Visfatin: the missing link between intra-abdominal obesity and diabetes?

Sethi, J.; Vidal-Puig, António

doi:10.1016/j.molmed.2005.06.010

Cited by 250 publications

(202 citation statements)

References 10 publications

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“…Over the past several years, a series of evidence has indicated that it is also ubiquitously present in most other tissues, such as adipose tissue, skeletal muscle, spleen, and liver (Sethi and Vidal-Puig 2005). Visfatin could stimulate the release of cytokines and is induced by inflammatory stimuli such as TNF-α, LPS, and IL-6 (Jia et al 2004;Nowell et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Visfatin induces cholesterol accumulation in macrophages through up-regulation of scavenger receptor-A and CD36

Zhou

Pan

Huang³

et al. 2013

Cell Stress and Chaperones

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As a new potential inflammatory mediator, visfatin plays an important role in inflammation and atherosclerosis. The formation of macrophage-derived foam cells occurs at the early stage of atherosclerosis and underlies the visible fatty streak. Recent studies have indicated that visfatin may be associated with the development of foam cells, but its exact effect and molecular mechanism remain unknown. This study aims to study the effect of visfatin on foamy cell formation and its underlying molecular mechanism. Visfatin levels were determined in apolipoprotein E (ApoE) knockout (KO) mice on a western diet for 16 weeks. Effects of visfatin in cholesterol accumulation were studied both in vivo and in vitro. The levels of scavenger receptors located in macrophage surface were measured in RAW264.7 cells after treatment with visfatin. Visfatin levels were much higher in ApoE KO mice than that in the control mice. Meanwhile, oxidized low-density lipoprotein induces both visfatin release from RAW264.7 cells and its cellular levels within 24 h. Visfatin promotes lipid accumulation mainly through excessive cholesterol uptake not only in RAW264.7 cells but also in peritoneal macrophages isolated from ApoE KO mice. Furthermore, visfatin induces the activation of scavenger receptors (SR)-A and cluster of differentiation (CD)36, but not that of SR-BI, ATP-binding cassette transporter (ABC)A1, or ABCG1 in RAW264.7 cells. Both transcriptional and posttranscriptional regulation may work in concert to mediate the expression of SR-A and CD36 in visfatin-treated cells. Visfatin induces cholesterol accumulation in macrophages and accelerates the process of atherosclerosis mainly through modulating the expression of SR-A and CD36.

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Section: Discussionmentioning

confidence: 99%

Visfatin induces cholesterol accumulation in macrophages through up-regulation of scavenger receptor-A and CD36

Zhou

Pan

Huang³

et al. 2013

Cell Stress and Chaperones

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“…Visfatin, a recently discovered adipokine, has been shown to play a role similar to insulin in insulin-sensitive tissues, such as liver, muscle, and fat (8). Visfatin may play a dual role: an endocrine role, by modulating insulin sensitivity in peripheral organs; and an autocrine/paracrine function on visceral adipose tissue, facilitating differentiation and fat deposition (14). Though Pagano (15) have reported decreased plasma visfatin and its messenger RNA in subcutaneous adipose tissue of obese subjects, several other studies have reported elevated blood visfatin levels in patients with T2DM (9,16) or in obese children (17).…”

Section: Effects Of Different Treatments On Visfatin Levels In Sat Pmentioning

confidence: 99%

Impact of metformin treatment and swimming exercise on visfatin levels in high-fat-induced obesity rats

