Abstract
Since arginase has been shown to compete with nitric oxide (NO) synthase, emerging evidence has reported that arginase inhibition improves obesity by increasing NO production. Semen cuscutae (SC), which is a well-known Chinese medicine, has multiple biological functions such as anti-oxidant function and immune regulation. In this study, we investigated whether the SC as a natural arginase inhibitor influences hepatic lipid abnormalities and whole-body adiposity in high-fat diet (HFD)-induced obese mice. The lipid accumulation was significantly reduced by SC treatment in oleic acid-induced hepatic steatosis in vitro. Additionally, SC supplementation substantially lowered HFD-induced increases in arginase activity and weights of liver and visceral fat tissue, while increasing hepatic NO. Furthermore, elevated mRNA expressions of sterol regulatory element-binding transcription factor 1 (SREBP-1c), fatty-acid synthase (FAS), peroxisome proliferator-activated receptor-gamma (PPAR-γ)1, and PPAR-γ2 in HFD-fed mice were significantly attenuated by SC supplementation. Taken together, SC, as a novel natural arginase inhibitor, showed anti-obesity properties by modulating hepatic arginase and NO production and metabolic pathways related to hepatic triglyceride (TG) metabolism.
Highlights
Arginase, which catalyzes the hydrolysis of l-arginine to urea, has been implicated in various diseases, such as obesity-associated vascular and metabolic dysfunction [1,2]
We found that the Semen cuscutae (SC) treatment dramatically reduced the arginase activity in a dose-dependent manner
To investigate the possible underlying mechanisms for SC’s effects, we evaluated the expression of several genes involved in hepatic TG metabolism (Figure 4A–F)
Summary
Arginase, which catalyzes the hydrolysis of l-arginine to urea, has been implicated in various diseases, such as obesity-associated vascular and metabolic dysfunction [1,2]. Previous studies reported that increased arginase activity was found in obese individuals and those who have obesity related metabolic disorders, such as metabolic syndrome and endothelial dysfunction [5,6,7]. Arginase is involved in the reduction of NO production, so the blockage of its activity may Nutrients 2019, 11, 3035; doi:10.3390/nu11123035 www.mdpi.com/journal/nutrients. Recent studies have shown that deletion of arginase 2 ameliorates high-fat induced obesity and the associated nonalcoholic fatty liver disease (NAFLD) [11,12]. It was assumed that upregulated arginase expression in an obese condition is associated with the reduction in NO production, and with abnormal hepatic triglyceride (TG) metabolism and relevant metabolic pathways. It is crucial to describe the beneficial effects of arginase suppression in NAFLD and the underlying mechanisms associated with obesity
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