Activation of SOCS-3 by Resistin

Steppan, Claire M.; Wang, Juan; Whiteman, Eileen L.; Birnbaum, Morris J.; Lazar, Mitchell A.

doi:10.1128/mcb.25.4.1569-1575.2005

Cited by 254 publications

(202 citation statements)

References 43 publications

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“…However, it attenuates the insulin-signaling pathway upon decreased insulindependent phosphorylation of the insulin receptor and subsequent reduction of downstream 9 signals [56]. Suppressor of cytokine signaling (SOCS) proteins are well known inhibitors of insulin signaling.…”

Section: Resistin Obesity and Markers Of Insulin Resistancementioning

confidence: 99%

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The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková

Haluzı́k

Šenolt

2009

Clinical Immunology

375

297

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Section: Resistin Obesity and Markers Of Insulin Resistancementioning

confidence: 99%

“…In adipocytes, resistin activates SOCS3 in a time-and dose-dependent manner and induces the association of SOCS3 with the insulin receptor. It is possible that SOCS3 could be a cellular mediator of the ability of resistin to antagonize insulin action in adipocytes [56].…”

Section: Resistin Obesity and Markers Of Insulin Resistancementioning

confidence: 99%

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková

Haluzı́k

Šenolt

2009

Clinical Immunology

375

297

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“…From this perspective, the ability of RETN to affect glucose metabolism is associated with activation of SOCS-3, an inhibitor of insulin signaling in adipocytes (Steppan et al, 2005). Although studies in animal models have consistently shown that RETN promotes insulin resistance, there is also evidence indicating that this effect in humans is less evident (Lee et al, 2003;Heilbronn et al, 2004).…”

Section: Resistinmentioning

confidence: 99%

Obesity, inflammation, and insulin resistance

Martins

Oliveira

Cruz

et al. 2014

Braz. J. Pharm. Sci.

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White adipose tissue (WAT) is considered an endocrine organ. When present in excess, WAT can influence metabolism via biologically active molecules. Following unregulated production of such molecules, adipose tissue dysfunction results, contributing to complications associated with obesity. Previous studies have implicated pro-and anti-inflammatory substances in the regulation of inflammatory response and in the development of insulin resistance. In obese individuals, pro-inflammatory molecules produced by adipose tissue contribute to the development of insulin resistance and increased risk of cardiovascular disease. On the other hand, the molecules with anti-inflammatory action, that have been associated with the improvement of insulin sensitivity, have your decreased production. Imbalance of these substances contributes significantly to metabolic disorders found in obese individuals. The current review aims to provide updated information regarding the activity of biomolecules produced by WAT.Uniterms: Obesity. Inflammation. Adipose tissue. Adipokines. Insulin resistance.O tecido adiposo branco (WAT) é considerado um órgão endócrino, que, em excesso, é capaz de controlar o metabolismo, pela ação de moléculas biologicamente ativas. A produção desregulada destas substâncias pela disfunção do tecido adiposo pode contribuir para as complicações presentes na obesidade. As pesquisas atuais têm esclarecido fatores e mecanismos envolvidos na atuação de substâncias pró e anti-inflamatórias na modulação da inflamação e da resistência à insulina. Em indivíduos obesos, as moléculas pró-inflamatórias produzidas pelo tecido adiposo têm sido implicadas como fator contribuinte para o desenvolvimento da resistência à insulina e aumento do risco de doença cardiovascular. Por outro lado, as moléculas com ação anti-inflamatória, que atuam na melhora da sensibilidade à insulina, têm sua produção reduzida. O desequilíbrio entre essas substâncias contribui de forma significativa para as desordens metabólicas presente em indivíduos obesos. Assim, esta revisão visa a trazer informações atualizadas sobre a atuação de moléculas secretadas pelo tecido adiposo. Unitermos:Obesidade. Inflamação. Tecido adiposo. Adipocinas. Resistência à insulina.

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“…Several reports have demonstrated that ectopic expression of SOCS3 may lead to insulin resistance (Senn et al 2003;Steppan et al 2005;Ye et al 2012;Jorgensen et al 2013). As shown in Fig.…”

Section: Discussionmentioning

confidence: 93%

“…Resistin antagonize several insulin actions in vitro, resulting in decreased basal and insulin-stimulated glucose uptake, oxidation and glycogen synthesis. For example, recombinant resistin attenuates insulin-stimulated glucose uptake by inducing the expression of SOCS3 in 3T3-L1 adipocytes (Steppan et al 2001;Steppan et al 2005). Basal and insulin-stimulated glucose uptake, oxidation and glycogen synthesis in L6 rat skeletal muscle cells were also decreased in the presence of resistin (Palanivel et al 2006).…”

Section: Introductionmentioning

confidence: 98%

Resistin disrupts glycogen synthesis under high insulin and high glucose levels by down-regulating the hepatic levels of GSK3β

Song¹,

Wang²,

Mao³

et al. 2013

Gene

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The effect of mouse resistin on hepatic insulin resistance in vivo and in vitro, and its possible molecular mechanism were examined. Focusing on liver glycogen metabolism and gluconeogenesis, which are important parts of glucose metabolism, in primary cultures of rat hepatocytes we found that glycogen content was significantly lower (P<0.05) after treatment with recombinant murine resistin only in the presence of insulin plus glucose stimulation. Protein levels of factors in the insulin signaling pathway involved in glycogen synthesis were examined by Western blot analysis, with the only significant change observed being the level of phosphorylated (at Ser 9) glycogen synthase kinase-3β (GSK-3β) (P<0.001). No differences in the protein levels for the insulin receptor β (IRβ), insulin receptor substrates (IRS1 and IRS2), phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt) or their phosphorylated forms were observed between control and resistin treated primary rat hepatocytes. In a mouse model with high liver-specific expression of resistin, fasting blood glucose levels and liver glycogen content changed. Fasting blood glucose levels were significantly higher (P<0.001) in the model mice, compared to the control mice, while the glycogen content of the liver tissue was about 60% of that of the control mice (P<0.05). The gluconeogenic response was not altered between the experimental and control mice. The level of phosphorylated GSK-3β in the liver tissue was also decreased (P<0.05) in the model mice, consistent with the results from the primary rat hepatocytes. Our results suggests that resistin reduces the levels of GSK-3β phosphorylated at Ser 9 leading to impaired hepatic insulin

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Activation of SOCS-3 by Resistin

Cited by 254 publications

References 43 publications

The role of resistin as a regulator of inflammation: Implications for various human pathologies

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Obesity, inflammation, and insulin resistance

Resistin disrupts glycogen synthesis under high insulin and high glucose levels by down-regulating the hepatic levels of GSK3β

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