Long-term effects of angiotensin-(1–7) on lipid metabolism in the adipose tissue and liver

Altered global microRNA expression in hepatic stellate cells LX-2 by angiotensin-(1–7) and miRNA-1914-5p identification as regulator of pro-fibrogenic elements and lipid metabolism

“…Singh et al (2010) demonstrated the effect of the ang-(1–7) in changing lipid composition in renal cortical tissue in diabetic rats. Other studies demonstrated the effect of the ang-(1–7) in reducing levels of lipids in the plasma and in the whole body (Moreira et al, 2017; Santos et al, 2010; Schuchard et al, 2015; Tang et al, 2017), in preventing or positive controlling hepatic steatosis (Cao et al, 2016; Feltenberger et al, 2013; Moreira et al, 2017; Simões et al, 2017), and in antifibrotic activity (Cai et al, 2016; Lubel et al, 2009; Simões et al, 2017). In our analyses, ang-(1–7) modulated pro-fibrotic markers, lipid metabolism and the expression pattern of miRNAs in LX-2 cells, including the miR-1914-5p.…”

Genetic Models

“…The increased levels of plasma Ang-(1-7) exerted antinatriuretic actions in the kidney resulting in reduced urinary flow and increased urinary osmolality [28]. Furthermore, TGR(A1-7)3292 rats exhibited metabolic improvements such as decreased plasma lipid levels, improved glucose tolerance, less fat tissue, decreased lipogenesis, and less cafeteria-diet-induced obesity [9,57,87,89]. Moreover, these rats presented a reduction in anxiety-like behavior [39] and in the response to stress [60].…”

Liver

“…The liver, under physiological conditions, plays a pivotal role in metabolic homeostasis, by regulating glucose and lipid metabolisms [12,13]. A great body of evidence has pointed out the RAS components as crucial regulators of hepaticassociated metabolic functions [12,[14][15][16][17].…”

“…The liver, under physiological conditions, plays a pivotal role in metabolic homeostasis, by regulating glucose and lipid metabolisms [12,13]. A great body of evidence has pointed out the RAS components as crucial regulators of hepaticassociated metabolic functions [12,[14][15][16][17]. For instance, the genetic deletion of the Mas receptor in FVB/N mice leads to a metabolic syndrome-like state characterized by dyslipidemia, increased abdominal fat mass, enhanced muscle triglycerides, glucose intolerance, and reduced insulin sensitivity, as well as a decrease in insulinstimulated glucose uptake by adipocytes [16,17].…”

“…A transgenic rat overexpressing Ang-(1-7) presented a decrease in adiposity index along with a reduction in lipogenesis, suggesting a direct effect of Ang-(1-7) on adipose tissue lipid metabolism, independent of the stimulatory effect of insulin. Moreover, specifically in the liver, overexpression of Ang-(1-7) decreased the concentration of triacylglycerol and inhibited fatty acid synthase (FAS) and fatty acid transport protein (FATP) expression in the liver, suggesting a decrease in de novo fatty acid synthesis and fatty acid uptake [12]. Interestingly, exercise training prevented metabolic syndrome and nonalcoholic fatty liver disease (NAFLD) in fructose-fed rats by increasing hepatic ACE2-Ang-(1-7)-Mas receptor axis activity [18].…”