Role of macrophage tissue infiltration in metabolic diseases

Bouloumié, Anne; Curat, Cyrile Anne; Sengenès, Coralie; Lolmède, Karine; Miranville, Alexandra; Busse, Rudi

doi:10.1097/01.mco.0000172571.41149.52

Cited by 234 publications

(170 citation statements)

References 93 publications

(57 reference statements)

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“…The maximal differentiation response of the omental preadipocytes was somewhat lower than that of subcutaneous preadipocytes as observed by others [20,26]. Interestingly, omental/visceral adipose tissue contains more macrophages than does subcutaneous fat in obese rodents and humans [11]. Also adipose tissue possesses anatomical site-specific properties [33], and these could potentially influence interactions with macrophages.…”

Section: Discussionmentioning

confidence: 77%

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Macrophage-conditioned medium inhibits the differentiation of 3T3-L1 and human abdominal preadipocytes

et al. 2006

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Aims/hypothesis: In obesity, a limited adipogenic capacity may promote adipocyte hypertrophy and increase the risk of insulin resistance and type 2 diabetes. Recent data indicate that macrophages reside within adipose tissue in obese rodents and humans. We hypothesised that secreted macrophage factors may inhibit adipogenesis.Materials and methods: Conditioned media from cultured murine J774 or human THP-1 macrophages were collected, and added to either murine 3T3-L1 preadipocytes or human abdominal stromal preadipocytes from subcutaneous or omental fat depots. Results: Macrophage-conditioned medium (MacCM) strongly inhibited 3T3-L1 adipogenesis. Dose-response studies with J774-MacCM revealed that 80 and 100% of J774-MacCM completely suppressed triacylglycerol accumulation as well as the induction of fatty acid synthase, peroxisome proliferator-activated receptor γ, CCAAT/enhancer binding protein α, and adiponectin. Similar inhibitory effects on 3T3-L1 preadipocytes were observed with THP-1-MacCM. Differentiation of human abdominal subcutaneous stromal preadipocytes was moderately reduced (subcutaneous>omental) by J744-MacCM. In contrast, the differentiation of both subcutaneous and omental stromal preadipocytes was completely inhibited by THP-1-MacCM, as determined on the basis of morphology and triacylglycerol accumulation, as well as fatty acid synthase and adiponectin protein expression. Conclusions/interpretation: Secreted macrophage products inhibit the differentiation of 3T3-L1 preadipocytes as well as human abdominal stromal preadipocytes.

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Section: Discussionmentioning

confidence: 77%

“…It appears that macrophages and adipose cells may influence each other via paracrine mediators or direct cellular processes [11]. For example, diapedesis and the infiltration of monocytes and their differentiation into macrophages in adipose tissue were shown to be modulated by factors secreted by adipose cells [12,13].…”

Section: Introductionmentioning

confidence: 99%

Macrophage-conditioned medium inhibits the differentiation of 3T3-L1 and human abdominal preadipocytes

et al. 2006

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“…Moreover, we stated an important role for post-translational modifications in the regulation of ER stress [26,27]. Activation of ER stress induces an increased release of NEFA, adipokines and inflammatory mediators [28,29], triggering infiltration and activation of macrophages in adipose tissue, contributing to insulin resistance [30,31]. These infiltrating immune cells further stimulate secretion of adipokines from adipocytes [31] and secrete pro-inflammatory cytokines of which TNFα and IL-6 are implicated in the induction of insulin resistance [32,33].…”

Section: Discussionmentioning

confidence: 99%

“…Activation of ER stress induces an increased release of NEFA, adipokines and inflammatory mediators [28,29], triggering infiltration and activation of macrophages in adipose tissue, contributing to insulin resistance [30,31]. These infiltrating immune cells further stimulate secretion of adipokines from adipocytes [31] and secrete pro-inflammatory cytokines of which TNFα and IL-6 are implicated in the induction of insulin resistance [32,33]. The absence of inflammation around the hypertrophic adipocytes of Chop −/− mice contrasts with the increased numbers of resident macrophages in adipose tissue of obese individuals [34] and suggests that CHOP provides a crucial proinflammatory signal in fat.…”

Section: Discussionmentioning

confidence: 99%

Deletion of C/EBP homologous protein (Chop) in C57Bl/6 mice dissociates obesity from insulin resistance

et al. 2012

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Aims/hypothesis Endoplasmic reticulum (ER) stress has been implicated in the development of type 2 diabetes, via effects on obesity, insulin resistance and pancreatic beta cell health. C/EBP homologous protein (CHOP) is induced by ER stress and has a central role in apoptotic execution pathways triggered by ER stress. The aim of this study was to characterise the role of CHOP in obesity and insulin resistance.Methods Metabolic studies were performed in Chop −/− and wild-type C57Bl/6 mice, and included euglycaemichyperinsulinaemic clamps and indirect calorimetry. The inflammatory state of liver and adipose tissue was determined by quantitative RT-PCR, immunohistology and macrophage cultures. Viability and absence of ER stress in islets of Langerhans was determined by electron microscopy, islet culture and quantitative RT-PCR. Results Systemic deletion of Chop induced abdominal obesity and hepatic steatosis. Despite marked obesity, Chop −/− mice had preserved normal glucose tolerance and insulin sensitivity. This discrepancy was accompanied by lower levels of pro-inflammatory cytokines and less infiltration of immune cells into fat and liver. Conclusions/interpretation These observations suggest that insulin resistance is not induced by fat accumulation per se, but rather by the inflammation induced by ectopic fat. CHOP may play a key role in the crosstalk between excessive fat deposition and induction of inflammation-mediated insulin resistance.

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“…Adipose tissue of obese subjects is characterized by increased macrophage infiltration and overexpression of inflammatory cytokines and chemokines (7,10,12). Liver fat has been shown to be associated with increased gene expression of macrophage-specific cell surface markers such as CD68 (18,25) and an increased number of macrophages (10,18) in adipose tissue.…”

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confidence: 99%

Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy

Sevastianova

Sutinen²,

Kannisto³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Role of macrophage tissue infiltration in metabolic diseases

Cited by 234 publications

References 93 publications

Macrophage-conditioned medium inhibits the differentiation of 3T3-L1 and human abdominal preadipocytes

Macrophage-conditioned medium inhibits the differentiation of 3T3-L1 and human abdominal preadipocytes

Deletion of C/EBP homologous protein (Chop) in C57Bl/6 mice dissociates obesity from insulin resistance

Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy

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