Modulation of Adipose Tissue Expression of Murine Matrix Metalloproteinases and Their Tissue Inhibitors With Obesity

Maquoi, Erik; Munaut, Carine; Colige, Alain; Collen, Désiré; Lijnen, H.R.

doi:10.2337/diabetes.51.4.1093

Cited by 251 publications

(260 citation statements)

References 33 publications

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“…These contradictory findings indicate that distinct pathways of matrix decomposition may be activated in different diseases. In agreement with our results, an interesting study performed on the adipose tissue of mice reported the presence of several members of MMPs and TIMPs, except MMP-8 [26]. A microarray study showed that while various MMP family members were strongly upregulated in adipocytes in a culture-conditioned medium, MMP-8 upregulation was not observed [27].…”

Section: Discussionsupporting

confidence: 92%

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Andrade

Petruceli

Belo

et al. 2012

Clinical Biochemistry

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Section: Discussionsupporting

confidence: 92%

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Andrade

Petruceli

Belo

et al. 2012

Clinical Biochemistry

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“…In parallel, specific tissue inhibitors of MMPs (TIMPs) can also be dysregulated. More specifically, TIMP1 is upregulated with obesity, and conversely, TIMP4 is downregulated in states of obesity (106). Such striking regulatory patterns of MMPs and their corresponding inhibitors suggest important roles of these factors in the pathophysiology of AT.…”

Section: Angiogenesis a Rate-limiting Step For At Expansion And Remomentioning

confidence: 96%

“…The function of several other MMPs highly expressed in AT remains to be further identified. Maquoi and colleagues further demonstrated that in DIO mice, expression levels of MMP3, -11, -12, -13, and -14 are all upregulated, whereas levels of MMP7, -9, -16, and -24 are downregulated (106). In parallel, specific tissue inhibitors of MMPs (TIMPs) can also be dysregulated.…”

Section: Angiogenesis a Rate-limiting Step For At Expansion And Remomentioning

confidence: 99%

Adipose tissue remodeling and obesity

Sun¹,

Kusminski²,

Scherer³

2011

J. Clin. Invest.

1,509

1,381

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To fulfill its role as the major energy-storing tissue, adipose has several unique properties that cannot be seen in any other organ, including an almost unlimited capacity to expand in a non-transformed state. As such, the tissue requires potent mechanisms to remodel, acutely and chronically. Adipocytes can rapidly reach the diffusional limit of oxygen during growth; hypoxia is therefore an early determinant that limits healthy expansion. Proper expansion requires a highly coordinated response among many different cell types, including endothelial precursor cells, immune cells, and preadipocytes. There are therefore remarkable similarities between adipose expansion and growth of solid tumors, a phenomenon that presents both an opportunity and a challenge, since pharmacological interventions supporting healthy adipose tissue adaptation can also facilitate tumor growth. IntroductionAdipose tissue (AT) can respond rapidly and dynamically to alterations in nutrient deprivation and excess through adipocyte hypertrophy and hyperplasia, thereby fulfilling its major role in wholebody energy homeostasis. AT remodeling is an ongoing process that is pathologically accelerated in the obese state, and thus, features such as reduced angiogenic remodeling, ECM overproduction, a heightened state of immune cell infiltration and subsequent proinflammatory responses prevail in many obese fat-pads (1). However, not all AT expansion is necessarily associated with pathological changes. The concept of the "metabolically healthy obese" state (2) suggests that some individuals can preserve systemic insulin sensitivity on the basis of "healthy" AT expansion, bypassing all of the aforementioned pathological consequences associated with obesity (3), thereby also avoiding the obesity-associated lipotoxic side effects. Many physiologically relevant processes important for human AT remodeling can be studied in rodent models, with the added advantage that processes related to AT expansion and reduction can occur at an extremely rapid rate. A 24-hour fast in a mouse is associated with a dramatic loss of AT mass and an acute remodeling process that involves rapid infiltration of macrophages; moreover, merely 24 to 48 hours of exposure to a high-fat diet (HFD) can cause a prompt increase in adipocyte size (4). AT is therefore an ideal model system to study rapid alterations in tissue expansion and reduction, as it adapts to a differential nutrient supply. Here, we will focus on key aspects of the intricate dynamics of AT remodeling and subsequent inflammatory consequences that arise from obesity.

