Adropin is a unique hormone encoded by the energy homeostasis-associated (Enho) gene. Adropin is produced in the liver and brain, and also in peripheral tissues such as in the heart and gastrointestinal tract. Furthermore, adropin is present in the circulatory system. A decade after its discovery, there is evidence that adropin may contribute to body weight regulation, glucose and lipid homeostasis, and cardiovascular system functions. In this review, we summarize and discuss the physiological, metabolic, and pathophysiological factors regulating Enho as well as adropin. Furthermore, we review the literature addressing the role of adropin in adiposity and type 2 diabetes. Finally, we elaborate on the role of adropin in the context of the cardiovascular system, liver diseases, and cancer.

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Peptide hormones play a prominent role in controlling energy homeostasis and metabolism. They have been implicated in controlling appetite, the function of the gastrointestinal and cardiovascular systems, energy expenditure, and reproduction. Furthermore, there is growing evidence indicating that peptide hormones and their receptors contribute to energy homeostasis regulation by interacting with white and brown adipose tissue. In this article, we review and discuss the literature addressing the role of selected peptide hormones discovered in the 21st century (adropin, apelin, elabela, irisin, kisspeptin, MOTS-c, phoenixin, spexin, and neuropeptides B and W) in controlling white and brown adipogenesis. Furthermore, we elaborate how these hormones control adipose tissue functions in vitro and in vivo.

neuropeptide B (nPB) regulates food intake, body weight and energy homeostasis by interacting with nPBW1/nPBW2 in humans and nPBW1 in rodents. nPB and nPBW1 are widely expressed in the central nervous system and peripheral tissues including pancreatic islets. although previous studies have demonstrated a prominent role for nPB and nPBW1 in controlling glucose and energy homeostasis, it remains unknown as to whether nPB modulates pancreatic β-cell functions. Therefore, the aim of the present study was to investigate the effects of nPB on insulin expression and secretion in vitro. Furthermore, the role of nPB in the modulation of inS-1e cell growth, viability and death was examined. Gene expression was assessed by reverse transcription-quantitative Pcr. cell proliferation and viability were determined by Brdu or MTT tests, respectively. apoptotic cell death was evaluated by relative quantification histone-complexed DNA fragments (mono-and oligonucleosomes). insulin secretion was studied using an eliSa test. Protein phosphorylation was assessed by western blot analysis. nPB and nPBW1 mrna was expressed in inS-1e cells and rat pancreatic islets. in inS-1e cells, nPB enhanced insulin 1 mrna expression via an erK1/2-dependent mechanism. Furthermore, nPB stimulated insulin secretion from inS-1e cells and rat pancreatic islets. By contrast, nPB failed to affect inS-1e cell growth or death. We conclude that nPB may regulate insulin secretion and expression in inS-1e cells and insulin secretion in rat pancreatic islets.

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.

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