S-resistin inhibits adipocyte differentiation and increases TNFα expression and secretion in 3T3-L1 cells

Fernández, Constantino Arce; Arco, Araceli del; Gallardo, Nilda; Aguado, Lidia; Rodríguez, María E; Ros, Manuel; Carrascosa, J.M.; Andrés, Antonio; Arribas, Carmen

doi:10.1016/j.bbamcr.2010.06.012

Cited by 8 publications

(16 citation statements)

References 41 publications

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“…This observation provides direct support for the evidence that, upon central leptin administration, the up-regulation of resistin levels in WAT can contribute to the inhibition of the insulin-stimulated glucose uptake in this tissue. Finally, our data are consistent with previous reports showing that resistin inhibits the early steps of insulin signaling pathway involved in glucose uptake in 3T3-L1 adipocytes (52,54) and L6 cells (53). Nevertheless, the contribution of other factors promoting insulin resistance in WAT upon central leptin administration should be taken into account.…”

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confidence: 82%

Regulation of Insulin-Stimulated Glucose Uptake in Rat White Adipose Tissue upon Chronic Central Leptin Infusion: Effects on Adiposity

et al. 2011

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Leptin enhances the glucose utilization in most insulin target tissues and paradoxically decreases it in white adipose tissue (WAT), but knowledge of the mechanisms underlying the inhibitory effect of central leptin on the insulin-dependent glucose uptake in WAT is limited. After 7 d intracerebroventricular leptin treatment (0.2 g/d) of rats, the overall insulin sensitivity and the responsiveness of WAT after acute in vivo insulin administration were analyzed. We also performed unilateral WAT denervation to clarify the role of the autonomic nervous system in leptin effects on the insulin-stimulated [ 3 H]-2-deoxyglucose transport in WAT. Central leptin improved the overall insulin sensitivity but decreased the in vivo insulin action in WAT, including insulin receptor autophosphorylation, insulin receptor substrate-1 tyrosine-phosphorylation, and Akt activation. In this tissue, insulin receptor substrate-1 and glucose transporter 4 mRNA and protein levels were down-regulated after central leptin treatment. Additionally, a remarkable up-regulation of resistin, together with an augmented expression of suppressor of cytokine signaling 3 in WAT, was also observed in leptin-treated rats. As a result, the insulin-stimulated glucose transporter 4 insertion at the plasma membrane and the glucose uptake in WAT were impaired in leptin-treated rats. Finally, denervation of WAT abolished the inhibitory effect of central leptin on glucose transport and decreased suppressor of cytokine signaling 3 and resistin levels in this tissue, suggesting that resistin, in an autocrine/paracrine manner, might be a mediator of central leptin antagonism of insulin action in WAT. We conclude that central leptin, inhibiting the insulin-stimulated glucose uptake in WAT, may regulate glucose availability for triacylglyceride formation and accumulation in this tissue, thereby contributing to the control of adiposity. (Endocrinology 152: 1366 -1377, 2011)

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confidence: 82%

Regulation of Insulin-Stimulated Glucose Uptake in Rat White Adipose Tissue upon Chronic Central Leptin Infusion: Effects on Adiposity

et al. 2011

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“…Cell lines and cell culture of 3T3-L1 cells Murine 3T3-L1 pre-adipocytes purchased from American Type Culture Collection, ATCC (ATTCC CL-173) was used as control and transduced cell lines 3T3-L1-res (resistin) and 3T3-L1-s-res (s-resistin) were previously obtained in our laboratory [8].…”

Section: Methodsmentioning

confidence: 99%

“…Fourteen days after initiation of differentiation, cells were incubated in DMEM without FBS during 8 h and then, they were incubated at different times with 100 nM insulin [8]. 3T3-L1 fibroblast or transduced cell lines were grown in p60 culture dishes.…”

