Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers

Simons, Peter J.; Pangaart, Petra S. van den; Roomen, Cindy P. A. A. van; Aerts, Johannes M. F. G.; Boon, Louis

doi:10.1016/j.cyto.2005.08.003

Cited by 105 publications

(92 citation statements)

References 54 publications

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“…It is noteworthy that leptin secretion was downregulated. This result agrees with that of Simons et al [39], who reported that, conversely to other proinflammatory cytokines, leptin secretion is reduced after stimulation with IFNγ, which is produced in high amounts by activated T lymphocytes. Furthermore, the conditioned media from activated lymphocytes reduced insulin responsiveness in adipocytes, probably due to altered adipocytokines and specific products of T lymphocytes.…”

Section: Discussionsupporting

confidence: 93%

The inflammatory receptor CD40 is expressed on human adipocytes: contribution to crosstalk between lymphocytes and adipocytes

et al. 2009

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Aims/hypothesis Obesity is associated with adipose tissue inflammation. The CD40 molecule, TNF receptor superfamily member 5 (CD40)/CD40 ligand (CD40L) pathway plays a role in the onset and maintenance of the inflammatory reaction, but has not been studied in human adipose tissue. Our aim was to examine CD40 expression by human adipocytes and its participation in adipose tissue inflammation. Methods CD40 expression was investigated in human whole adipose tissue and during adipocyte differentiation by real-time PCR, Western blot and immunohistochemistry. The CD40/CD40L pathway was studied using recombinant CD40L (rCD40L) in adipocyte culture and neutralising antibodies in lymphocyte/adipocyte co-culture. Results CD40 mRNA levels in subcutaneous adipose tissue were higher in the adipocyte than in the stromal-vascular fraction. CD40 expression was upregulated during adipocyte differentiation. Addition of rCD40L to adipocytes induced mitogen activated protein kinase (MAPK) activation, stimulated inflammatory adipocytokine production, and decreased insulin-induced glucose transport in parallel with a downregulation of IRS1 and GLUT4 (also known as SCL2A4). rCD40L decreased the expression of lipogenic genes and increased lipolysis. CD40 mRNA levels were significantly higher in subcutaneous adipose tissue than in visceral adipose tissue of obese patients and were positively correlated with BMI, and with IL6 and leptin mRNA levels. Lymphocyte/adipocyte co-culture led to an upregulation of proinflammatory adipocytokines and a downregulation of leptin and adiponectin. Physical separation of the two cell types attenuated these effects, suggesting the involvement of a cell-cell contact. Blocking the CD40/CD40L interaction with neutralising antibodies reduced IL-6 secretion from adipocytes. Conclusions/interpretation Adipocyte CD40 may contribute to obesity-related inflammation and insulin resistance. T lymphocytes regulate adipocytokine production through both the release of soluble factor(s) and heterotypic contact with adipocytes involving CD40.

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Section: Discussionsupporting

confidence: 93%

The inflammatory receptor CD40 is expressed on human adipocytes: contribution to crosstalk between lymphocytes and adipocytes

et al. 2009

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“…One study has reported an inhibition of the differentiation of subcutaneous abdominal preadipocytes (Simons et al 2005), but used only one concentration of IL1b that was much higher at 10 000 vs the 500 pg/ml range in our study. Another group, studying orbital human preadipocytes, also used only one dose of IL1b at 10 000 pg/ml to demonstrate its anti-adipogenic effect (Yoon et al 2011).…”

Section: Discussionmentioning

confidence: 99%

The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes

Gagnon

Foster

Landry

et al. 2013

Journal of Endocrinology

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When adipose tissue accumulates in obesity, the ability of preadipocytes to differentiate permits a hyperplastic expansion of functional adipocytes that preserves insulin sensitivity. Adipose infiltration by macrophages is associated with an adipogenic deficit and the appearance of inflamed, insulin-resistant hypertrophied adipocytes. Interleukin 1b (IL1b) has been reported to account for the anti-adipogenic action of macrophages in a mouse model. Using the THP-1 human macrophage cell line and human primary preadipocytes, our objective was to determine whether IL1b was necessary for the ability of conditioned medium from THP-1 macrophages (THP-1-MacCM) to: i) stimulate human preadipocyte inhibitor of kB kinase b (IKKb) and ii) inhibit human adipocyte differentiation. IL1b is present in THP-1-MacCM, and THP-1-MacCM or IL1b (500 pg/ml; its concentration in THP-1-MacCM) acutely stimulated IKKb phosphorylation and inhibitor of kB (IkB) degradation in preadipocytes. IL1b was sufficient to inhibit adipogenesis on its own, and this was blocked by SC-514, an IKKb inhibitor, as has been reported for THP-1-MacCM. IkB degradation by IL1b-immunodepleted THP-1-MacCM was attenuated, whereas IKKb phosphorylation and the inhibition of adipocyte differentiation were unchanged. Therefore, in contrast to what has been suggested for mouse cell models, IL1b is not required for the ability of MacCM to inhibit adipogenesis in human cell models.

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“…Among pro-inflammatory cytokines, TNF-a has been reported to decrease adiponectin production from adipocytes (Kappes & Löffler 2000, Simons et al 2005. Furthermore, TNF inhibits the differentiation of human adipocyte precursor cells and also promotes the delipidation of mature fat cells (Petruschke & Hauner 1993).…”

Section: Discussionmentioning

confidence: 99%

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

Martín¹,

Castillero²,

Granado³

et al. 2008

Journal of Endocrinology

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Adjuvant-induced arthritis is a model of rheumatoid arthritis that induces cachexia. In other cachectic situations, there is an increase in lipolysis resulting in a loss of adipose tissue mass. The aim of this work was to analyse the effect of chronic arthritis, induced by adjuvant injection, on white adipose tissue (WAT). For this purpose, rats were killed 10 days after adjuvant injection, when the first external symptoms appeared, on days 15 and 22 when the external signs of the illness reach their severest level. As arthritis decreases food intake, a pair-fed group was also included. Serum concentrations of insulin, leptin, adiponectin, glycerol and nitrites, as well as gene expression of leptin, adiponectin, hormonesensitive lipase (HSL), fatty acid synthase (FAS), tumour necrosis factor a and zinc-a 2 -glycoprotein (ZAG) were determined. Arthritis decreased food intake between days 5 and 16, but not during the last 5 days of the experiment. There was a marked decrease in relative adipose tissue weight and in serum leptin and adiponectin as well as in their gene expression in WAT in arthritic rats. Arthritis decreased the gene expression of FAS in the WAT. However, none of these effects was found in pair-fed rats. Arthritis did not increase lipolysis, since arthritic rats have lower serum concentrations of glycerol, HSL mRNA in WAT, as well as liver ZAG mRNA than the pair-fed or control rats. These data suggest that in chronic arthritis the decrease in white adipose mass is secondary to a reduced adipose lipogenesis, and this effect is not mainly due to the decrease in food intake.

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Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers

Cited by 105 publications

References 54 publications

The inflammatory receptor CD40 is expressed on human adipocytes: contribution to crosstalk between lymphocytes and adipocytes

The inflammatory receptor CD40 is expressed on human adipocytes: contribution to crosstalk between lymphocytes and adipocytes

The role of interleukin 1β in the anti-adipogenic action of macrophages on human preadipocytes

Adipose tissue loss in adjuvant arthritis is associated with a decrease in lipogenesis, but not with an increase in lipolysis

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