Gao

Wang

Pan

et al. 2014

Arq Bras Endocrinol Metab

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Objective: Visfatin is a recently discovered adipocytokine that contributes to glucose and obesityrelated conditions. Until now, its responses to the insulin-sensitizing agent metformin and to exercise are largely unknown. We aim to investigate the impact of metformin treatment and/or swimming exercise on serum visfatin and visfatin levels in subcutaneous adipose tissue (SAT), peri-renal adipose tissue (PAT) and skeletal muscle (SM) of high-fat-induced obesity rats. Materials and methods:Sprague-Dawley rats were fed a normal diet or a high-fat diet for 16 weeks to develop obesity model. The high-fat-induced obesity model rats were then randomized to metformin (MET), swimming exercise (SWI), or adjunctive therapy of metformin and swimming exercise (MAS), besides high-fat obesity control group and a normal control group, all with 10 rats per group. Zoometric and glycemic parameters, lipid profile, and serum visfatin levels were assessed at baseline and after 6 weeks of therapy. Visfatin levels in SAT, PAT and SM were determined by Western Blot. Results: Metformin and swimming exercise improved lipid profile, and increased insulin sensitivity and body weight reduction were observed. Both metformin and swimming exercise down-regulated visfatin levels in SAT and PAT, while the adjunctive therapy conferred greater benefits, but no changes of visfatin levels were observed in SM. Conclusion: Our results indicate that visfatin down-regulation in SAT and PAT may be one of the mechanisms by which metformin and swimming exercise inhibit obesity.Arq Bras Endocrinol Metab. 2014;58(1):42-7 Keywords Endocrinology; metabolic syndrome; adipocytokine RESUMO Objetivo: A visfatina é uma adipocina recentemente descoberta que contribui com as condições relacionadas à glicose e à obesidade. Até hoje, pouco se sabe da sua resposta à metformina, um agente sensibilizador de insulina, e ao exercício. Nosso objetivo foi investigar o impacto do tratamento com metformina e/ou da natação sobre a visfatina no soro e no tecido adiposo subcutâneo (TAS), tecido adiposo perirrenal (TAP) e músculo esquelético (ME) em ratos com obesidade induzida por dieta com alto teor de gordura. Materiais e métodos: Ratos Sprague-Dawley foram alimentados com uma dieta normal ou com alto teor de gordura por 16 semanas para o desenvolvimento de um modelo de obesidade. Os ratos do modelo de obesidade foram, então, randomizados para a metformina, natação ou terapia de combinação com metformina e natação, além do grupo controle de obesidade induzida por alto teor de gordura e do grupo controle normal. Cada grupo apresentava 10 ratos. Parâmetros zoométricos e glicêmicos, perfil lipídico e níveis de visfatina sérica foram avaliados no momento inicial e após seis semanas de tratamento. Os níveis de visfatina em TAS, TAP e ME foram determinados por Western Blot. Resultados: A metformina e a natação melhoraram o perfil lipídico e aumentaram a sensibilidade à insulina, com redução do peso corporal. Tanto a metformina quanto a natação levaram à regulação para baixo do...

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“…25 Furthermore, the fact that visfatin increases in plasma following a high-fat diet suggests that it has an important role in diet-or obesityinduced insulin resistance. 24 A significant positive correlation was found between visfatin and circulating markers of inflammation such as C-reactive protein, suggesting a possible role of visfatin in the cardiovascular system. 27 In conclusion, the novel finding of this study is the association of the mutant type group A358C of FAAH with a better metabolic profile (insulin, glucose, visfatin and HOMA levels) than of the wild-type group.…”

Section: Discussionmentioning

confidence: 93%

“…Although the affinity of visfatin for the insulin receptors appears to be similar to insulin, its concentration in plasma is much lower than the insulin concentration under fasting conditions. 24 It remains to be established whether visfatin production is a compensatory response to tissue-specific insulin resistance or more simply a marker of tissue-specific inflammatory cytokine action. Perhaps a new hypothesis could explain the contradictory results of the literature.…”

Section: Discussionmentioning

confidence: 99%

C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females

et al. 2010

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Background: Recently, it has been shown that the polymorphism 385 C/A of FAAH (fatty acid amide hydrolase) was associated with overweight and obesity. Visfatin has been identified as a protein expressed in visceral adipose tissue with contradictory functions in glucose metabolism. Objective: The aim of our study was to investigate the relationship between polymorphism (cDNA 385 C-4A) of the FAAH gene and visfatin levels in obese women. Design: A population of 143 females with obesity was analyzed. Indirect calorimetry, tetrapolar electrical bioimpedance, blood pressure and serial assessment of nutritional intake with 3-day written food records and biochemical analysis (lipid profile, visfatin, insulin, C-reactive protein and homeostasis model assessment for insulin sensitivity (HOMA)) were performed. Results: Ninety-four patients (65.7%) had the genotype C358C (wild-type group) and 49 (34.3%) patients had the genotype C358A (mutant type group). No differences were detected between groups in anthropometric parameters and dietary intakes. Insulin (15.6±7.6 vs 14.1±10.1 mUI l À1 ; Po0.05), glucose (101.2±21.9 vs 92.3±10.5 mg per 100 ml; Po0.05) and HOMA values (3.96 ± 2.3 vs 3.15 ± 2.8; Po0.05) were higher in the wild type-group than in the mutant type group. Visfatin levels were lower in the wild-type group than in the mutant type group (47.83±57.5 vs 65.71±55 ng ml À1 ; Po0.05). Conclusion:The novel finding of this study is the association of the mutant type group A358C of FAAH with lower glucose, insulin and HOMA levels than of the wild-type group with higher visfatin levels.

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Visfatin: the missing link between intra-abdominal obesity and diabetes?

Cited by 250 publications

References 10 publications

Visfatin induces cholesterol accumulation in macrophages through up-regulation of scavenger receptor-A and CD36

Visfatin induces cholesterol accumulation in macrophages through up-regulation of scavenger receptor-A and CD36

Impact of metformin treatment and swimming exercise on visfatin levels in high-fat-induced obesity rats

C358A missense polymorphism of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH) and visfatin levels in obese females

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