Mechanisms of adiponectin regulation and use as a pharmacological target

Phillips, Susan A.; Kung, Jacqueline

doi:10.1016/j.coph.2010.08.002

Cited by 72 publications

(47 citation statements)

References 77 publications

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“…In contrast, mice with NASH benefit from the use of rosiglitazone as it inhibited cell proliferation and diminished collagen expression in hepatic stellate cells in vivo and in vitro [59,60] . In addition, the increase in insulin sensitivity due to enhanced adiponectin transcription and reduced levels of tumor necrosis factor (TNF)-alpha is crucial to the treatment of NASH with rosiglitazone in murine models [61,62] . Humans with NASH also benefit from the regular use of rosiglitazone.…”

Section: Targeting Ppars To Treat Nafldmentioning

confidence: 99%

Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

Souza-Mello¹

2015

WJH

147

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and microsomal omega-oxidation, being markedly decreased by high-fat (HF) intake. PPAR-beta/delta is crucial to the regulation of forkhead box-containing protein O subfamily-1 expression and, hence, the modulation of enzymes that trigger hepatic gluconeogenesis. In addition, PPAR-beta/delta can activate hepatic stellate cells aiming to the hepatic recovery from chronic insult. On the contrary, PPAR-gamma upregulation by HF diets maximizes NAFLD through the induction of lipogenic factors, which are implicated in the fatty acid synthesis. Excessive dietary sugars also upregulate PPAR-gamma, triggering de novo lipogenesis and the consequent lipid droplets deposition within hepatocytes. Targeting PPARs to treat NAFLD seems a fruitful approach as PPAR-alpha agonist elicits expressive decrease in hepatic steatosis by increasing mitochondrial beta-oxidation, besides reduced lipogenesis. PPAR-beta/delta ameliorates hepatic insulin resistance by decreasing hepatic gluconeogenesis at postprandial stage. Total PPAR-gamma activation can exert noxious effects by stimulating hepatic lipogenesis. However, partial PPAR-gamma activation leads to benefits, mainly mediated by increased adiponectin expression and decreased insulin resistance. Further studies are necessary aiming at translational approaches useful to treat NAFLD in humans worldwide by targeting PPARs. AbstractLately, the world has faced tremendous progress in the understanding of non-alcoholic fatty liver disease (NAFLD) pathogenesis due to rising obesity rates. Peroxisome proliferator-activated receptors (PPARs) are transcription factors that modulate the expression of genes involved in lipid metabolism, energy homeostasis and inflammation, being altered in diet-induced obesity. Experimental evidences show that PPAR-alpha is the master regulator of hepatic beta-oxidation (mitochondrial and peroxisomal)

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Section: Targeting Ppars To Treat Nafldmentioning

confidence: 99%

Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

Souza-Mello¹

2015

WJH

147

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“…ADPN, also called Acrp30, apM1, AdipoQ, and GBP28, is an important protein that exists in three forms in the serum: trimer, hexamer, and a high molecular weight form (Phillips and Kung, 2010;. ADPN possesses insulin-sensitizing, anti-inflammatory, anti-atherogenic, and antiangiogenic properties, among which the anti-inflammatory effect has been widely confirmed (Gu et al, 2013;Fiaschi et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Correlation between adiponectin and hemorrhagic shock in mice

Gong

Yao

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to explore the relationship between adiponectin (ADPN) and hemorrhagic shock (HS) and the recovery after HS. This is significant for further understanding of the pathophysiological processes of HS and the development of better treatments. In total, 72 male C57BL/6 mice were assigned randomly to three groups: control, HS, and recovery (N = 24). The HS mouse model was constructed by hemorrhage of the carotid artery and recovery was achieved by tail vein injection of Ringer's solution. The level of ADPN in the peripheral blood of mice before and after recovery was detected by enzyme-linked immunosorbent assay. Compared to control, HS mice showed significantly decreased ADPN levels with the extension of HS time while the level of ADPN in recovery mice increased significantly and remained high. The variation of ADPN levels was closely associated with the occurrence of HS in mice and their recovery, suggesting that ADPN might act as a biomarker of inflammation and have potential for the treatment of HS.

