Diet Induction of Monocyte Chemoattractant Protein‐1 and its Impact on Obesity

Chen, Airu; Mumick, Sheena; Zhang, Chunsheng; Lamb, John; Dai, Hongyue; Weingarth, Drew T.; Mudgett, John S.; Chen, Howard; MacNeil, Douglas J.; Reitman, Marc L.; Su, Qian

doi:10.1038/oby.2005.159

Cited by 208 publications

(160 citation statements)

References 27 publications

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“…Studies of high-fat diet-induced obesity in mice deficient in chemokine CC motif receptor 2 (CCR2) are somewhat controversial, one study showing that these mice are unprotected from adipose inflammation and insulin resistance and another indicating protection [5,30]. It is indeed possible that CCR2 deficiency may not duplicate the results of MCP-1 deficiency, because CCR2 is not an exclusive receptor for MCP-1, and other ligands capable of binding CCR2, such as MCP-3, are also increased in adipose tissue during obesity [30].…”

Section: Discussionmentioning

confidence: 99%

“…It is indeed possible that CCR2 deficiency may not duplicate the results of MCP-1 deficiency, because CCR2 is not an exclusive receptor for MCP-1, and other ligands capable of binding CCR2, such as MCP-3, are also increased in adipose tissue during obesity [30]. In addition, adipose levels of MCP-1 and macrophage expression of CCR2 may not be equivalent in different mouse models of obesity, which may lead to variations in the severity and mechanisms of inflammation in adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

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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

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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“…Circulating concentrations and adipose tissue expression levels of CCL2 positively correlate to adiposity (9) . In addition, 3T3-L1 adipocytes treated with CCL2 exhibited a marked reduction in insulin-simulated glucose uptake in vitro (92,93) . Absence of CCR2 in DIO mouse model partially ameliorated HFD-induced obesity, hepatic steatosis coincident with attenuated systemic IR.…”

Section: Obesity-induced Adipose Tissue Macrophage Recruitmentmentioning

confidence: 99%

“…The role of CCL2 in obesity maybe further confounded by the effect of CCL2 on metabolism. Lack of CCR2 reduced HFDinduced obesity, while plasma CCL2 levels decreased exponentially with pharmacological-induced weight reduction in DIO mice (51,93) . A number of studies have disputed the involvement of the CCR2/MCP-1 axis in obesity and IR (93,96) .…”

Section: Obesity-induced Adipose Tissue Macrophage Recruitmentmentioning

confidence: 99%

“…Lack of CCR2 reduced HFDinduced obesity, while plasma CCL2 levels decreased exponentially with pharmacological-induced weight reduction in DIO mice (51,93) . A number of studies have disputed the involvement of the CCR2/MCP-1 axis in obesity and IR (93,96) . Abrogating CCR2 in DIO mice did not alter body weight, glucose homoeostasis or ATM infiltration (93) .…”

Section: Obesity-induced Adipose Tissue Macrophage Recruitmentmentioning

confidence: 99%

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Insights into the role of macrophage migration inhibitory factor in obesity and insulin resistance

et al. 2012

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High-fat diet (HFD)-induced obesity has emerged as a state of chronic low-grade inflammation characterised by a progressive infiltration of immune cells, particularly macrophages, into obese adipose tissue. Adipose tissue macrophages (ATM) present immense plasticity. In early obesity, M2 anti-inflammatory macrophages acquire an M1 pro-inflammatory phenotype. Pro-inflammatory cytokines including TNF-α, IL-6 and IL-1β produced by M1 ATM exacerbate local inflammation promoting insulin resistance (IR), which consequently, can lead to type-2 diabetes mellitus (T2DM). However, the triggers responsible for ATM recruitment and activation are not fully understood. Adipose tissue-derived chemokines are significant players in driving ATM recruitment during obesity. Macrophage migration inhibitory factor (MIF), a chemokine-like inflammatory regulator, is enhanced during obesity and is directly associated with the degree of peripheral IR. This review focuses on the functional role of macrophages in obesity-induced IR and highlights the importance of the unique inflammatory cytokine MIF in propagating obesity-induced inflammation and IR. Given MIF chemotactic properties, MIF may be a primary candidate promoting ATM recruitment during obesity. Manipulating MIF inflammatory activities in obesity, using pharmacological agents or functional foods, may be therapeutically beneficial for the treatment and prevention of obesity-related metabolic diseases.

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Adipokine Production by Adipose Tissue: A Novel Target for Treating Metabolic Syndrome and its Sequelae

et al. 2011

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Diet Induction of Monocyte Chemoattractant Protein‐1 and its Impact on Obesity

Cited by 208 publications

References 27 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

Insights into the role of macrophage migration inhibitory factor in obesity and insulin resistance

Adipokine Production by Adipose Tissue: A Novel Target for Treating Metabolic Syndrome and its Sequelae

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