Section: Insulin Incubationsmentioning

confidence: 99%

“…Several studies showed that overexpression of resistin in 3T3-L1 fibroblast increased the expression and secretion of proinflammatory cytokines such as tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6) and decreased the insulin stimulated glucose uptake. These results suggest that an inflammatory pathway might mediate resistin effects impairing insulin action and adipogenesis [8,10]. Although the resistin receptor has not been identified yet, it was described that some mouse receptors, as an isoform of decorin or the tyrosine kinase-like orphan receptor (ROR) 1, could act as functional resistin receptors and therefore, mediate some resistin functions such glucose uptake and adipogenesis [5,29].…”

Section: Introductionmentioning

confidence: 95%

“…Likewise, both isoforms impair at different degrees the insulin-stimulated glucose transport, and promote IL-6 and plasminogen activity inhibitor type 1 (PAI-1) secretion, but only s-resistin increased the TNFα expression and secretion in early and intermediate stages of adipocyte differentiation. These data suggest that the s-resistin variant carries out additional functions in insulin response and adipocyte differentiation [8].…”

Section: Introductionmentioning

confidence: 98%

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S-resistin, a non secretable resistin isoform, impairs the insulin signalling pathway in 3T3-L1 adipocytes

et al. 2015

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S-resistin is a non-secretable resistin spliced variant, which is expressed mainly in the white adipose tissue from Wistar rats. Previous results confirmed that 3T3-L1 cells expressing s-resistin (3T3-L1-s-res) showed an inflammatory response and exhibited a decrease in glucose transport, both basal and insulin-stimulated. Here we present evidences demonstrating for the first time that s-resistin, like resistin, blocks insulin signalling pathway by inhibiting insulin receptor, insulin receptor substrate 1, protein kinase B/Akt and the mammalian target of rapamycin phosphorylation, and increasing the suppressor of cytokine signalling 3 levels being the later probably due to augmented of leptin expression. Thus, our data suggest that s-resistin could act by a still unknown intracrine pathway as an intracellular sensor, regulating the adipocyte insulin sensitivity.

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Resistin impairs glucose permeability in EA.hy926 cells by down-regulating GLUT1 expression

Cai

Huang

et al. 2016

Molecular and Cellular Endocrinology

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Type 2 diabetes mellitus (T2DM) is a chronic disease which is now affecting the health of more and more people in the world. Resistin, discovered in 2001, is considered to be closely related to metabolic dysfunction and obesity. Previous study showed that hyperglycemia is always accompanied by a high serum resistin concentration. We therefore investigated whether resistin can mediate glucose transfer across the blood-tissue barrier. Here, we employed a transwell system to analyze glucose permeability in EA.hy926 human endothelial cells treated without or with human resistin. In EA.hy926 cells treated with resistin, the permeability to glucose was heavily impaired. This was due to the down-regulation of GLUT1 expression as a result of the treatment, rather than regulation of tight junctions. In addition, overexpression of GLUT1 in EA.hy926 cells was able to recover the blocking effect of resistin on glucose permeability. We further found that resistin could inhibit the expression of peroxisome proliferator-activated receptor gamma (PPARγ) and consequently impede the transcription of GLUT1. The results of the present study suggested that resistin could cause glucose retention in serum and thus result in hyperglycemia. This provides a novel explanation for hyperglycemia and a potential new way of treating type 2 diabetes mellitus.

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S-resistin inhibits adipocyte differentiation and increases TNFα expression and secretion in 3T3-L1 cells

Cited by 8 publications

References 41 publications

Regulation of Insulin-Stimulated Glucose Uptake in Rat White Adipose Tissue upon Chronic Central Leptin Infusion: Effects on Adiposity

Regulation of Insulin-Stimulated Glucose Uptake in Rat White Adipose Tissue upon Chronic Central Leptin Infusion: Effects on Adiposity

S-resistin, a non secretable resistin isoform, impairs the insulin signalling pathway in 3T3-L1 adipocytes

Resistin impairs glucose permeability in EA.hy926 cells by down-regulating GLUT1 expression

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