Abstract
Simple SummaryNesfatin-1 is a newly identified molecule derived from the precursor protein NEFA/nucleobindin2. In this minireview we analyzed the research on the nesfatin-1 localization in the gastrointestinal tract of the mammals. We also referred to the effects of the protein on disorders in the gastrointestinal tract.Nesfatin-1, discovered in 2006, is an anorexigenic molecule derived from the precursor protein NEFA/nucleobindin2. It is generally postulated that this molecule acts through a specific G protein-coupled receptor, as yet unidentified. Research conducted over the last 15 years has revealed both central and peripheral actions of nesfatin-1. Given its major central role, studies determining its inhibitory effect on food intake seem to be of major scientific interest. However, in recent years a number of experiments have found that peripheral organs, including those of the gastrointestinal tract (GIT), may also be a source (possibly even the predominant source) of nesfatin-1. This mini-review aimed to summarize the current state of knowledge regarding the expression and immunoreactivity of nesfatin-1 and its possible involvement (both physiological and pathological) in the mammalian GIT. Research thus far has shown very promising abilities of nesfatin-1 to restore the balance between pro-oxidants and antioxidants, to interplay with the gut microbiota, and to alter the structure of the intestinal barrier. This necessitates more extensive research on the peripheral actions of this molecule. More in-depth knowledge of such mechanisms (especially those leading to anti-inflammatory and anti-apoptotic effects) is important for a better understanding of the involvement of nefatin-1 in GIT pathophysiological conditions and/or for future therapeutic approaches.
Highlights
Introduction published maps and institutional affilThe history of nesfatin-1 begins in 2006 when a group of researchers led by ShinsukeOh-I identified a new anorexigenic molecule in the hypothalamus of the rat [1]
In a series of experiments involving immunohistochemistry (IHC) and in situ hybridization (ISH) techniques, they located a new protein encoded in the precursor protein NEFA/nucleobindin2, in the arcuate nucleus, paraventricular nucleus (PVN), supraoptic nucleus, lateral hypothalamic area, zona incerta, and nucleus tractus solitarius (NTS), which are believed to be hypothalamic nuclei involved in appetite regulation
Nesfatin-1 was shown to stimulate Ca+2 influx in cultured hypothalamic neurons, and this elevation was significantly reduced by specific protein kinase A inhibitor KT 5720, which indicates an interaction between nesfatin-1 and G protein-coupled receptor [7]
Summary
Before characterizing the significance of nesfatin-1, the review will outline the current state of knowledge about possible mechanisms of its action. There are several indications that nesfatin-1 acts through a specific receptor. Nesfatin-1 was shown to stimulate Ca+2 influx in cultured hypothalamic neurons, and this elevation was significantly reduced by specific protein kinase A inhibitor KT 5720, which indicates an interaction between nesfatin-1 and G protein-coupled receptor [7]. As shown in cultured dorsal root ganglia neurons, the elevated Ca+2 levels resulting from nesfatin activity may be achieved through a protein kinase C-dependent mechanism [8]. Electron microscopy confirmed that nesfatin-1 is located in the secretory vesicles of PVN neurons and when released is able to activate the adjacent oxytocin-IR nervous cells, which strongly supports the hypothesis of a paracrine/autocrine mode of action [12]. It is noteworthy that in the cells of peripheral organs, nesfatin-1 is usually visualized as granules exclusively limited to the cytoplasm and not present in the nucleus or cell membrane [14]
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