Abstract

Adropin is a peptide hormone which modulates energy homeostasis and metabolism. In animals with diet-induced obesity, adropin attenuates adiposity and improves lipid and glucose homeostasis. Adropin promotes the proliferation of rodent white preadipocytes and suppresses their differentiation into adipocytes. By contrast, the effects of adropin on mature white adipocytes are unknown. Therefore, we aimed to evaluate the effects of adropin on lipolysis, lipogenesis and glucose uptake in white rodent adipocytes. We assessed the effects of adropin on the mRNA expression of adiponectin, resistin and visfatin. White preadipocytes were isolated from male Wistar rats. Differentiated 3T3-L1 cells were used as a surrogate model of white adipocytes. Lipolysis was measured by the evaluation of glycerol and free fatty acid secretion using colorimetric kits. The effects of adropin on lipogenesis and glucose uptake were measured using radioactive-labelled glucose. The expression of adipokine mRNA was studied using real-time PCR. Our results show that adropin slightly promotes lipolysis in rat adipocytes and 3T3-L1 cells. Adropin suppresses lipogenesis in rat adipocytes without influencing glucose uptake. In addition, adropin stimulates adiponectin mRNA expression and suppresses the expression of resistin and visfatin. These results indicate that adropin may be involved in controlling lipid metabolism and adipokine expression in white rodent adipocytes.

Highlights

  • Adropin is a peptide hormone encoded by energy homeostasis-associated (Enho), which was originally identified in 2008 by Kumar et al [1]

  • We studied whether adropin is able to modulate the mRNA expression of adiponectin, resistin and visfatin

  • We studied the effects of adropin on the mRNA expression and phosphorylation of hormone-sensitive lipase (HSL) in rat adipocytes

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Summary

Introduction

Adropin is a peptide hormone encoded by energy homeostasis-associated (Enho), which was originally identified in 2008 by Kumar et al [1]. More than a decade after the identification of adropin, there is convincing evidence demonstrating numerous beneficial effects of this peptide hormone on metabolic diseases such as obesity and diabetes. It was found that the overproduction or administration of adropin enhances insulin sensitivity, attenuates hepatic steatosis and delays the development of obesity in mice fed a diet enriched in fat [1]. Adropin deficiency in mice leads to impaired insulin sensitivity, abnormal glucose metabolism and increased adiposity [10]. It was found that adropin may modulate glucose homeostasis by suppressing hepatic glucose production in obese mice [11,12] and by promoting glucose oxidation in skeletal muscle [13]. The direct effects of adropin on mature fat cell functions, such as glucose and lipid metabolism, as well as endocrine activity, are largely unknown. We studied whether adropin is able to modulate the mRNA expression of adiponectin, resistin and visfatin

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