Effect of matrix metalloproteinase inhibition on adipose tissue development

Demeulemeester, Diego; Collen, Désiré; Lijnen, H.R.

doi:10.1016/j.bbrc.2005.01.103

Cited by 60 publications

(47 citation statements)

References 25 publications

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“…12,15,16,44 Treatment with MMP inhibitors impairs adipose tissue development in mice fed a high fat diet. 10,45 Furthermore, the secretion of MMP-2 and MMP-9 increases during adipocyte differentiation in both human adipocytes and mouse preadipocyte cell lines. 12,15,16 This suggests that Ob-X can regulate growth and development of adipose tissue by inhibiting MMP activities.…”

Section: Inhibition Of Obesity By Angiogenesis Inhibitormentioning

confidence: 99%

The anti-angiogenic herbal composition Ob-X inhibits adipose tissue growth in obese mice

My¹,

By²,

Hs³

et al. 2010

Int J Obes

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Objective: The growth and development of adipose tissue are thought to be associated with angiogenesis and extracellular matrix remodeling. As the composition of the herbal extract called Ob-X has been shown to have both anti-angiogenic and matrix metalloproteinase (MMP)-inhibiting activities, we hypothesized that growth of adipose tissue can be regulated by Ob-X. Materials and methods: The effects of Ob-X on angiogenesis and extracellular matrix remodeling were measured using in vitro and ex vivo assays. The effects of Ob-X on adipose tissue growth were investigated in nutritionally obese mice. Results: Ob-X inhibited angiogenesis in a dose-dependent manner in the human umbilical vein endothelial cell tube formation assay in vitro and the rat aortic ring assay ex vivo. Ob-X also suppressed MMP activity in vitro. Administration of Ob-X to high fat diet-induced obese mice produced significant reductions in body weight gain and adipose tissue mass compared with control. The mass of both visceral (VSC) and subcutaneous (SC) fat was reduced in Ob-X-treated mice. The size of adipocytes in VSC and SC adipose tissues was also significantly reduced in Ob-X-treated mice. Ob-X treatment decreased the blood vessel density and MMP activity in VSC adipose tissues of nutritionally obese mice. Ob-X reduced mRNA levels of angiogenic factors (VEGF-A and FGF-2) and MMPs (MMP-2 and MMP-9), whereas it increased mRNA levels of angiogenic inhibitors (TSP-1, TIMP-1 and TIMP-2) in SC and VSC adipose tissues of nutritionally obese mice. Conclusion: Ob-X, which has anti-angiogenic and MMP-inhibitory activities, reduces adipose tissue mass in nutritionally induced obese mice, providing evidence that adipose tissue growth and development may be prevented by inhibiting angiogenesis. In addition, these data suggest that regulation of adipose tissue growth by inhibiting angiogenesis may alter the expression of genes involved in angiogenesis and the MMP system.

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Section: Inhibition Of Obesity By Angiogenesis Inhibitormentioning

confidence: 99%

The anti-angiogenic herbal composition Ob-X inhibits adipose tissue growth in obese mice

My¹,

By²,

Hs³

et al. 2010

Int J Obes

View full text Add to dashboard Cite

show abstract

“…Interestingly, both studies suggest that the effects of TIMP-1 on proliferation and apoptosis are not due to metalloproteinase inhibition (12,13). These findings are of special interest since pharmacological inhibition of MMPs, in contrast to TIMP-1, leads to impaired adipogenesis in vitro and in vivo (5,6,14,15). Taking these studies into account, TIMP-1 appears to maintain fat mass independent of MMP inhibition in rodents possibly via increased proliferation and/or decreased apoptosis.…”

Section: Discussionmentioning

confidence: 92%

Tissue inhibitor of metalloproteinase-1 predicts adiposity in humans

Kralisch¹,

Blüher²,

Tönjes³

et al. 2007

eur j endocrinol

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Objective: Tissue inhibitor of metalloproteinase (TIMP)-1 is upregulated in fat of obese rodents and promotes adipose tissue development in these animals. However, it is unclear whether TIMP-1 independently predicts adiposity in humans and whether serum levels are increased in s.c. and visceral obesity. Design: Twenty-four lean, 16 s.c. obese, and 20 visceral obese subjects were studied. Methods: Plasma TIMP-1 concentrations were quantified using ELISAs and correlated to clinical parameters. Results: Plasma TIMP-1 levels were significantly different between lean (156G42 mg/l), s.c. obese (186G52 mg/l), and visceral obese (198G42 mg/l) subjects (P!0.01). Furthermore, TIMP-1 correlated positively with body mass index (BMI), waist-to-hip ratio (WHR), % body fat, fasting insulin, free fatty acids, cholesterol, leptin, interleukin-6, and negatively with adiponectin (P!0.05). Moreover, TIMP-1 serum levels predicted % body fat but not WHR independent of age, sex, and plasma insulin. Conclusions: We demonstrate that increased TIMP-1 serum levels are found with increased adiposity in humans.

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“…TIMP-1 -/-mice also had a similar phenotype [81]. Finally, studies utilizing inhibitors of MMPs have shown a reduction in AT mass in mice that have reduced MMP activity [82,83]. Interestingly, dietary fish oils have been shown to inhibit the increase in MMPs noted in highfat fed mice [84].…”

Section: Matrix Metalloproteinases and Tissue Inhibitors Of Metalloprotmentioning

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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Effect of matrix metalloproteinase inhibition on adipose tissue development

Cited by 60 publications

References 25 publications

The anti-angiogenic herbal composition Ob-X inhibits adipose tissue growth in obese mice

The anti-angiogenic herbal composition Ob-X inhibits adipose tissue growth in obese mice

Tissue inhibitor of metalloproteinase-1 predicts adiposity in humans

Macrophage infiltration into adipose tissue: initiation, propagation and remodeling

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