PAQRs: A Counteracting Force to Ceramides?: 
            Figure 1.

Holland, William L.; Scherer, Philipp E.

doi:10.1124/mol.109.054817

Cited by 26 publications

(13 citation statements)

References 29 publications

(32 reference statements)

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“…Adiponectin exerts its effects by binding to two receptors, AdipoR1 and AdipoR2., which belong to the progesterone and adiponectin Q receptor (PAQR) family. [68] Because some PAQR receptors enhance ceramidase activity, Holland et al tested whether AdipoR1 and AdipoR2 might mediate the ability of adiponectin to lower ceramide. Adiponectin increased ceramidase activity in mouse embryonic fibroblasts (MEFs) with intact adiponectin receptors but failed to do so in MEFs in which both isoforms were deleted.…”

Section: Cross-talk Between Adiponectin and Ceramidementioning

confidence: 99%

Lipotoxicity contributes to endothelial dysfunction: A focus on the contribution from ceramide

Symons

Abel

2013

Rev Endocr Metab Disord

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Cardiovascular complications are the leading causes of morbidity and mortality in individuals with obesity, type 2 diabetes mellitus (T2DM), and insulin resistance. Complications include pathologies specific to large (atherosclerosis, cardiomyopathy) and small (retinopathy, nephropathy, neuropathy) vessels. Common among all of these pathologies is an altered endothelial cell phenotype i.e., endothelial dysfunction. A crucial aspect of endothelial dysfunction is reduced nitric oxide (NO) bioavailability. Hyperglycemia, oxidative stress, activation of the renin-angiotensin system, and increased pro-inflammatory cytokines are systemic disturbances in individuals with obesity, T2DM, and insulin resistance and each of these contribute independently and synergistically to decreasing NO bioavailability. This review will examine the contribution from elevated circulating fatty acids in these subjects that lead to lipotoxicity. Particular focus will be placed on the fatty acid metabolite ceramide.

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Section: Cross-talk Between Adiponectin and Ceramidementioning

confidence: 99%

Lipotoxicity contributes to endothelial dysfunction: A focus on the contribution from ceramide

Symons

Abel

2013

Rev Endocr Metab Disord

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“…AdipoR1 and AdipoR2 enhance ceramidase activity [164]. An accumulation of ceramide promotes an array of activities related to metabolic diseases, often in direct opposition to adiponectin [165]. The activity of ceramidase converts ceramide to S1P, a potent inducer of proliferation and inhibitor of apoptosis [166].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms linking obesity and cancer

Louie¹,

Roberts²,

Nomura³

2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

121

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The incidence of obesity in US adults has been steadily increasing over the past few decades. Many comorbidities associated with obesity have been well-established such as type 2 diabetes and cardiovascular diseases. However, more recently an epidemiological relationship between obesity and the prevalence of a variety of cancers has also been uncovered. The shift of the paradigm surrounding white adipose tissue function from purely an energy storage tissue, to one that has both endocrine and metabolic relevance, has led to several mechanisms implicated in how obesity drives cancer prevalence and cancer deaths. Currently, there are four categories into which these mechanisms fall – increased lipids and lipid signaling, inflammatory responses, insulin resistance, and adipokines. In this review, we examine each of these categories and the mechanisms through which they drive cancer pathogenesis. Understanding the relationship(s) between obesity and cancer and especially the nodal points of control in these cascades will be essential in developing effective therapeutics or interventions for combating this deadly combination.

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“…Adiponectin research took a significant step forward when it was found that adiponectin receptors contain inherent ceramidase activity, degrading ceramide and forming sphingosine and S1P [45,111]. Indeed, it appears that many of adiponectin's beneficial effects are mediated by accumulation of S1P, including the activation of AMPK [44].…”

Section: Adiponectinmentioning

confidence: 99%

A role for sphingolipids in the pathophysiology of obesity-induced inflammation

Bikman

2012

Cell. Mol. Life Sci.

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Following the initial discovery that adipose tissue actively synthesizes and secretes cytokines, obesity-induced inflammation has been implicated in the etiology of a host of disease states related to obesity, including cardiovascular disease and type II diabetes. Interestingly, a growing body of evidence similarly implicates sphingolipids as prime instigators in these same diseases. From the recent discovery that obesity-related inflammatory pathways modulate sphingolipid metabolism comes a novel perspective—sphingolipids may act as the dominant mediators of deleterious events stemming from obesity-induced inflammation. This paradigm may identify sphingolipids as an effective target for future therapeutics aimed at ameliorating diseases associated with chronic inflammation.

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PAQRs: A Counteracting Force to Ceramides?: Figure 1.

Cited by 26 publications

References 29 publications

Lipotoxicity contributes to endothelial dysfunction: A focus on the contribution from ceramide

Lipotoxicity contributes to endothelial dysfunction: A focus on the contribution from ceramide

Mechanisms linking obesity and cancer

A role for sphingolipids in the pathophysiology of obesity-induced inflammation

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