Stimulation of interleukin-6 release by interleukin-1β from isolated human adipocytes

Flower, Louise; Gray, Rosaire; Pinkney, Jonathan; Mohamed‐Ali, Vidya

doi:10.1016/s1043-4666(02)00495-7

Cited by 72 publications

(39 citation statements)

References 28 publications

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“…Similarly it has been shown that TNF-α and IL6 strongly suppress adiponectin production [41], consistent with the antagonism between the action of adiponectin and proinflammatory cytokines [42]. Since IL1B can increase IL6 secretion in cultured adipocytes [17], part of the IL1B effect could be mediated by upregulation of IL6 release. Our finding that IL1B is also a potent inhibitor of adiponectin production in murine and human adipose cells is in line with data showing that IL1B suppresses the mRNA expression of adiponectin in human adipose tissue explants [13].…”

Section: Discussionsupporting

confidence: 57%

“…In addition, treatment of human adipose tissue explants with IL1B decreased the level of mRNA for adiponectin [13], an adipocyte-secreted protein that plays a positive role in insulin sensitivity [14,15]. In adipose tissue and isolated adipocytes, IL1B has been shown to upregulate the release and expression of IL6 [16,17]. IL1B could also play a role in the increased production of monocyte chemoattractant protein 1 [18,19], a chemokine involved in the recruitment of macrophages to inflammation sites and the mRNA content of which is elevated in adipose tissue of obese subjects [20].…”

Section: Introductionmentioning

confidence: 99%

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Long-term treatment with interleukin-1β induces insulin resistance in murine and human adipocytes

et al. 2006

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Aims/hypothesis Adipose tissue inflammation has recently been implicated in the pathogenesis of insulin resistance and is probably linked to high local levels of cytokines. IL1B, a proinflammatory cytokine, may participate in this alteration. Materials and methods We evaluated the chronic effect (1-10 days) of IL1B (0.1-20 ng/ml) on insulin signalling in differentiating 3T3-F442A and differentiated 3T3-L1 murine adipocytes and in human adipocytes. We also assessed expression of the gene encoding IL1B in adipose tissue of wild-type and insulin-resistant mice (diet-induced and genetically obese ob/ob mice). Results IL1B inhibited insulin-induced phosphorylation of the insulin receptor β subunit, insulin receptor substrate 1, Akt/protein kinase B and extracellular regulated kinase 1/2 in murine and human adipocytes. Accordingly, IL1B suppressed insulin-induced glucose transport and lipogenesis. Long-term treatment of adipose cells with IL1B decreased cellular lipid content. This could result from enhanced lipolysis and/or decreased expression of genes involved in lipid metabolism (acetyl-CoA carboxylase, fatty acid synthase). Down-regulation of peroxisome proliferating-activated receptor γ and CCAAT/enhancer-binding protein α in response to IL1B may have contributed to the altered phenotype of IL1B-treated adipocytes. Moreover, IL1B altered adipocyte differentiation status in longterm cultures. IL1B also decreased the production of adiponectin, an adipocyte-specific protein that plays a positive role in insulin sensitivity. Expression of the gene encoding IL1B was increased in epididymal adipose tissue of obese insulin-resistant mice. Conclusions/interpretation IL1B is upregulated in adipose tissue of obese and insulin-resistant mouse models and may play an important role in the development of insulin resistance in murine and human adipose cells.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

Long-term treatment with interleukin-1β induces insulin resistance in murine and human adipocytes

et al. 2006

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“…IL-1β is an important immune cytokine released by a large variety of cells, including adipocytes [47], in which it may have a paracrine effect. IL-1β has been shown to inhibit adipocyte maturation and lipid accumulation [48] and to suppress expression of adiponectin [49] and leptin [50].…”

