ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice

Brake, Danett K.; Smith, E. O’Brian; Mersmann, Harry J.; Smith, C. Wayne; Robker, Rebecca L.

doi:10.1152/ajpcell.00008.2006

Cited by 137 publications

(116 citation statements)

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“…Previous studies reported that the expression of adhesion molecules in visceral adipose tissue was increased by obesity [36,37]. In another study, obese mice did not exhibit macrophage infiltration into adipose tissue after ICAM-1 antagonist treatment [38].…”

Section: Discussionmentioning

confidence: 88%

“…Previous reports showed that the expression of adhesion molecules in adipose tissue was increased in the obese condition [5,6] and a different study indicated that HFD induced obese mice exhibited higher expression of Intercellular adhesion molecule 1(ICAM-1) and Vascular cell adhesion [7]. Thus, adhesion molecules affect obesity-induced macrophage infiltration into adipose tissue.…”

Section: Introduction *mentioning

confidence: 97%

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The effects of either resveratrol or exercise on macrophage infiltration and switching from M1 to M2 in high fat diet mice

Jeong

Lee

Park

et al. 2015

J. Exerc. Nutr, Biochem.

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The effects of either resveratrol or exercise on macrophage infiltration and switching from M1 to M2 in high fat diet mice. JENB., Vol. 19, No. 2, pp.65-72, 2015 [Purpose] The aim of this study was to compare the effectiveness of either resveratrol supplementation or exercise training on macrophage infiltration and switching from M1 to M2 kupffer cells in high fat diet mice.[Methods] C57BL/6 mice were separated into 5 groups: normal diet (ND; n = 6), high-fat diet (HD; n = 6), high-fat diet with resveratrol (HR; n = 6), high-fat diet with exercise (HE; n = 6) or high-fat diet with resveratrol and exercise (HRE; n = 6). Resveratrol supplementation mice were orally gavaged with resveratrol (25mg/kg of body weight) dissolved in 50% propylene glycol. Exercise mice ran on a treadmill at 12-20 m/min for 30-60 min/day, 5 times/week for 12 weeks.[Results] After 12 weeks of intervention, the liver was analyzed. F4/80 expression was evaluated by western blot while CD11c and CD163 mRNA expressions were evaluated by RT-PCR. The weights of the body and liver were significantly increased in the HD and HR group compared to the ND group (p < 0.01). However, the weights were most effectively reduced in the HE and HRE groups compared to the HD group (p < 0.05). The macrophage marker, F4/80 expression was significantly lower in the HE and HRE groups compared to the HD group (p < 0.05). mRNA expression of the M1 macrophage marker, CD11c, in the HD group was significantly increased compared to the ND group (p < 0.01). mRNA expression of the M2 macrophage specific marker, CD163, in the HE and HRE groups were significantly increased compared to the HD group (p < 0.05). The mRNA expressions of TLR4, ICAM-1 and VCAM-1, which induce pro-inflammatory cytokine production, were strongly decreased in the HR, HE, and HRE groups compared to the HD group.[Conclusion] These results suggest that moderate exercise training inhibits macrophage infiltration and up regulation of CD163 expression. However, resveratrol supplementation is not enough to ameliorate obesity-induced macrophage infiltration and switching.

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Section: Discussionmentioning

confidence: 88%

Section: Introduction *mentioning

confidence: 97%

The effects of either resveratrol or exercise on macrophage infiltration and switching from M1 to M2 in high fat diet mice

Jeong

Lee

Park

et al. 2015

J. Exerc. Nutr, Biochem.

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“…Adhesion molecules such as intercellular adhesion molecule (ICAM)-1 have been shown to be expressed in murine AT [33]. Furthermore, it has been shown in mice that within 3 weeks of high-fat feeding, AT expression of ICAM-1 was increased, and after 6 months of feeding, soluble ICAM-1 in plasma correlated with bodyweight and fat mass [34]. Most recently, Nishimura et al used in vivo imaging to show that leukocyte-EC interactions are increased in the microcirculation of the subcutaneous AT of obese mice, and that administration of antibody to ICAM-1 normalized these interactions [35].…”

