Association of adipocyte genes with ASP expression: a microarray analysis of subcutaneous and omental adipose tissue in morbidly obese subjects

MacLaren, Robin; Cui, Wei; Lü, Huiling; Simard, Serge; Cianflone, Katherine

doi:10.1186/1755-8794-3-3

Cited by 61 publications

(52 citation statements)

References 57 publications

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“…ASP is produced in the adipose tissue by the posttranslational cleavage of C3 complement factor [13]. Few studies have examined C3 gene expression in adipose tissue [27][28][29][30][31]. Our study is the first to compare the ASP precursor (C3) gene expression in SAT and VAT from morbidly obese patients with low IR and with high IR or T2DM, obese patients with low IR and lean healthy subjects.…”

Section: Discussionmentioning

confidence: 94%

162 Adipose Tissue Gene Expression of Factors Related to Lipid Processing in Obesity

Clemente‐Postigo¹,

Tinahones²,

Cardona³

2011

Atherosclerosis Supplements

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Section: Discussionmentioning

confidence: 94%

162 Adipose Tissue Gene Expression of Factors Related to Lipid Processing in Obesity

Clemente‐Postigo¹,

Tinahones²,

Cardona³

2011

Atherosclerosis Supplements

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“…Obesity-related datasets were retrieved from published studies: zebrafish DIO (GSE18566) (Oka et al 2010), rat DIO (GSE8700) (Li et al 2008), mice DIO (GSE11790) (Poussin et al 2008), and human adipocytes in obesity (GSE15524 and GSE2952) (Nadler et al 2000, MacLaren et al 2010. For the LPS comparison, the curated group of datasets C7 (immunological signatures) of the MSigDB was used.…”

Section: Microarray Analysesmentioning

confidence: 99%

Liver immune responses to inflammatory stimuli in a diet-induced obesity model of zebrafish

Forn-Cuní¹,

Varela²,

Fernández-Rodrı́guez³

et al. 2014

Journal of Endocrinology

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Obesity-and metabolic syndrome-related diseases are becoming important medical challenges for the western world. Non-alcoholic fatty liver disease (NAFLD) is a manifestation of these altered conditions in the liver, and inflammation appears to be a factor that is tightly connected to its evolution. In this study, we used a diet-induced obesity approach in zebrafish (Danio rerio) based on overfeeding to analyze liver transcriptomic modulation in the disease and to determine how obesity affects the immune response against an acute inflammatory stimulus such as lipopolysaccharide (LPS). Overfed zebrafish developed an obese phenotype, showed signs of liver steatosis, and its modulation profile resembled that observed in humans, with overexpression of tac4, col4a3, col4a5, lysyl oxidases, and genes involved in retinoid metabolism. In response to LPS, healthy fish exhibited a typical host defense reaction comparable to that which occurs in mammals, whereas there was no significant gene modulation when comparing expression in the liver of LPS-stimulated and non-stimulated obese zebrafish at the same statistical level. The stimulation of obese fish represents a double-hit to the already damaged liver and can help understand the evolution of the disease. Finally, a comparison of the differential gene activation between stimulated healthy and obese zebrafish revealed the expected difference in the metabolic state between healthy and diseased liver. The differentially modulated genes are currently being studied as putative new pathological markers in NAFLD-stimulated liver in humans.

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“…These three genes also correlated closely with other genes and have been called the "ASP triad" (MacLaren et al, 2010).…”

mentioning

confidence: 93%

Letter to the Editor Reply to commentary by A. Fisette on the article “Relationship between the acylation-stimulating protein gene and coronary heart disease in the Xinjiang Uygur and Han populations of China” published in Genetics and Molecular Research 13 (2):

Chen

2014

Genet. Mol. Res.

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In answer to the questioning of the terminology we used in our manuscript (Chen et al., 2014), ASP is a 76-amino acid (8932 Da) fragment, which is identical to C3adesArg, a cleavage product of complement C3. Cleavage of complement C3 is mediated via the alternate complement pathway by the interaction of C3, factor B and adipsin (Factor D, a serine protease enzyme), which generates C3a. Rapid cleavage of the C terminal arginine of C3a by carboxypeptidase N generates ASP (Hugli, 1990). Activation of this pathway is initiated through the C3b component of C3 (ASP precursor) associated with the plasma membrane. In the presence of Mg 2+ , Factor B binds to the activated C3b to form a C3bB complex. This, in turn, induces a conformational change of Factor B, permitting proteolytic cleavage by adipsin. The action of adipsin on C3b-bound Factor B generates a C3bBb fragment (a C3 convertase),

show abstract

Association of adipocyte genes with ASP expression: a microarray analysis of subcutaneous and omental adipose tissue in morbidly obese subjects

Cited by 61 publications

References 57 publications

162 Adipose Tissue Gene Expression of Factors Related to Lipid Processing in Obesity

162 Adipose Tissue Gene Expression of Factors Related to Lipid Processing in Obesity

Liver immune responses to inflammatory stimuli in a diet-induced obesity model of zebrafish

Letter to the Editor Reply to commentary by A. Fisette on the article “Relationship between the acylation-stimulating protein gene and coronary heart disease in the Xinjiang Uygur and Han populations of China” published in Genetics and Molecular Research 13 (2):

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