Section: Discussionmentioning

confidence: 99%

Adipokines and the insulin resistance syndrome in familial partial lipodystrophy caused by a mutation in lamin A/C

et al. 2005

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Aims/hypothesis: Familial partial lipodystrophy (FPLD) and obesity are both associated with increased risks of type 2 diabetes and cardiovascular disease. Although adipokines have been implicated, few data exist in subjects with FPLD; therefore we investigated a family with FPLD due to a lamin A/C mutation in order to determine how abnormalities of the plasma adipokine profile relate to insulin resistance and the metabolic syndrome. Methods: Plasma levels of adiponectin, leptin, resistin, IL-1β, IL-6 and TNF-α in 30 subjects (ten patients, 20 controls) were correlated with indices of metabolic syndrome. Results: Compared with controls, FPLD patients had significantly lower plasma levels of adiponectin (3.7±1.0 in FDLP cases vs 7.1±0.72 μg/ml in controls, p=0.02), leptin (1.23±0.4 vs 9.0±1.3 ng/ml, p=0.002) and IL-6 (0.59±0.12 vs 1.04±0.17 pg/ml, p=0.047) and elevated TNF-α (34.8±8.1 vs 13.7±2.7 pg/ml, p=0.028), whereas IL-1β and resistin were unchanged. In both groups, adiponectin levels were inversely correlated with body fat mass (controls, r=−0.44, p=0.036; FDLP, r=−0.67, p=0.025), insulin resistance (controls, r=−0.62, p=0.003; FDLP, r=−0.70, p=0.025) and other features of the metabolic syndrome. TNF-α concentrations were positively related to fat mass (controls, r=0.68, p=0.001; FDLP, r=0.64, p=0.048) and insulin resistance (controls, r=0.86, p=0.001; FDLP, r=0.75, p=0.013). IL-6, IL-1β and resistin did not demonstrate any correlations with the metabolic syndrome in either group. Conclusions/interpretation: Low adiponectin and leptin and high TNF-α were identified as the major plasma adipokine abnormalities in FPLD, consistent with the hypothesis that low adiponectin and high TNF-α production may be mechanistically related, and perhaps responsible for the development of insulin resistance and cardiovascular disease in FPLD.

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“…22 Human adipose tissue expresses IL-6, and adipocytes in culture express IL-6 constitutively. 23 IL-6 also exerts its effects on the central nervous system, where it is known that cytokines from the IL-6 family regulate glial cell activation. 24 The Role of IL-6 in Human Disease IL-6 is an important factor in many disease states including, rheumatoid arthritis, 25 systemic-onset FIGURE 1.…”

Section: Biologic Activities Of Il-6mentioning

confidence: 99%

Interleukin‐6 and its receptor in cancer

Hong

Angelo

Kurzrock

2007

Cancer

342

127

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Interleukin-6 (IL-6) plays a major role in the response to injury or infection and is involved in the immune response, inflammation, and hematopoiesis. Its deregulation impacts numerous disease states, including many types of cancer. Consequently, modulating IL-6 may be an innovative therapeutic strategy in several diseases. A review of relevant published literature regarding IL-6 and its receptor was performed. In addition, a review of the relevance of this cytokine system to human illness, particularly in cancer, was undertaken. IL-6 is a pleiotropic cytokine that is involved in the physiology of virtually every organ system. Aberrant expression of this cytokine has been implicated in diverse human illnesses, most notably inflammatory and autoimmune disorders, coronary artery and neurologic disease, gestational problems, and neoplasms. In cancer, high levels of circulating IL-6 are observed in almost every type of tumor studied and predict a poor outcome.

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Stimulation of interleukin-6 release by interleukin-1β from isolated human adipocytes

Cited by 72 publications

References 28 publications

Long-term treatment with interleukin-1β induces insulin resistance in murine and human adipocytes

Long-term treatment with interleukin-1β induces insulin resistance in murine and human adipocytes

Adipokines and the insulin resistance syndrome in familial partial lipodystrophy caused by a mutation in lamin A/C

Interleukin‐6 and its receptor in cancer

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