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“…The modulation of extracellular matrix components via the production of metalloproteinases is an important regulator of fat tissue remodeling. The metalloproteinase 9 (Mmp-9) gene, known to be expressed at higher levels in preadipocytes than in adipocytes, decreased over generations in accordance with its downregulation in nutritionally induced obesity of C57BL/6J mice ( 36 ).…”

Section: Gene Expression Analysis Of Stromal Vascular Cellsmentioning

confidence: 97%

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

Massiéra

Barbry

Guesnet

et al. 2010

Journal of Lipid Research

163

128

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This article is available online at http://www.jlr.org able to genetic factors as it has occurred relatively recently and is observed in a wide range of human populations. High-fat diets are considered to be obesogenic in that they produce a consistent increase in fat mass that is directly related to the content of the diet and duration of feeding. However, the contribution of dietary fats compared with an excess energy intake in increasing body weight remains controversial, as no major change in the total amount of ingested fats has occurred in the last two decades ( 1, 2 ).In addition to caloric excess, a qualitative issue has emerged as a risk factor for obesity in rodents and possibly in humans; i.e., the disequilibrium in polyunsaturated fatty acid (PUFA) metabolism with a high ratio of linoleic acid (C18:2 6, LA) versus ␣ -linolenic acid (C18:3 3, LNA) ( 3 ). Notably, in rodents, reducing this ratio from 59 to 2 under isolipidic, isoenergetic conditions (40% energy as fat) by inclusion of dietary LNA counteracted the enhancing effects of LA on body weight and fat mass, which then became similar to that observed with a chow diet ( 4 ).6 PUFAs were more potent than 3 PUFAs in promoting adipogenesis ( 5-7 ). When combined with high carbohydrate content, a linoleic acid-enriched diet was found to be pro-adipogenic in vivo through cAMP-dependent signaling ( 8 ). LA acts through arachidonic acid (C20:4 6, ARA) and prostacyclin, as pups from mice invalidated for the prostacyclin receptor (IP-R) and fed a LA-rich diet exhibit reduced body weight and fat mass compared with wild-type mice fed the same diet ( 4 ). Overall, these results emphasize the importance of adipose tissue development Abstract The prevalence of obesity has steadily increased over the last few decades. During this time, populations of industrialized countries have been exposed to diets rich in fat with a high content of linoleic acid and a low content of ␣ -linolenic acid compared with recommended intake. To assess the contribution of dietary fatty acids, male and female mice fed a high-fat diet (35% energy as fat, linoleic acid: ␣ -linolenic acid ratio of 28) were mated randomly and maintained after breeding on the same diet for successive generations. Offspring showed, over four generations, a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in food intake. Transgenerational alterations in adipokine levels were accompa nied by hyperinsulinemia. Gene expression analyses of the stromal vascular fraction of adipose tissue, over generations, revealed discrete and steady changes in certain important players, such as CSF3 and Nocturnin. Thus, under conditions of genome stability and with no change in the regimen over four generations, we show that a Western-like fat diet induces a gradual fat mass enhancement, in accordance with the increasing prevalence of obesity observed in humans. -Massiera, F., P. Barbry, P. Guesnet, A. Joly, S. The prevalence of obesity and the risk of developing associated diseases ha...

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Modulation of Adipose Tissue Expression of Murine Matrix Metalloproteinases and Their Tissue Inhibitors With Obesity

Cited by 251 publications

References 33 publications

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Evaluation of plasmatic MMP-8, MMP-9, TIMP-1 and MPO levels in obese and lean women

Adipose tissue remodeling and obesity

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

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