Obesity modifies bone marrow microenvironment and directs bone marrow mesenchymal cells to adipogenesis

Silva, Simone Vargas da; Renovato-Martins, Mariana; Ribeiro-Pereira, Cristiane; Citelli, Marta; Barja‐Fidalgo, Christina

doi:10.1002/oby.21660

Cited by 54 publications

(38 citation statements)

References 34 publications

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“…Male mice fed a HFD developed increased bone marrow cellularity and TNF-α production, and their bone marrow mesenchymal stem cells were primed towards adipogenesis 160 . ATM in visceral adipose tissue release cytokines such as IL-1β that increase bone marrow proliferation, resulting in monocytosis and neutrophilia 161 .…”

Section: Macrophage and Adipocyte Dysfunction In Obese Adipose Tissuementioning

confidence: 99%

Macrophage functions in lean and obese adipose tissue

2017

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Summary Interactions between macrophages and adipocytes influence both metabolism and inflammation. Obesity-induced changes to macrophages and adipocytes lead to chronic inflammation and insulin resistance. This paper reviews the various functions of macrophages in lean and obese adipose tissue and how obesity alters adipose tissue macrophage phenotypes. Metabolic disease and insulin resistance shift the balance between numerous pro- and anti-inflammatory regulators of macrophages and create a feed-forward loop of increasing inflammatory macrophage activation and worsening adipocyte dysfunction. This ultimately leads to adipose tissue fibrosis and diabetes. The molecular mechanisms underlying these processes have therapeutic implications for obesity, metabolic syndrome, and diabetes.

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Section: Macrophage and Adipocyte Dysfunction In Obese Adipose Tissuementioning

confidence: 99%

Macrophage functions in lean and obese adipose tissue

2017

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“…Obesity and its co-morbidities have been closely associated with a functional decline in the HSC compartment [20][21][22][23] . In our previous study, we showed that hypercholesterolemia, a major co-morbidity of obesity, caused a significant reduction in long-term HSC populations, telomere length, and reconstitution capacity of HSCs 24 .…”

Section: Expression Of the Tet1 Catalytic Domain In Hscs Effectively mentioning

confidence: 99%

Hypercholesterolemia Accelerates the Aging Phenotypes of Hematopoietic Stem Cells by a Tet1-Dependent Pathway

Tie

Yan

Khair

et al. 2020

Sci Rep

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“…231,232 Diet-induced obesity also reduced the proliferative and self-renewing capacity of hematopoietic stem and progenitor cells in the bone marrow, in turn gradually impeding B lymphopoiesis. Evidence for this possibility has come from experiments in murine models of obesity, including high-fat diet fed mice or leptin-leptin receptor deficient animals.…”

Section: Obesitymentioning

confidence: 99%

“…Bone marrow resident mesenchymal stem cells from mice on a high-fat diet as well as from mesenchymal stem cell-specific lepR fl/fl mice expressed gene signatures associated with adipogenesis, suggesting that obesity can induce an altered differentiation route for these multipotent cells. 231,232 Diet-induced obesity also reduced the proliferative and self-renewing capacity of hematopoietic stem and progenitor cells in the bone marrow, in turn gradually impeding B lymphopoiesis. [233][234][235] This gradual lymphopenia may help explain poor immune responses in aged individuals.…”

Section: Obesitymentioning

confidence: 99%

Plasma cells: You are what you eat

D'Souza

Bhattacharya

2019

Immunological Reviews

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Summary Plasma cells are terminally differentiated B lymphocytes that constitutively secrete antibodies. These antibodies can provide protection against pathogens, and their quantity and quality are the best clinical correlates of vaccine efficacy. As such, plasma cell lifespan is the primary determinant of the duration of humoral immunity. Yet dysregulation of plasma cell function can cause autoimmunity or multiple myeloma. The longevity of plasma cells is primarily dictated by nutrient uptake and non‐transcriptionally regulated metabolic pathways. We have previously shown a positive effect of glucose uptake and catabolism on plasma cell longevity and function. In this review, we discuss these findings with an emphasis on nutrient uptake and its effects on respiratory capacity, lifespan, endoplasmic reticulum stress, and antibody secretion in plasma cells. We further discuss how some of these pathways may be dysregulated in multiple myeloma, potentially providing new therapeutic targets. Finally, we speculate on the connection between plasma cell intrinsic metabolism and systemic changes in nutrient availability and metabolic diseases.

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Obesity modifies bone marrow microenvironment and directs bone marrow mesenchymal cells to adipogenesis

Abstract: The data suggest that obesity promotes an inflammatory microenvironment in bone marrow that commits BM-MSC to adipogenesis.

Cited by 54 publications

References 34 publications

Macrophage functions in lean and obese adipose tissue

Macrophage functions in lean and obese adipose tissue

Hypercholesterolemia Accelerates the Aging Phenotypes of Hematopoietic Stem Cells by a Tet1-Dependent Pathway

Plasma cells: You are what you eat

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