Immune cells in adipose tissue: Key players in metabolic disorders

Lolmède, Karine; Duffaut, Carine; Zakaroff-Girard, Alexia; Bouloumié, Anne

doi:10.1016/j.diabet.2011.03.002

Cited by 91 publications

(83 citation statements)

References 101 publications

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“…As such, this study provides the first, to our knowledge, empirical evidence supporting a mammalian function for GPR1 as a modifier of glucose homeostasis during obesity. The varied population of adipose stem cells and leukocytes within the SVF supports WAT differentiation and expansion and connects energy homeostasis with immunity and inflammation (Lolmede et al 2011). Although Gpr1 mRNA has been reported previously in adipocytes (Regard et al 2008), we report here for the first time, to our knowledge, that Gpr1 mRNA expression was markedly higher in the SVF than in adipocytes.…”

Section: Figurementioning

confidence: 37%

Gpr1 is an active chemerin receptor influencing glucose homeostasis in obese mice

Rourke¹,

Muruganandan²,

Dranse³

et al. 2014

Journal of Endocrinology

109

120

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Chemerin is an adipose-derived signaling protein (adipokine) that regulates adipocyte differentiation and function, immune function, metabolism, and glucose homeostasis through activation of chemokine-like receptor 1 (CMKLR1). A second chemerin receptor, G protein-coupled receptor 1 (GPR1) in mammals, binds chemerin with an affinity similar to CMKLR1; however, the function of GPR1 in mammals is essentially unknown. Herein, we report that expression of murine Gpr1 mRNA is high in brown adipose tissue and white adipose tissue (WAT) and skeletal muscle. In contrast to chemerin (Rarres2) and Cmklr1, Gpr1 expression predominates in the non-adipocyte stromal vascular fraction of WAT. Heterozygous and homozygous Gpr1-knockout mice fed on a high-fat diet developed more severe glucose intolerance than WT mice despite having no difference in body weight, adiposity, or energy expenditure. Moreover, mice lacking Gpr1 exhibited reduced glucose-stimulated insulin levels and elevated glucose levels in a pyruvate tolerance test. This study is the first, to our knowledge, to report the effects of Gpr1 deficiency on adiposity, energy balance, and glucose homeostasis in vivo. Moreover, these novel results demonstrate that GPR1 is an active chemerin receptor that contributes to the regulation of glucose homeostasis during obesity.

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Section: Figurementioning

confidence: 37%

Gpr1 is an active chemerin receptor influencing glucose homeostasis in obese mice

Rourke¹,

Muruganandan²,

Dranse³

et al. 2014

Journal of Endocrinology

109

120

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“…The inflammatory processes associated with obesity have not been fully established, though there is much interest in the role of adipose tissue macrophages in the inflammation characteristically observed in obesity [14]. Monocyte chemoattractant protein-1 (MCP-1) is known to induce macrophage infiltration into adipose tissue.…”

Section: Cerk Deficiency Prevents Infiltration Of Macrophages Into Admentioning

confidence: 99%

Ceramide kinase deficiency improves diet‐induced obesity and insulin resistance

et al. 2012

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a b s t r a c tCeramide kinase (CERK) is an enzyme that phosphorylates ceramide to produce ceramide 1-phosphate. Recently, evidence has emerged that CERK has a role in inflammatory signaling of immune cells. Since obesity is accompanied by chronic, low-grade inflammation, we examined whether CERK might be involved using CERK-null mice. We determined that CERK deficiency suppresses dietinduced increases in body weight, and improves glucose intolerance. Furthermore, we demonstrated that CERK deficiency attenuates MCP-1/CCR2 signaling in macrophages infiltrating the adipose tissue, resulting in the suppression of inflammation in adipocytes, which might otherwise lead to obesity and diabetes.

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“…Several chemokines and chemokine receptors, namely CCL2, CCL5, CCL7, CCL8, C-C motif chemokine receptor (CCR)2, C-X-C chemokine ligand (CXCL)12, CXCL14, C-X-C chemokine receptor (CXCR)2, have been implicated in the process of WAT inflammation in obesity [1,8,9]. The causal link between obesity and WAT inflammation was recognised more than a decade ago.…”

Section: Introductionmentioning

confidence: 99%

Lymphocytes in obesity-related adipose tissue inflammation

et al. 2012

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Inflammation in the white adipose tissue (WAT) is considered a major player in the development of insulin resistance. The role of macrophages accumulating in the WAT during obesity, promoting WAT inflammation and insulin resistance is well established. In contrast, less is known about the role of lymphocytes. Recent studies have implicated different lymphocyte subsets in WAT inflammation. For instance, cytotoxic CD8 + T cells infiltrating the WAT may contribute to the recruitment, differentiation and activation of macrophages. On the other hand, a differential role for CD4 + Th1 and CD4 + Th2 cells has been suggested.Levels of WAT regulatory T cells decrease during the course of obesity and may represent a crucial factor for the maintenance of insulin sensitivity. Moreover, activation of natural killer T cells, an innate-like T cell population, which recognises lipid antigens, promotes insulin resistance and WAT inflammation. Finally, B cells may infiltrate WAT very early in response to high-fat feeding and worsen glucose metabolism through modulation of T cells and the production of pathogenic antibodies. These interesting new findings however bear controversies and introduce novel, yet unanswered, questions. Here, we review and discuss the impact of the different lymphocyte subsets in obesityrelated WAT inflammation and attempt to identify the open questions to be answered by future studies.

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Immune cells in adipose tissue: Key players in metabolic disorders

Cited by 91 publications

References 101 publications

Gpr1 is an active chemerin receptor influencing glucose homeostasis in obese mice

Gpr1 is an active chemerin receptor influencing glucose homeostasis in obese mice

Ceramide kinase deficiency improves diet‐induced obesity and insulin resistance

Lymphocytes in obesity-related adipose tissue inflammation

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