•Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease.•Açai (Euterpe oleracea) fruit contains high levels of polyphenols, e.g. anthocyanins.•Mice with high-fat diet-induced ...NAFLD received oral aqueous açai extract (AAE).•AAE increased adiponectin levels, insulin sensitivity and PPAR-α-mediated fatty acid oxidation, decreasing liver lipids.
Polyphenols, especially anthocyanins, have been considered promising for the prevention of nonalcoholic fatty liver disease (NAFLD). This study investigated whether açai (Euterpe oleracea Mart.), a source of anthocyanins and recognized as one of the new “superfruits”, could alleviate high-fat diet (HFD)-induced NAFLD in mice. In HFD mice, aqueous açai extract (AAE) administration (3 g/kg) for six weeks improved insulin resistance index and increased adiponectin mRNA expression in adipose tissue and serum levels. Furthermore, AAE decreased the total liver triacylglycerol content and attenuated HFD-induced hepatic steatosis. This reduced hepatic lipid content was associated with AAE-mediated up-regulation of genes involved in adiponectin signaling, including adiponectin receptor 2, PPAR-α, and its target gene, carnitine palmitoyltransferase. Thus, dietary açai can protect liver from steatosis through its enhancement of adiponectin levels, improvement of insulin sensitivity, and increase in PPAR-α-mediated fatty acid oxidation.
Aldosterone acts on its target tissue through a classical mechanism or through the rapid pathway through a putative membrane-bound receptor. Our goal here was to better understand the molecular and ...biochemical rapid mechanisms responsible for aldosterone-induced cardiomyocyte hypertrophy. We have evaluated the hypertrophic process through the levels of ANP, which was confirmed by the analysis of the superficial area of cardiomyocytes. Aldosterone increased the levels of ANP and the cellular area of the cardiomyocytes; spironolactone reduced the aldosterone-increased ANP level and cellular area of cardiomyocytes. Aldosterone or spironolactone alone did not increase the level of cyclic 3',5'-adenosine monophosphate (cAMP), but aldosterone plus spironolactone led to increased cAMP level; the treatment with aldosterone + spironolactone + BAPTA-AM reduced the levels of cAMP. These data suggest that aldosterone-induced cAMP increase is independent of mineralocorticoid receptor (MR) and dependent on Ca
2+
. Next, we have evaluated the role of A-kinase anchor proteins (AKAP) in the aldosterone-induced hypertrophic response. We have found that St-Ht31 (AKAP inhibitor) reduced the increased level of ANP which was induced by aldosterone; in addition, we have found an increase on protein kinase C (PKC) and extracellular signal-regulated kinase 5 (ERK5) activity when cells were treated with aldosterone alone, spironolactone alone and with a combination of both. Our data suggest that PKC could be responsible for ERK5 aldosterone-induced phosphorylation. Our study suggests that the aldosterone through its rapid effects promotes a hypertrophic response in cardiomyocytes that is controlled by an AKAP, being dependent on ERK5 and PKC, but not on cAMP/cAMP-dependent protein kinase signaling pathways. Lastly, we provide evidence that the targeting of AKAPs could be relevant in patients with aldosterone-induced cardiac hypertrophy and heart failure.
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