant to human biology. While obesity is associated with changes in the cell composition of bone marrow, including HSPC 33 , little is known of its effects on stem cells in human BAT.…”

Section: Discussionmentioning

confidence: 99%

Metabolic dysfunction induced by high-fat diet modulates hematopoietic stem and myeloid progenitor cells in brown adipose tissue of mice

Mincham¹,

Panchal²,

Hart³

et al. 2021

Preprint

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Brown adipose tissue (BAT) may be an important metabolic regulator of whole-body glucose. While important roles have been ascribed to macrophages in regulating metabolic functions in BAT, little known is known of the roles of other immune cells subsets, particularly dendritic cells (DCs). Eating a high fat diet may compromise the development of hematopoietic stem and progenitor cells (HSPC), which give rise to DCs, in bone marrow, with less known of its effects in BAT. We have previously demonstrated that ongoing exposure to low-dose ultraviolet radiation (UVR) significantly reduced the whitening effect of eating a high-fat diet upon interscapular (i)BAT of mice. Here, we examined whether this observation may be linked to changes in the phenotype of HSPC and myeloid-derived immune cells in iBAT and bone marrow of mice using 12-colour flow cytometry. Many HSPC subsets declined in both iBAT and bone marrow with increasing metabolic dysfunction. Conversely, with rising adiposity and metabolic dysfunction, conventional (c)DCs increased in both of these tissues. When compared to low-fat diet, consumption of high-fat diet significantly reduced proportions of myeloid, common myeloid and megakaryocyte-erythrocyte progenitors in iBAT, and short-term hematopoietic stem cells in bone marrow. In mice fed a high-fat diet, exposure to low-dose UVR significantly reduced proportions of cDCs in iBAT, independently of nitric oxide release from irradiated skin (blocked using the scavenger, cPTIO), but did not significantly modify HSPC subsets in either tissue. Further studies are needed to determine whether changes in these cell populations contribute towards metabolic dysfunction.

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“…Recent studies on obesity have demonstrated that a rise in bone marrow adiposity promotes osteoporosis and impairs several immune-associated functions [216,217]. An increase in bone marrow adiposity can have an impact on bone marrow stem cell lineage differentiation towards myelopoiesis.…”

Section: Adiposity and Cns Injurymentioning

confidence: 99%

“…SCI individuals not only experience increased adiposity in these two common regions of the body, but also a rise in bone marrow adipose tissue [ 197 ]. Recent studies on obesity have demonstrated that a rise in bone marrow adiposity promotes osteoporosis and impairs several immune-associated functions [ 216 , 217 ]. An increase in bone marrow adiposity can have an impact on bone marrow stem cell lineage differentiation towards myelopoiesis.…”

Section: Energy Balance Lipid Accumulation and Adipose Tissuementioning

confidence: 99%

The Role of Lipids, Lipid Metabolism and Ectopic Lipid Accumulation in Axon Growth, Regeneration and Repair after CNS Injury and Disease

Roy

Tedeschi

2021

Cells

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Axons in the adult mammalian nervous system can extend over formidable distances, up to one meter or more in humans. During development, axonal and dendritic growth requires continuous addition of new membrane. Of the three major kinds of membrane lipids, phospholipids are the most abundant in all cell membranes, including neurons. Not only immature axons, but also severed axons in the adult require large amounts of lipids for axon regeneration to occur. Lipids also serve as energy storage, signaling molecules and they contribute to tissue physiology, as demonstrated by a variety of metabolic disorders in which harmful amounts of lipids accumulate in various tissues through the body. Detrimental changes in lipid metabolism and excess accumulation of lipids contribute to a lack of axon regeneration, poor neurological outcome and complications after a variety of central nervous system (CNS) trauma including brain and spinal cord injury. Recent evidence indicates that rewiring lipid metabolism can be manipulated for therapeutic gain, as it favors conditions for axon regeneration and CNS repair. Here, we review the role of lipids, lipid metabolism and ectopic lipid accumulation in axon growth, regeneration and CNS repair. In addition, we outline molecular and pharmacological strategies to fine-tune lipid composition and energy metabolism in neurons and non-neuronal cells that can be exploited to improve neurological recovery after CNS trauma and disease.

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Obesity-Induced Changes in Bone Marrow Homeostasis

Cited by 71 publications

References 199 publications

Iron Metabolism in Obesity and Metabolic Syndrome

Iron Metabolism in Obesity and Metabolic Syndrome

Metabolic dysfunction induced by high-fat diet modulates hematopoietic stem and myeloid progenitor cells in brown adipose tissue of mice

The Role of Lipids, Lipid Metabolism and Ectopic Lipid Accumulation in Axon Growth, Regeneration and Repair after CNS Injury and Disease

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