Genetics of adiponectin

Breitfeld, Jana; Stümvoll, Michael; Kovacs, Peter

doi:10.1016/j.biochi.2012.03.004

Cited by 44 publications

(46 citation statements)

References 84 publications

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“…Indeed, we now demonstrate that type 2 diabetes and reduced circulating levels of adiponectin are related to increased NADPH oxidase activity in the human arterial wall, even after correcting for other cardiovascular risk factors such as smoking or hypertension. The genetic variability of the ADIPOQ locus, which defines the capacity of adipose tissue to release adiponectin (15,19), also leads to parallel effects on vascular NADPH oxidase activity. We now demonstrate that ADIPOQ gene expression and adiponectin release from Th-AT (which is distant from large vessels) are inversely correlated with NADPH oxidase activity in the human arterial wall.…”

Section: Discussionmentioning

confidence: 99%

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Adiponectin as a Link Between Type 2 Diabetes and Vascular NADPH Oxidase Activity in the Human Arterial Wall: The Regulatory Role of Perivascular Adipose Tissue

et al. 2014

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Oxidative stress plays a critical role in the vascular complications of type 2 diabetes. We examined the effect of type 2 diabetes on NADPH oxidase in human vessels and explored the mechanisms of this interaction. Segments of internal mammary arteries (IMAs) with their perivascular adipose tissue (PVAT) and thoracic adipose tissue were obtained from 386 patients undergoing coronary bypass surgery (127 with type 2 diabetes). Type 2 diabetes was strongly correlated with hypoadiponectinemia and increased vascular NADPH oxidase-derived superoxide anions (O 2 _ 2 ). The genetic variability of the ADIPOQ gene and circulating adiponectin (but not interleukin-6) were independent predictors of NADPH oxidasederived O 2 _ 2 . However, adiponectin expression in PVAT was positively correlated with vascular NADPH oxidasederived O 2 _ 2 . Recombinant adiponectin directly inhibited NADPH oxidase in human arteries ex vivo by preventing the activation/membrane translocation of Rac1 and downregulating p22 phox through a phosphoinositide 3-kinase/Akt-mediated mechanism. In ex vivo coincubation models of IMA/PVAT, the activation of arterial NADPH oxidase triggered a peroxisome proliferator-activated receptor-g-mediated upregulation of the adiponectin gene in the neighboring PVAT via the release of vascular oxidation products. We demonstrate for the first time in humans that reduced adiponectin levels in individuals with type 2 diabetes stimulates vascular NADPH oxidase, while PVAT "senses" the increased NADPH oxidase activity in the underlying vessel and responds by upregulating adiponectin gene expression. This PVAT-vessel interaction is identified as a novel therapeutic target for the prevention of vascular complications of type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

“…These two functional single nucleotide polymorphisms (SNPs) have shown an effect on adiponectin levels in recent genome-wide association studies (19).…”

Section: Dna Extraction and Genotypingmentioning

confidence: 99%

Adiponectin as a Link Between Type 2 Diabetes and Vascular NADPH Oxidase Activity in the Human Arterial Wall: The Regulatory Role of Perivascular Adipose Tissue

et al. 2014

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“…A decrease in this adipokine is associated with deterioration in virtually all parameters of the metabolic syndrome, including T2D and cardiovascular disease (CVD) [17]. Variants of the ADIPOQ gene seem to cause substantial changes in adiponectin levels; this finding was replicated in independent study populations (see detailed review in Breitfeld et al, 2011) [17].…”

Section: Adiponectin (Adipoq)mentioning

confidence: 96%

“…[17] rs17373414 C/T ADIPOQ C ↓ 7% variability attributed to ADIPOQ SNPs [26]; <5% [27] [26]; [27] rs1403696 C/T ADIPOQ T ↓ 7% variability attributed to ADIPOQ SNPs…”

Section: Leptin (Lep)mentioning

confidence: 99%

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Genetic Determination of Serum Levels of Diabetes-Associated Adipokines

Schleinitz¹

2016

Rev Diabet Stud

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■ AbstractAdipose tissue secretes an abundance of proteins. Some of these proteins are known as adipokines and adipose-derived hormones which have been linked with metabolic disorders, including type 2 diabetes, and even with cancer. Variance in serum adipokine concentration is often closely associated with an increase (obesity) or decrease (lipodystrophy) in fat tissue mass, and it is affected by age, gender, and localization of the adipose tissue. However, there may be genetic variants which, in consequence, influence the serum concentration of a certain adipokine, and thereby promote metabolic disturbances or, with regard to the "protective" allele, exert beneficial effects. This review focuses on the genetic determination of serum levels of the following adipokines: adiponectin, chemerin, leptin, progranulin, resistin, retinol binding protein 4, vaspin, adipsin, apelin, and omentin. The article reports on the latest findings from genome-wide association studies (GWAS) and candidate gene studies, showing variants located in/nearby the adipokine genes and other (non-receptor) genes. An extra chapter highlights adipokine-receptor variants. Epigenetic studies on adipokines are also addressed.

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