Chemokines control fat accumulation and leptin secretion by cultured human adipocytes

Gerhardt, C.C.; Romero, Ignacio A.; Cancello, Raffaella; Camoin, Luc; Strosberg, A. Donny

doi:10.1016/s0303-7207(01)00394-x

Cited by 299 publications

(263 citation statements)

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“…The finding that adipose inflammation in obese db/db mice is independent of MCP-1 suggests that other mechanisms are responsible for adipose macrophage accumulation. Additional macrophage chemokines, including macrophage inhibitory protein-1α, macrophage migration inhibitory factor and macrophage-colony stimulating factor (M-CSF), are produced by adipocytes and may be important for adipose macrophage recruitment and activation [17,31,32]. In addition, M-CSF is known to promote tissue macrophage accrual by inducing local proliferation [33], and this may be a contributing mechanism for macrophage accumulation in adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

“…MCP-1 levels are increased in plasma and adipose tissue in mouse models of obesity [15,16], and correlate with the number of CD11b + monocytes in these animals [16]. Primary cultures of human preadipocytes constitutively produce MCP-1 but these levels are reduced upon maturation [17]. Stimulation with TNF-α or insulin increases expression of the gene encoding MCP-1 (Ccl2) in adipocytes differentiated in vitro [15,17].…”

mentioning

confidence: 99%

“…Primary cultures of human preadipocytes constitutively produce MCP-1 but these levels are reduced upon maturation [17]. Stimulation with TNF-α or insulin increases expression of the gene encoding MCP-1 (Ccl2) in adipocytes differentiated in vitro [15,17]. Addition of MCP-1 to differentiated adipocytes in vitro decreases insulin-stimulated glucose uptake and the expression of several adipogenic genes, suggesting that MCP-1 may also affect adipocyte function [17].…”

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confidence: 99%

“…Stimulation with TNF-α or insulin increases expression of the gene encoding MCP-1 (Ccl2) in adipocytes differentiated in vitro [15,17]. Addition of MCP-1 to differentiated adipocytes in vitro decreases insulin-stimulated glucose uptake and the expression of several adipogenic genes, suggesting that MCP-1 may also affect adipocyte function [17]. In diabetic kidneys, Ccl2 expression increases with macrophage accumulation and disease progression [4] and appears to be dependent on both the diabetic milieu [18] and activation of the renin-angiotensin system [19].…”

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Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

et al. 2006

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Aims/hypothesis Tissue macrophage accumulation is thought to induce insulin resistance during obesity and stimulate the progression of diabetic nephropathy. Monocyte chemoattractant protein-1 (MCP-1) is a potent stimulator of macrophage recruitment. It is increased in adipose tissue during obesity and in diabetic kidneys, suggesting that inflammation of these tissues may be MCP-1-dependent. Based on these findings, the aim of this study was to examine whether a deficiency in MCP-1 would alter the development of type 2 diabetes and its renal complications. Materials and methods The role of MCP-1 in the progression of type 2 diabetes and its associated renal injury was assessed in obese db/db mice that were deficient in the gene encoding MCP-1 (Ccl2). Results The incidence and development of type 2 diabetes were similar in Ccl2 +/+ and Ccl2 −/− db/db mice between 8 and 32 weeks of age. Body mass, hyperglycaemia, hyperinsulinaemia, glucose and insulin tolerance, plasma triacylglycerol and serum NEFA were not different between these strains. Pathological changes in epididymal adipose tissue, including increases in macrophage accumulation and Tnfa mRNA and reductions in Adipoq mRNA, were unaffected by the absence of MCP-1. In contrast, kidney macrophage accumulation and the progression of diabetic renal injury (albuminuria, histopathology, renal fibrosis) were substantially reduced in Ccl2 −/− compared with Ccl2 +/+ db/db mice with equivalent diabetes. Conclusions/interpretation Our study demonstrates that MCP-1 promotes type 2 diabetic renal injury but does not influence the development of obesity, insulin resistance or type 2 diabetes in db/db mice. MCP-1 plays a critical role in inflammation of the kidney, but not adipose tissue, during the progression of type 2 diabetes.

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Section: Discussionmentioning

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Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

et al. 2006

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“…Gerhardt et al 27 showed that prolonged stimulation of cultured human adipocytes with exogenous cytokines, including IL-8, leads to a decrease in lipid content. Ferrer et al 28 reported the presence of IL-8 in tissue sections from patients with CaP, but not in patients with benign prostatic hyperplasia.…”

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Elevation of cytokine levels in cachectic patients with prostate carcinoma

Pfitzenmaier

Vessella

Higano

et al. 2003

Cancer

144

100

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BACKGROUNDApproximately 60–70% of patients with advanced prostate carcinoma (CaP) suffer from cachexia, one of the most devastating conditions associated with advanced malignant disease. The pathophysiology of cachexia is multifactorial, and several cytokines, such as tumor necrosis factor α (TNFα) and interleukin 1 (IL‐1), IL‐6, and IL‐8, may be involved. The objective of the current study was to determine whether cachexia associated with advanced CaP is accompanied by increased serum levels of TNFα, IL‐1β, IL‐6, and IL‐8.METHODSThe levels of TNFα, IL‐1β, IL‐6, IL‐8, and prostate specific antigen (PSA) were examined in serum samples from normal donors (n = 10 donors), from patients with organ‐confined CaP (n = 19 patients), from patients with advanced CaP without cachexia (n = 17 patients), and from patients with cachectic CaP (n = 26 patients). DPC Immulite and Abbott IMx Total‐PSA assays were used to determine cytokine and PSA levels, respectively.RESULTSLevels of TNFα, IL‐6, and IL‐8 were elevated significantly in the group of patients with advanced, cachectic CaP compared with patients who were without cachexia. In the cachectic patients, levels of TNFα were correlated positively with IL‐8, and there was no correlation between PSA levels and any of the cytokine levels. IL‐1β levels were below the limit of detection in all samples.CONCLUSIONSThe current results show that levels of TNFα, IL‐6, and IL‐8 were increased in CaP patients with cachexia. Increased levels of these cytokines were not correlated with PSA levels, suggesting that they are regulated by a mechanism that is independent of PSA synthesis. Additional fundamental research is needed to determine the mechanisms involved and to identify potential therapeutic targets in patients with cachexia. Cancer 2003;97:1211–6. © 2003 American Cancer Society.DOI 10.1002/cncr.11178

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2018

Cardiovascular Disease

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Chemokines control fat accumulation and leptin secretion by cultured human adipocytes

Cited by 299 publications

References 50 publications

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

Elevation of cytokine levels in cachectic patients with prostate carcinoma

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