Section: Endothelial Cell-mediated Adhesionmentioning

confidence: 99%

Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

2008

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It has long been known that adipose tissue in obesity is in a heightened state of inflammation. Recently, our understanding of this has been transformed by the knowledge that immune cells such as macrophages and T cells can infiltrate adipose tissue and are responsible for the majority of inflammatory cytokine production. These seminal findings have opened up a new area in biology that is garnering the interest of scientists involved in research relating to cell motility, inflammation, obesity, physiology, diabetes and cardiovascular disease. Some important general questions relevant to this field are: how are macrophages recruited to adipose tissue in obesity? What are the physiological consequences of macrophage-adipocyte interactions? Do these inflammatory macrophages contribute to pathophysiological conditions associated with obesity, such as insulin resistance, dyslipidemia, diabetes and cardiovascular disease? This review focuses on the first of these important questions. Keywords activation; adipose tissue; chemokines; crown-like structures; hypoxia; inflammation; insulin resistance; leptin; lymphocytes; macrophages During the past two decades, the complex nature of adipose tissue (AT) has become an area of intense investigation. This is in part due to the growing worldwide obesity epidemic, and in part to the identification of leptin as an adipokine secreted from AT. Since the discovery of leptin, many other adipokines, such as adiponectin, resistin, visfatin and omentin, have also been identified. These discoveries have led to the first revolution in the field of AT biology, the identification of AT as an endocrine organ. More recently, it has been discovered that not only adipocytes, but also immune cells, such as macrophages [1,2] and T lymphocytes [3][4][5], reside in AT, and that these cells may induce insulin resistance by promoting a proinflammatory milieu within the AT. This discovery has led to the second revolution in the field of AT biology,

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“…In obese mice and humans, M⌽s infiltrate AT as circulating monocytes in response to AT secretion of MCP-1, which recruits monocytes expressing the C-C chemokine receptor (CCR)2 (1,2,10 -12,13). CCR2ϩ M⌽s expressing the M⌽ differentiation marker F4/80 and CD11c, a dendritic cell (DC) marker (13) upregulated in M⌽ foam cells (14), were recently reported to infiltrate AT of obese mice and were distinguished from noninflammatory resident ATM⌽s (F4/ 80ϩ/CCR2Ϫ/CD11cϪ) isolated from nonobese mice (12,15). However, the relationship between this obesityassociated ATM⌽ "phenotypic switch" (12) and the development and progression of obesity complications is unclear (16,17).…”

mentioning

confidence: 99%

Adipocyte Death, Adipose Tissue Remodeling, and Obesity Complications

Strissel

Stancheva²,

Miyoshi³

et al. 2007

Diabetes

857

807

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OBJECTIVE-We sought to determine the role of adipocyte death in obesity-induced adipose tissue (AT) inflammation and obesity complications.RESEARCH DESIGN AND METHODS-Male C57BL/6 mice were fed a high-fat diet for 20 weeks to induce obesity. Every 4 weeks, insulin resistance was assessed by intraperitoneal insulin tolerance tests, and epididymal (eAT) and inguinal subcutaneous AT (iAT) and livers were harvested for histological, immunohistochemical, and gene expression analyses.RESULTS-Frequency of adipocyte death in eAT increased from Ͻ0.1% at baseline to 16% at week 12, coincident with increases in 1) depot weight; 2) AT macrophages (ATM⌽s) expressing F4/80 and CD11c; 3) mRNA for tumor necrosis factor (TNF)-␣, monocyte chemotactic protein (MCP)-1, and interleukin (IL)-10; and 4) insulin resistance. ATM⌽s in crown-like structures surrounding dead adipocytes expressed TNF-␣ and IL-6 proteins. Adipocyte number began to decline at week 12. At week 16, adipocyte death reached ϳ80%, coincident with maximal expression of CD11c and inflammatory genes, loss (40%) of eAT mass, widespread collagen deposition, and accelerated hepatic macrosteatosis. By week 20, adipocyte number was restored with small adipocytes, coincident with reduced adipocyte death (fourfold), CD11c and MCP-1 gene expression (twofold), and insulin resistance (35%). eAT weight did not increase at week 20 and was inversely correlated with liver weight after week 12 (r ϭ Ϫ0. 85, P Ͻ 0.001). In iAT, adipocyte death was first detected at week 12 and remained Յ3%.CONCLUSIONS-These results implicate depot-selective adipocyte death and M⌽-mediated AT remodeling in inflammatory and metabolic complications of murine obesity. Diabetes

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ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice

Abstract: . ICAM-1 expression in adipose tissue: effects of diet-induced obesity in mice.

Cited by 137 publications

References 56 publications

The effects of either resveratrol or exercise on macrophage infiltration and switching from M1 to M2 in high fat diet mice

The effects of either resveratrol or exercise on macrophage infiltration and switching from M1 to M2 in high fat diet mice

Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

Adipocyte Death, Adipose Tissue Remodeling, and Obesity Complications

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