Abstract
BackgroundNesfatin-1 is a recently discovered anorexigen encoded in the precursor peptide, nucleobindin-2 (NUCB2) in mammals. To date, nesfatin-1 has not been described in any non-mammalian species, although some information is available in the sequenced genomes of several species. Our objective was to characterize nesfatin-1 in fish.Methodology/Principal FindingsIn the present study, we employed molecular, immunohistochemical, and physiological studies to characterize the structure, distribution, and appetite regulatory effects of nesfatin-1 in a non-mammalian vertebrate. A very high conservation in NUCB2 sequences, especially in the nesfatin-1 region was found in lower vertebrates. Abundant expression of NUCB2 mRNA was detected in several tissues including the brain and liver of goldfish. Nesfatin-1-like immunoreactive cells are present in the feeding regulatory nucleus of the hypothalamus and in the gastrointestinal tract of goldfish. Approximately 6-fold increase in NUCB2 mRNA levels was found in the liver after 7-day food-deprivation, and a similar increase was also found after short-term fasting. This points toward a possible liver specific role for NUCB2 in the control of metabolism during food-deprivation. Meanwhile, ∼2-fold increase at 1 and 3 h post-feeding and an ∼3-fold reduction after a 7-day food-deprivation was observed in NUCB2 mRNA in the goldfish hypothalamus. In vivo, a single intraperitoneal injection of the full-length native (goldfish; gf) nesfatin-1 at a dose of 50 ng/g body weight induced a 23% reduction of food intake one hour post-injection in goldfish. Furthermore, intracerebroventricular injection of gfnesfatin-1 at a dose of 5 ng/g body weight resulted in ∼50% reduction in food intake.Conclusions/SignificanceOur results provide molecular, anatomical and functional evidences to support potential anorectic and metabolic roles for endogenous nesfatin-1 in goldfish. Collectively, we provide novel information on NUCB2 in non-mammals and an anorexigenic role for nesfatin-1 in goldfish.
Highlights
Nesfatin-1 is a recently identified anorectic peptide cleaved from the N-terminal of the precursor protein nucleobindin 2 (NUCB2) [1]
NUCB2A in Takifugu rubripes and Tetraodon nigroviridis both have 12 exons interspaced by 11 introns and this appears to be due to the deletion of exon 1. (Figure 1A)
There have been no reports on the processing of nesfatin-1 from NUCB1 or any reports of the involvement of NUCB1 in food intake or glucose homeostasis
Summary
Nesfatin-1 is a recently identified anorectic peptide cleaved from the N-terminal of the precursor protein nucleobindin 2 (NUCB2) [1]. Nesfatin-1 has been detected in both rat cerebrospinal fluid [1] and in the peripheral circulation of humans and rodents [9,12,13,14]. Acute administration of nesfatin-1, by central or peripheral injections has been shown to reduce food intake in rats for up to 6 hours [1,13,14,15]. Nesfatin-1 has been shown to regulate cardiac functions [16], reduce blood glucose levels in diabetic mice [14], and induce fear and anxiety like behaviors [17]. Nesfatin-1 is a recently discovered anorexigen encoded in the precursor peptide, nucleobindin-2 (NUCB2) in mammals.
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