Globular adiponectin increases GLUT4 translocation and glucose uptake but reduces glycogen synthesis in rat skeletal muscle cells

Ceddia, Rolando B.; Somwar, Romel; Maida, Adriano; Fang, Xia; Bikopoulos, George; Sweeney, Gary

doi:10.1007/s00125-004-1609-y

Cited by 295 publications

(227 citation statements)

References 38 publications

(65 reference statements)

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“…Down-regulation of Glut4 in mice was reported to be associated with hepatic lipid production, which subsequently contributed to fat accumulation and insulin resistance [29]. Activation of the expression of both Glut4 and adiponectin by the coconut water vinegar treatment may help to increase the translocation and uptake of glucose in obese mice [35], increase lipid metabolism in the liver [29], and thus contribute to less lipid accumulation. Acetic acid is a major active ingredient in coconut water vinegar [18].…”

Section: Discussionmentioning

confidence: 99%

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Mohamad

Yeap

Kỳ

et al. 2017

Food & Nutrition Research

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Obesity has become a serious health problem worldwide. Various types of healthy food, including vinegar, have been proposed to manage obesity. However, different types of vinegar may have different bioactivities. This study was performed to evaluate the anti-obesity and anti-inflammatory effects of coconut water vinegar on high-fat-diet (HFD)-induced obese mice. Changes in the gut microbiota of the mice were also evaluated. To induce obesity, C57/BL mice were continuously fed an HFD for 33 weeks. Coconut water vinegar (0.08 and 2 ml/kg body weight) was fed to the obese mice from early in week 24 to the end of week 33. Changes in the body weight, fat-pad weight, serum lipid profile, expression of adipogenesis-related genes and adipokines in the fat pad, expression of inflammatory-related genes, and nitric oxide levels in the livers of the untreated and coconut water vinegar-treated mice were evaluated. Faecal samples from the untreated and coconut water vinegar-treated mice (2 ml/kg body weight) were subjected to 16S metagenomic analysis to compare their gut microbiota. The oral intake of coconut water vinegar significantly (p < 0.05) reduced the body weight, fat-pad weight, and serum lipid profile of the HFD-induced obese mice in a dose-dependent manner. We also observed up-regulation of adiponectin and down-regulation of sterol regulatory element-binding protein-1, retinol-binding protein-4, and resistin expression. The coconut water vinegar also reduced HFD-induced inflammation by down-regulating nuclear factor-κB and inducible nitric oxide synthase expression, which consequently reduced the nitric oxide level in the liver. Alterations in the gut microbiota due to an increase in the populations of the Bacteroides and Akkermansia genera by the coconut water vinegar may have helped to overcome the obesity and inflammation caused by the HFD. These results provide valuable insights into coconut water vinegar as a potential food ingredient with anti-obesity and anti-inflammatory effects.

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Section: Discussionmentioning

confidence: 99%

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Mohamad

Yeap

Kỳ

et al. 2017

Food & Nutrition Research

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“…Subsequently, glucose transport was assayed for 5 min at room temperature as previously described [27]. The incubation medium was aspirated, the cells were washed with ice-cold saline, and 200 μl of KOH (1 mol/l) was added to each well.…”

Section: Methodsmentioning

confidence: 99%

“…The amount of GLUT4-myc present at the cell surface was measured by an antibody-coupled colorimetric assay as described previously [27]. The L6GLUT4-myc cells are stably transfected to express GLUT4 tagged on its first exofacial loop with a myc epitope.…”

Section: Determination Of Cell Surface Glut4-mycmentioning

confidence: 99%

“…We also treated cells with lactacystin (10 μmol/l, 1 h pretreatment) to prepare lysates for examination of IRS-1 or Akt1 protein content. Lysates were prepared exactly as we previously described [27]. Prior to loading onto SDS-PAGE gels, the samples were diluted 1:1 (v/v) with 2 × Laemmli sample buffer (62.5 mmol/l Tris-HCl [pH 6.8], 2% [w/v] SDS, 50 mmol/l dithiothreitol, 0.01% [w/v] bromophenol blue).…”

Section: Western Blottingmentioning

confidence: 99%

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Regulation of insulin signalling, glucose uptake and metabolism in rat skeletal muscle cells upon prolonged exposure to resistin

et al. 2005

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Aims/hypothesis: Debate exists regarding the role of resistin in the pathophysiology of insulin resistance. The aim of this study was to directly assess the effects of resistin (0-24 h) on basal and insulin-stimulated glucose uptake and metabolism in skeletal muscle cells and to investigate the mechanisms responsible for the effects of resistin. Methods: We used L6 rat skeletal muscle cells and examined [ 3 H]2-deoxyglucose uptake, GLUT4 translocation and GLUT protein content. We assessed glucose metabolism by measuring the incorporation of D-[U-14 C] glucose into glycogen, 14 CO 2 and lactate production, as well as the phosphorylation level and total protein content of insulin signalling proteins, including insulin receptor β-subunit (IRβ), insulin receptor substrate (IRS), Akt and glycogen synthase kinase-3β (GSK-3β). Results: Treatment of L6 rat skeletal muscle cells with recombinant resistin (50 nmol/l, 0-24 h) reduced levels of basal and insulin-stimulated 2-deoxyglucose uptake and decreased insulin-stimulated GLUT4myc content at the cell surface, with no alteration in the production of GLUT4 or GLUT1. Resistin also decreased glycogen synthesis and GSK-3β phosphorylation. Insulin-stimulated oxidation of glucose via the Krebs cycle was reduced by resistin, whereas lactate production was unaltered. Although insulin receptor protein level and phosphorylation were unaltered by resistin, production of IRS-1, but not IRS-2, was downregulated and a decreased tyrosine phosphorylation of IRS-1 was detected. Reduced phosphorylation of Akt on T308 and S473 was observed, while total Akt and Akt1, but not Akt2 or Akt3, production was decreased. Conclusions/ interpretation: Our data show that resistin regulates the function of IRS-1 and Akt1 and decreases GLUT4 translocation and glucose uptake in response to insulin. Selective decreases in insulin-stimulated glucose metabolism via oxidation and conversion to glycogen were also induced by resistin. These observations highlight the potential role of resistin in the pathophysiology of type 2 diabetes in obesity.

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“…Dans le muscle, l'activation de l'AMPK par l'adiponectine conduit à l'inactivation de l'acétylCoA, ce qui augmente l'oxydation des acides gras [14,15]. Dans ce tissu, l'adiponectine favorise également l'utilisation du glucose en facilitant la translocation des transporteurs GLUT4 sensibles à l'insuline [16]. Chez l'homme, le rôle de la résistine dans le méta-bolisme est moins connu que celui de l'adiponectine.…”

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Adiponectine et résistine

et al. 2013

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Globular adiponectin increases GLUT4 translocation and glucose uptake but reduces glycogen synthesis in rat skeletal muscle cells

Cited by 295 publications

References 38 publications

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Dietary coconut water vinegar for improvement of obesity-associated inflammation in high-fat-diet-treated mice

Regulation of insulin signalling, glucose uptake and metabolism in rat skeletal muscle cells upon prolonged exposure to resistin

Adiponectine et résistine

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