Resistin and insulin resistance in hepatocytes: Resistin disturbs glycogen metabolism at the protein level

Yang, Yang; Xiao, Mei-Fang; Mao, Youdong; Li, Hui; Zhao, Shuyong; Gu, Yun; Wang, Rong; Yu, Jian‐Qiang; Zhang, Xuemei; Irwin, David M.; Niu, Gang; H, Tan

doi:10.1016/j.biopha.2008.06.033

Cited by 23 publications

(13 citation statements)

References 37 publications

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“…This indicates that the effect of resistin on Akt and ERK1/2 phosphorylation is independent of IR signaling. These results contrast with previous reports documenting that resistin has no effect on insulin receptor content and phosphorylation (39,40). It is of note that these studies were performed in primary cell culture derived from liver and skeletal muscle, and the current study, to our knowledge, is the first investigation describing such resistin effects in vivo.…”

Section: Discussioncontrasting

confidence: 99%

Central Resistin Overexposure Induces Insulin Resistance Through Toll-Like Receptor 4

Benomar

Gertler

Lacy³

et al. 2012

Diabetes

154

111

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Resistin promotes both inflammation and insulin resistance associated with energy homeostasis impairment. However, the resistin receptor and the molecular mechanisms mediating its effects in the hypothalamus, crucial for energy homeostasis control, and key insulin-sensitive tissues are still unknown. In the current study, we report that chronic resistin infusion in the lateral cerebral ventricle of normal rats markedly affects both hypothalamic and peripheral insulin responsiveness. Central resistin treatment inhibited insulin-dependent phosphorylation of insulin receptor (IR), AKT, and extracellular signal–related kinase 1/2 associated with reduced IR expression and with upregulation of suppressor of cytokine signaling-3 and phosphotyrosine phosphatase 1B, two negative regulators of insulin signaling. Additionally, central resistin promotes the activation of the serine kinases Jun NH2-terminal kinase and p38 mitogen-activated protein kinase, enhances the serine phosphorylation of insulin receptor substrate-1, and increases the expression of the proinflammatory cytokine interleukin-6 in the hypothalamus and key peripheral insulin-sensitive tissues. Interestingly, we also report for the first time, to our knowledge, the direct binding of resistin to Toll-like receptor (TLR) 4 receptors in the hypothalamus, leading to the activation of the associated proinflammatory pathways. Taken together, our findings clearly identify TLR4 as the binding site for resistin in the hypothalamus and bring new insight into the molecular mechanisms involved in resistin-induced inflammation and insulin resistance in the whole animal.

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Section: Discussioncontrasting

confidence: 99%

Central Resistin Overexposure Induces Insulin Resistance Through Toll-Like Receptor 4

Benomar

Gertler

Lacy³

et al. 2012

Diabetes

154

111

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show abstract

“…In skeletal muscle of mice it promoted insulin resistance, hyperglycemia and hyperlipdemia [145,146], involving regulation of key enzymes of hepatic glycogen synthesis [147] and decreased activation of IRS-1 in response to insulin [148,149]. Likewise, mice that developed obesity-associated NASH exhibited increased serum levels of resistin [150].…”

Section: Adipocytokinesmentioning

confidence: 94%

Diabetes and apoptosis: liver

Schattenberg

Schuchmann

2009

Apoptosis

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The liver is a central regulator of glucose homeostasis and stores or releases glucose according to metabolic demands. In insulin resistant states or diabetes the dysregulation of hepatic glucose release contributes significantly to the pathophysiology of these conditions. Acute or chronic liver disease can aggravate insulin resistance and the physiological effects of insulin on hepatocytes are disturbed. Insulin resistance has also been recognized as an independent risk factor for the development of liver injury. In the healthy liver tissue homeostasis is achieved through cell turnover by apoptosis and dysregulation of the physiological process resulting in too much or too little cell death can have potentially devastating effects on liver tissue. The delineation of the signaling pathways that mediate apoptosis changed the paradigms of understanding of many liver diseases. These signaling events include cell surface based receptor-ligand systems and intracellular signaling pathways that are regulated through kinases on multiple levels. The dissection of these signaling pathways has shown that the regulators of apoptosis signaling events in hepatocytes can also modulate insulin signaling pathways and that mediators of insulin resistance in turn influence liver cell apoptosis. This review will summarize the potential crosstalk between apoptosis and insulin resistance signaling events and discuss the involved mediators.

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“…It is well known that elevated resistin level may be associated with insulin resistance and chronic inflammation [11,12]. Resistin is a protein hormone thought to modulate glucose tolerance and insulin action and it has been shown to antagonize insulin action [13]. In a screen of candidate genes, a region on chromosome 19p13.3 was identified that shows significant evidence for both linkage and association with PCOS.…”

Section: Introductionmentioning

confidence: 98%

Serum resistin and adiponectin levels in young non-obese women with polycystic ovary syndrome

Arıkan¹,

Bahçeci²,

Tuzcu³

et al. 2009

Gynecological Endocrinology

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Resistin and insulin resistance in hepatocytes: Resistin disturbs glycogen metabolism at the protein level

Cited by 23 publications

References 37 publications

Central Resistin Overexposure Induces Insulin Resistance Through Toll-Like Receptor 4

Central Resistin Overexposure Induces Insulin Resistance Through Toll-Like Receptor 4

Diabetes and apoptosis: liver

Serum resistin and adiponectin levels in young non-obese women with polycystic ovary syndrome

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