Visfatin, a novel adipokine, stimulates glucose uptake through the Ca2+-dependent AMPK–p38 MAPK pathway in C2C12 skeletal muscle cells

Lee, Jung Ok; Kim, Nami; Lee, Hye Jeong; Lee, Yong Woo; Kim, Joong Kwan; Kim, Hyung Ip; Lee, Soo Kyung; Kim, Su Jin; Park, Sun Hwa; Kim, Hyeon Soo

doi:10.1530/jme-14-0274

Cited by 33 publications

(31 citation statements)

References 62 publications

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“…In the present study, we proposed a mechanism by which MR blockade improves adiponectin expression. The activation of the AMPK/p38 MAPK signaling cascade stimulates glucose uptake in adult cardiomyocytes, and the inhibition of the p38 MAPK signaling pathway abolishes the stimulation of glucose uptake in response to hypoxia [28,29]. In muscle cells, adiponectin activates AMPK and p38MAPK, which sequentially stimulates PPARα activity [30].…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Receptor Blockade Improves Insulin Sensitivity in the Rat Heart and a Possible Molecular Mechanism

Wang

Zhou

et al. 2016

Cell Physiol Biochem

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Background/Aims: Extensive research has explored the role of aldosterone in insulin resistance. Recent evidence suggests that the mineralocorticoid receptor (MR) mediates aldosterone-induced dysregulation of cytokines, and most of this research has focused on adjustments in fat tissue and adipocytes. However, the direct effect of MR blockade on insulin resistance in cardiomyocytes remains largely unknown. In the present study, we investigated whether MR blockade improves insulin-sensitizing factors in insulin-resistant rats and attenuates the dysregulation of the aldosterone-related transport of adiponectin and glucose in cardiomyocytes and examined the underlying mechanisms. Methods: The effects of aldosterone, MR inhibitors (e.g., eplerenone), a peroxisome proliferator-activated receptor (PPAR) α agonist, and a p38 mitogen-activated protein kinase (MAPK) inhibitor on adiponectin and glucose transport were studied at the mRNA and protein levels in vitro and in vivo. Results: Our data revealed that aldosterone reduced the expression of adiponectin and inhibited the transport of glucose in cardiomyocytes and that MR blockade reversed these affects. In vivo, MR blockade improved insulin-sensitive parameters and increased adiponectin expression in the myocardia of high-fat diet rats. Furthermore, aldosterone promoted p38MAPK expression but negatively affected PPARα expression, and the downregulation of adiponectin by aldosterone was reversed by MR blockade, a PPARα agonist, and a p38 MAPK inhibitor. Conclusion: The above results suggested that aldosterone promoted insulin resistance in the heart and that this effect could be partly reversed by MR blockade through signal transduction in the P38 MAPK pathway and PPARα.

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Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Receptor Blockade Improves Insulin Sensitivity in the Rat Heart and a Possible Molecular Mechanism

Wang

Zhou

et al. 2016

Cell Physiol Biochem

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“…pathways. Recent studies also indicated that visfatin and isoeugenol causes increased uptake of glucose in adipocytes and myocytes (Kim et al, 2016), in which AMPKa2 subunit promotes GLUT4 gene expression (Lee et al, 2015), consistent with earlier studies showing that AICAR/ AMPK enhanced glucose intake in muscle (Sakoda et al, 2002). In addition, overexpression of HDAC5 represses GLUT4 gene expression, and AICAR/AMPKa2 phosphorylates HDAC5 at S259 and S498 reduces nuclear HDAC5 resulting in decrease of HDAC5 binding with the GLUT4 promoter thereby promoting GLUT4 gene expression (Li et al, 2008) (Figure 2).…”

Section: Ampk and Glucose/fatty Acid Transportmentioning

confidence: 99%

Mechanisms of AMPK in the maintenance of ATP balance during energy metabolism

Liu

et al. 2018

Cell Biology International

305

190

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AMP-activated protein kinase (AMPK) is a conserved sensor of cellular energy change and is activated by increased AMP/ATP and/or ADP/ATP ratios. AMPK maintains the energy balance by decreasing the ATP-consuming processes such as transcription of synthetic fat genes and rRNA, the translation of ribosomal proteins, synthesis of cholesterol and fatty acid, while the metabolic pathways such as glucose and fatty transport, fatty acid oxidation, autophagy, mitochondrial synthesis and oxidative metabolism are increased to preserve ATP during energy deficiency. Recent advance has demonstrated that AMPK activity has a close association with the initiation and progression in various cancers. Here we review the mechanisms that AMPK controls energy metabolism through regulating ATP synthesis and consumption, and further discuss the deregulation of AMPK in cancers.

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“…Most recently, experimental and clinical studies suggest that novel adipokines such as adipsin and visfatin might have an energetic role in the cascade of the events leading to diabetes mellitus. Namely, adipsin has a beneficial role in maintaining β cell function and visfatin plays an important role in glucose metabolism (2,3).…”

Section: Introductionmentioning

confidence: 99%

Reciprocal changes of serum adispin and visfatin levels in patients with type 2 diabetes after an overnight fast

Legakis

Mantzouridis²,

Bouboulis

et al. 2016

Arch. Endocrinol. Metab.

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Objective: In order to elucidate the interrelationship of adipokines in glucose hemiostasis, we determined the concentration of visfatin and adipsin in blood samples in patients with type 2 diabetes and age-matched controls after an overnight fast. Subjects and methods: We enrolled 37 patients with known type 2 diabetes -21 males and 16 females, aged 62.95 ± 15.72 years and 43 controls-28 males and 15 females, aged 60.79 ± 12.67 years. Blood samples were collected after an overnight fast and routine biochemical parameters such as glucose, cholesterol, HDL, LDL, triglycerides along with Hb1Ac, insulin and c-peptide, in addition to circulating visfatin and adipsin were determined in all samples. Data were considered significant at a level of p < 0.05. Results: In patients with type 2 diabetes, circulating adipsin levels were decreased and inversely related with glucose levels while circulating visfatin was increased significantly in the fasting state. Conclusion: These results implicate the adipokines adipsin and visfatin as possible participants in the pathogenesis of type 2 diabetes.Arch Endocrinol Metab. 2016;60(1):76-8

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Visfatin, a novel adipokine, stimulates glucose uptake through the Ca2+-dependent AMPK–p38 MAPK pathway in C2C12 skeletal muscle cells

Cited by 33 publications

References 62 publications

Mineralocorticoid Receptor Blockade Improves Insulin Sensitivity in the Rat Heart and a Possible Molecular Mechanism

Mineralocorticoid Receptor Blockade Improves Insulin Sensitivity in the Rat Heart and a Possible Molecular Mechanism

Mechanisms of AMPK in the maintenance of ATP balance during energy metabolism

Reciprocal changes of serum adispin and visfatin levels in patients with type 2 diabetes after an overnight fast

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