Resistin: Insulin resistance to malignancy

Codoñer‐Franch, Pilar; Alonso‐Iglesias, Eulalia

doi:10.1016/j.cca.2014.07.043

Cited by 119 publications

(134 citation statements)

References 142 publications

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“…It was initially correlated to the pathogenesis of insulin resistance in obesity and some cardiovascular diseases (CVD) but now is also considered an important link between obesity and inflammation [34]. Resistin has been found in areas of inflammation and seems to be mediated by IL-6 and TNF α [35].…”

Section: Resistinmentioning

confidence: 99%

Adipokines in rheumatoid arthritis

et al. 2018

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Rheumatoid arthritis affects millions of people worldwide and is considered a chronic multisystem disease whose causes are unknown. In general, the main objective of rheumatoid arthritis treatment is to improve the quality of life of patients by relieving pain, maintaining or improving functional capacity, preventing thus, disability. In recent years the role of adipokines in the pathogenesis of rheumatoid arthritis has been discussed but results are still conflicting. Although results from some studies have shown the implications of adipokines in the pathophysiology of autoimmune diseases, including rheumatoid arthritis, their role in the pathogenesis of disease progression is not clear. Thus, this review aimed to describe the association of key adipokines (leptin, resistin, visfatin and adiponectin) and rheumatoid arthritis, given the high prevalence of this disease and the important social impact caused by this chronic disabling disease.

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Section: Resistinmentioning

confidence: 99%

Adipokines in rheumatoid arthritis

et al. 2018

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“…Currently, several studies indicate that WAT is an endocrine organ producing numerous proteins with broad biological activity [73][74][75][76][77][78][79]. The secretory products of WAT, collectively referred to as adipocytokines (usually abbreviated as adipokines) include about 50 different proteins as [72,73,77,78,80] leptin, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), transforming growth factor beta (TGF-beta), plasminogen activator inhibitor-1 (PAI-1), metallothionein, adiponectin, resistin, angiotensinogen, adipsin, acylation stimulating protein (ASP), apelin and visfatin, among other products.…”

Section: Adipose Tissue and Adipocytokinesmentioning

confidence: 99%

“…ed protein (AgRP) neurons, and by contrast, proopiomelanocortin (POMC) and cocaine amphetamine-regulated transcript (CART) neurons are activated by hormone leptin [74,79,85]. In other words, leptin stimulates the anorexigenic pathway and inhibits the orexigenic pathway.…”

Section: Leptinmentioning

confidence: 99%

Therapeutic Methods Against Insulin Resistance

Rafael¹

2016

J Endocrinol Metab

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Clinical, neurosurgical and autopsy findings show that type 2 diabetes mellitus is caused by progressive ischemia in the anterior hypothalamus and endocrine pancreas due to atherosclerosis, and associated with insulin resistance. The hypothalamic ischemia provokes neuroendocrinological disorders through descending projections, and the pancreatic ischemia causes an inappropriate insulin secretion. Both ischemic structures can be improved by means of omental implantation (omental transplantation or transposition) or with anti-inflammatory drugs. Likewise, experimental and clinical observations suggest that insulin resistance is caused by inflammatory action of tumor necrosis factor alpha and resistin in the insulin receptor. Because, in contrast to this, high-dose aspirin or resveratrol can reduce hyperglycemia to normal or near normal in diabetic patients. That is, both drugs are almost specific for the treatment of insulin resistance. Finally, the use of clonazepam at night can have a beneficial effect on glucose homeostasis, because it can reduce the effects of stressful stimuli and normalize the sleep disorders or loss.

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“…Also, (iii) such new knowledge will enable future utilization of RA to modulate pathologic situations in which local or systemic resistin activity has been convincingly shown to play pathological role such as cancer and CVD. ough the later aspects of resistin function are not covered in the present review, blocking resistin action maybe highly bene cial in several types of malignancy as summarized in recent reviews (83)(84)(85)(86) and in ameliorating elevated serum low density lipoprotein and thereby atherosclerotic CVD in obese humans (87)(88)(89).…”

Section: Discussionmentioning

confidence: 99%

Resistin activity in mice and humans affecting obesity, insulin resistance and T2DM: Blocking resistin action by resistin antagonis

Gertler

2014

Adipobiology

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Resistin, that was originally discovered in 2001 is named for its capacity to resist insulin action shown mainly in mice. However, there is a controversial history regarding its role in the pathogenesis of insulin resistance and type 2 diabetes mellitus (T2DM) in humans as most of the research was based on association between resistin blood levels and T2DM or other pathologies and so far the pharmacological e ect of recombinant resistin has not been tested in humans or even in primates. Resistin is a 12 kD cysteine-rich small protein acting as covalent dimer. Although human and mouse resistin genes and protein sequences share only approximately 60% homology, which is less than most hormones conserved across species, the genes are syntenic, with the mouse gene encoding resistin being located at a similar distance from the insulin receptor gene. Unlike mouse resistin which is mainly expressed in adipocytes, human resistin is synthesized predominantly in monocytes and macrophages, especially in the visceral adipose tissue. Resistin's e ects are mediated via paracrine and endocrine mechanisms of action through a receptor on the surface of target cells that remains controversial. Others and our study has shown that resistin interacts with the Toll-like receptor 4 (TLR4), however other putative receptors such as an isoform of decorin, mouse receptor tyrosine kinase-like orphan receptor 1 (ROR1) and adenylyl cyclase-associated protein 1 (CAP1) have been also proposed. Downstream targets of resistin provide indirect evidence for its function in intracellular pathways, involving impairment of insulin signaling, response to in ammation and proliferation. Despite the lack of in vivo data concerning the resistin receptor and signaling in primates or humans, there is a need to explore the in ammatory, metabolic and oncogenic e ects of resistin on human diseases. To address this challenge we have recently developed resistin mutant (C6A), acting as resistin antagonist which in several in vitro bioassays inhibited resistin action and in mice fed high fat diet (HFD) reduced weight, visceral fat, restored insulin sensitivity and attenuated HFD-induced neuroin amation. 2014; 6: 5-14 Adipobiology

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Resistin: Insulin resistance to malignancy

Cited by 119 publications

References 142 publications

Adipokines in rheumatoid arthritis

Adipokines in rheumatoid arthritis

Therapeutic Methods Against Insulin Resistance

Resistin activity in mice and humans affecting obesity, insulin resistance and T2DM: Blocking resistin action by resistin antagonis

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