Adiponectin: A multitasking player in the field of liver diseases

Silva, T.E.; Colombo, G; Schiavon, Leonardo de Lucca

doi:10.1016/j.diabet.2013.11.004

Cited by 57 publications

(46 citation statements)

References 147 publications

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“…Adiponectin is the most abundant peptide secreted by adipocytes [3,22], being a key component in the interrelationship between adiposity, insulin resistance and inflammation [22]. Central obesity accompanied by insulin resistance is a key factor in the development of MS and future macrovascular complications [23].…”

Section: Introductionmentioning

confidence: 99%

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Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Fisman

Tenenbaum

2014

Cardiovasc Diabetol

206

157

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Adiponectin is the most abundant peptide secreted by adipocytes, being a key component in the interrelationship between adiposity, insulin resistance and inflammation. Central obesity accompanied by insulin resistance is a key factor in the development of metabolic syndrome (MS) and future macrovascular complications. Moreover, the remarkable correlation between coronary artery disease (CAD) and alterations in glucose metabolism has raised the likelihood that atherosclerosis and type 2 diabetes mellitus (T2DM) may share a common biological background. We summarize here the current knowledge about the influence of adiponectin on insulin sensitivity and endothelial function, discussing its forthcoming prospects and potential role as a therapeutic target for MS, T2DM, and cardiovascular disease. Adiponectin is present in the circulation as a dimer, trimer or protein complex of high molecular weight hexamers, >400 kDa. AdipoR1 and AdipoR2 are its major receptors in vivo mediating the metabolic actions. Adiponectin stimulates phosphorylation and AMP (adenosin mono phosphate) kinase activation, exerting direct effects on vascular endothelium, diminishing the inflammatory response to mechanical injury and enhancing endothelium protection in cases of apolipoprotein E deficiency. Hypoadiponectinemia is consistently associated with obesity, MS, atherosclerosis, CAD, T2DM. Lifestyle correction helps to favorably modify plasma adiponectin levels. Low adiponectinemia in obese patients is raised via continued weight loss programs in both diabetic and nondiabetic individuals and is also accompanied by reductions in pro-inflammatory factors. Diet modifications, like intake of fish, omega-3 supplementation, adherence to a Mediterranean dietary pattern and coffee consumption also increase adiponectin levels. Antidiabetic and cardiovascular pharmacological agents, like glitazones, glimepiride, angiotensin converting enzyme inhibitors and angiotensin receptor blockers are also able to improve adiponectin concentration. Fibric acid derivatives, like bezafibrate and fenofibrate, have been reported to enhance adiponectin levels as well. T-cadherin, a membrane-associated adiponectin-binding protein lacking intracellular domain seems to be a main mediator of the antiatherogenic adiponectin actions. The finding of novel pharmacologic agents proficient to improve adiponectin plasma levels should be target of exhaustive research. Interesting future approaches could be the development of adiponectin-targeted drugs chemically designed to induce the activaton of its receptors and/or postreceptor signaling pathways, or the development of specific adiponectin agonists.

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Section: Introductionmentioning

confidence: 99%

“…Adiponectin can exist in plasma in its complete form or in globular fragments; the first appears to be the most common form. It circulates at physiological concentrations that represent about 0.05% of all plasma proteins [22]. …”

Section: Introductionmentioning

confidence: 99%

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Fisman

Tenenbaum

2014

Cardiovasc Diabetol

206

157

View full text Add to dashboard Cite

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“…Its concentration may reach up to 0.530 μg/ mL in the systemic circulation, accounting for 0.05% of the total plasma protein 4 . Previous studies con firmed that APN may improve insulin resistance, ath erosclerosis, inflammation, and lipid metabolism 4,5 . Recent studies suggest that APN may have some an tifibrotic effects 6 .…”

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confidence: 99%

“…Adiponectin (APN) is a hormone secreted by fat cells 3,4 . Its concentration may reach up to 0.530 μg/ mL in the systemic circulation, accounting for 0.05% of the total plasma protein 4 .…”

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confidence: 99%

Protective effect of adiponectin on paraquat-induced pulmonary fibrosis in mice

Yao

Zeng

Liang

et al. 2015

Mol. Cell. Toxicol.

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Pulmonary fibrosis (PF) is the most com mon complication of paraquat (PQ) toxicity, which lacks an effective treatment. This study aimed to inve stigate whether exogenous administration of globular adiponectin (APN) isoform provided protection ag ainst PQinduced PF, and examined the possible me chanisms underlying these effects. Eighty BALB/C mice were randomly divided into control, PQ, low dose APN, and highdose APN groups. Human lung WI-38 fibroblasts were similarly divided into control, PQ, and APN groups and examined at 24 h, 48 h, and 72 h after PQ exposure. Hematoxylin and eosin (HE) and Masson trichrome staining were used to compare the histopathologic changes in the mouse lung tissues. Western blot and realtime quantitativePCR (RT PCR) were used to measure the protein and mRNA expression of transforming growth factor β1 (TGF-β1) in mice lung tissues and α-SMA, type III collagen, and NFκB p65 in lung fibroblasts. Dihydroethidium (DHE) was used to detect intracellular superoxide anion (O2 -) in fibroblasts. APN administration significantly ameliorated PQmediated fibrosis histologically and reduced the protein and mRNA expression levels of TGF-β1 in mouse lung tissues in a dosedependent manner (P<0.05). When fibroblasts were pretreated with APN, the expression of α-SMA and NF-κB p65 were downregulated, and O2 -decreased. Expression of the anti-inflammatory factor IL-1Ra was upregulated following PQ exposure (P<0.05). This study revealed the beneficial effects of APN against PQinduced PF, which may have occurred through suppression of NF κB dependent inflammatory and TGF-β1 mediated fibrotic events.

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“…Simultaneously, it hampers gluconeogenesis by inhibiting the hepatic enzyme phosphoenolpyruvate carboxylase, inhibits the synthesis of fatty acids and stimulates their oxidation. [10][11] Serum adiponectin is inversely related to body fat mass and to the degree of insulin resistance. Its concentration is particularly low in adults with T2DM or CAD.…”

Section: Introductionmentioning

confidence: 99%