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“…A previous study showed that APN could lower serum triglycerides through enhancement of the catabolism of triglyceride-rich lipoproteins (Christou and Kiortsis 2013). Furthermore, statins were found to raise APN levels as well as decrease the cIMT mainly by improving the lipid profile, and suppression of miR29 will decrease hepatic cholesterol synthesis (Phillips and Kung 2010;Chrusciel et al 2016). In addition, APN exerts its anti-inflammatory effects in multiple ways.…”

Section: Discussionmentioning

confidence: 99%

Elevated Plasma miR-29a Levels Are Associated with Increased Carotid Intima-Media Thickness in Atherosclerosis Patients

Liu

Zhong

Huang

2017

Tohoku J. Exp. Med.

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Atherosclerotic cardiovascular diseases, such as coronary heart disease, have become a major public health problem all over the world. MicroRNA-29a (miR-29a) modulates expression levels of collagen, inflammatory reaction and other extracellular matrix mRNAs, while adiponectin (APN), a circulating protein secreted by adipocytes, has anti-inflammatory properties. Both play multifaceted roles in angiogenesis or vascular remodelling. However, little is known about plasma miR-29a and APN levels in patients with atherosclerosis. We therefore investigated the relationship between the plasma levels of miR-29a or APN and carotid intima-media thickness (cIMT) in atherosclerosis patients (n = 85, cIMT ≥ 1.2 mm) and the controls (n = 85, cIMT < 1.2 mm). We found that the atherosclerosis group showed higher miR-29a levels (31.15 ± 3.99 vs. 26.39 ± 1.05 Ct, P < 0.001) and lower APN levels (15.93 ± 4.61 vs. 21.80 ± 7.74 ng/ml, P < 0.001), compared with control group. Thus, increased cIMT was associated with higher plasma miR-29a levels (r = 0.688, P < 0.001) and with lower plasma APN levels (r = −0.494, P < 0.001). Furthermore, multiple logistic regression analysis indicated that higher miR-29a levels (OR: 1.136, 95% CI: 1.042-1.240, P = 0.004) increased the risk for atherosclerosis, whereas higher APN levels appeared to be protective (OR: 0.122, 95% CI: 0.055-0.271, P < 0.001). The present study indicates that elevated miR-29a levels and reduced APN levels are associated with atherosclerosis.Keywords: adiponectin; atherosclerosis; carotid intima-media thickness; microRNA; miR-29a Tohoku J. Exp. Med., 2017 March, 241 (3), 183-188. © 2017 Tohoku University Medical Press IntroductionAtherosclerotic cardiovascular diseases such as coronary heart disease and stroke have become a major public health problem all over the world (Murray et al. 2012). It is necessary to detect atherosclerotic cardiovascular diseases at earlier stages. In recent decades, microRNAs (miRs) are short non-coding RNA able to bind specific sequences on target mRNAs, thereby modulating gene expression (Gaudet and Brisson 2015). They are involved in almost every aspect of cellular or biological processes, and dysregulation of miRs correlated with cardiovascular diseases, such as atherosclerosis ). MiR-29a was one of the members of the miR-29 family (Hysolli et al. 2016). The miR-29 family, modulating mRNA level of collagen, inflammatory reaction and other extracellular matrix genes, play a multifaceted role in tissue remodelling and vessels injury Bretschneider et al. 2016). It was reported that miR-29 were up-regulated in the region of the heart adjacent to a myocardial infarction (MI) (van Rooij et al. 2008). Among other miRs, circulating miR-29a levels may represent one of the new biomarkers which significantly correlate with cardiovascular diseases (Roncarati et al. 2014). In addition, a previous study showed that miR-29b was involved in vascular smooth muscle cell migration and proliferation by mediating an epigenetic mechanism (Chen et al. 2011), which wa...

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Mechanisms of adiponectin regulation and use as a pharmacological target

Cited by 72 publications

References 77 publications

Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

Peroxisome proliferator-activated receptors as targets to treat non-alcoholic fatty liver disease

Correlation between adiponectin and hemorrhagic shock in mice

Elevated Plasma miR-29a Levels Are Associated with Increased Carotid Intima-Media Thickness in Atherosclerosis Patients

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