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

Bonzón-Kulichenko, Elena; Fernández-Agulló, Teresa; Moltó, Eduardo; Serrano, Rosario; Fernández, Alejandro; Ros, Manuel; Carrascosa, Jóse M.; Arribas, Carmen; Martı́nez, Carmen; Andrés, Antonio; Gallardo, Nilda

doi:10.1210/en.2010-0858

Cited by 16 publications

(17 citation statements)

References 61 publications

(70 reference statements)

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“…[ 3 H]-2-deoxyglucose uptake in mouse epididymal adipose tissue was determined immediately after death, as described previously (27,28). Adipose tissue (50 mg) was preincubated for 10 min at 37°C in 1 ml of Krebs-Ringer-HEPES (KRH) buffer (50 mM HEPES, pH 7.4; 137 mM NaCl; 4.8 mM KCl; 1.85 mM CaCl 2 ; and 1.3 mM MgSO 4 ), also used for subsequent incubations.…”

Section: Glucose Uptake In Mouse Wat Explantsmentioning

confidence: 99%

Obestatin regulates adipocyte function and protects against diet‐induced insulin resistance and inflammation

et al. 2012

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The metabolic actions of the ghrelin gene-derived peptide obestatin are still unclear. We investigated obestatin effects in vitro, on adipocyte function, and in vivo, on insulin resistance and inflammation in mice fed a high-fat diet (HFD). Obestatin effects on apoptosis, differentiation, lipolysis, and glucose uptake were determined in vitro in mouse 3T3-L1 and in human subcutaneous (hSC) and omental (hOM) adipocytes. In vivo, the influence of obestatin on glucose metabolism was assessed in mice fed an HFD for 8 wk. 3T3-L1, hSC, and hOM preadipocytes and adipocytes secreted obestatin and showed specific binding for the hormone. Obestatin prevented apoptosis in 3T3-L1 preadipocytes by increasing phosphoinositide 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK)1/2 signaling. In both mice and human adipocytes, obestatin inhibited isoproterenol-induced lipolysis, promoted AMP-activated protein kinase phosphorylation, induced adiponectin, and reduced leptin secretion. Obestatin also enhanced glucose uptake in either the absence or presence of insulin, promoted GLUT4 translocation, and increased Akt phosphorylation and sirtuin 1 (SIRT1) protein expression. Inhibition of SIRT1 by small interfering RNA reduced obestatin-induced glucose uptake. In HFD-fed mice, obestatin reduced insulin resistance, increased insulin secretion from pancreatic islets, and reduced adipocyte apoptosis and inflammation in metabolic tissues. These results provide evidence of a novel role for obestatin in adipocyte function and glucose metabolism and suggest potential therapeutic perspectives in insulin resistance and metabolic dysfunctions.

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Section: Glucose Uptake In Mouse Wat Explantsmentioning

confidence: 99%

Obestatin regulates adipocyte function and protects against diet‐induced insulin resistance and inflammation

et al. 2012

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“…Glucose uptake in WAT explants was evaluated as reported (19). Briefly, fat pad explants (20 mg), after exclusion of visible connective tissue and vessels, were placed in 0.…”

Section: Glucose Uptake In Wat Explantsmentioning

confidence: 99%

Growth Hormone Is Necessary for the p53-Mediated, Obesity-Induced Insulin Resistance in Male C57BL/6J × CBA Mice

et al. 2013

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Insulin resistance is a key marker of both obesity and GH excess. The purpose of the study was to assess the role of GH on p53-mediated insulin resistance of male mice with obesity due to a high-fat diet. C57BL/6J × CBA male mice fed on a high-fat diet (Obe) were studied; male mice fed a normal diet (Lean) or transgenic mice for bovine GH under the same genetic background (Acro) served as controls. The convergence of p53 and GH pathways was evaluated by Western blot. Obe mice had insulin resistance, which was sustained by a selective increased expression of p53 in adipose tissue. Normal insulin sensitivity was restored, and adipose p53 expression normalized when the GH pathway was blocked. Only the adipose p53 expression was sensitive to the GH blockage, which occurred through the p38 pathway. Adipose tissue of Obe mice had a coordinate overexpression of suppressors of cytokine signal 1-3 and signal transducers and activators of transcription-1, -3, and -5b, not different from that of Acro mice, suggesting an increased sensitivity of adipose tissue to GH. On the contrary, Lean mice were unaffected by changes of GH action. GH seems to be necessary for the increased adipose p53 expression and for insulin resistance of obese mice.

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“…Furthermore, intracerebroventricular leptin injections in Wistar rats induced SOCS-3 expression and protein levels in adipose tissue, contributing to reduce the insulin response from this tissue [4]. Our results show that the mRNA levels of leptin are significantly increased by s-resistin and especially by the resistin isoform, concomitantly with the increase in SOCS-3 levels, indicating the important role of resistin isoforms in the development of adipocyte leptin resistance.…”

Section: Discussionmentioning

confidence: 57%

“…There are several studies analyzing the effect of insulin on resistin expression in adipose tissue [3,4], in isolated adipocytes and in 3T3-L1 cells [12,17]. Specifically, it has been reported that insulin inhibits resistin expression in 3T3-L1 adipocytes, even at subphysiological concentrations [12].…”

Section: Discussionmentioning

confidence: 99%

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

Cited by 16 publications

References 61 publications

Obestatin regulates adipocyte function and protects against diet‐induced insulin resistance and inflammation

Obestatin regulates adipocyte function and protects against diet‐induced insulin resistance and inflammation

Growth Hormone Is Necessary for the p53-Mediated, Obesity-Induced Insulin Resistance in Male C57BL/6J × CBA Mice

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

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