Plasma Nesfatin-1 Is Not Affected by Long-Term Food Restriction and Does Not Predict Rematuration among Iteroparous Female Rainbow Trout (Oncorhynchus mykiss)

Abstract

The metabolic peptide hormone nesfatin-1 has been linked to the reproductive axis in fishes. The purpose of this study was to determine how energy availability after spawning affects plasma levels of nesfatin-1, the metabolic peptide hormone ghrelin, and sex steroid hormones in rematuring female rainbow trout (Oncorhynchus mykiss). To limit reproductive maturation, a group of female trout was food-restricted after spawning and compared with a control group that was fed a standard broodstock ration. The experiment was conducted twice, once using two-year-old trout (second-time spawners) and once using three-year-old trout (third-time spawners). During monthly sampling, blood was collected from all fish, and a subset of fish from each treatment was sacrificed for pituitaries. Pituitary follicle-stimulating hormone-beta (fsh-β) mRNA expression was analyzed with q-RT-PCR; plasma hormone levels were quantified by radioimmunoassay (17β-estradiol and ghrelin) and enzyme-linked immunosorbent assay (11-keto-testosterone and nesfatin-1). Although plasma nesfatin-1 levels increased significantly in the months immediately after spawning within both feeding treatments, plasma nesfatin-1 did not differ significantly between the two treatments at any point. Similarly, plasma ghrelin levels did not differ significantly between the two treatments at any point. Food restriction arrested ovarian development by 15–20 weeks after spawning, shown by significantly lower plasma E2 levels among restricted-ration fish. Pituitary fsh-β mRNA levels were higher among control-ration fish than restricted-ration fish starting at 20 weeks, but did not differ significantly between treatment groups until 30 weeks after spawning. Within both treatment groups, plasma 11-KT was elevated immediately after spawning and rapidly decreased to and persisted at low levels; starting between 20 and 25 weeks after spawning, plasma 11-KT was higher among control-ration fish than restricted-ration fish. The results from these experiments do not provide support for plasma nesfatin-1 as a signal for the initiation of reproductive development in rematuring female rainbow trout.

Nutrient status modulates the expression of nesfatin-1 encoding nucleobindin 2A and 2B mRNAs in zebrafish gut, liver and brain

“…Food restriction suppresses ovarian development in female rainbow trout after spawning. There were no differences in circulating nesfatin-1 in control and food restricted group, suggesting that endogenous is possibly not involved in regulating reproduction in rainbow trout (Caldwell et al, 2014). This result also highlights the species-specificity in endogenous nesfatin-1 and its biological actions.…”

“…Given that nesfatin-1 could be processed from both NUCB2A and NUCB2B, it is possible that these two genes are equally important in providing the biologically active endogenous nesfatin-1. In contrast, no association between circulating nesfatin-1 and reproduction in female rainbow trout were found (Caldwell et al, 2014). While plasma nesfatin-1 increased during a period preceding spawning, feed restriction caused no changes in circulating nesfatin-1.…”

“…Further studies are required to elucidate the liver specific roles of nesfatin-1 in fish. Serum nesfatin-1 was not altered due to food deprivation in female rainbow trout, and it might be due to several reasons, including the carnivory exhibited by this fish (Caldwell et al, 2014). Further characterization of trout nesfatin-1 will enable us to address the scope and functions of endogenous nesfatin-1 in this species.…”

“…NUCB2A mRNA is expressed in the brain (hypothalamus), pituitary, liver, hepatopancreas, intestine and gonads of goldfish (Gonzalez et al, 2010) and Ya fish (Lin et al, 2014). More recently, nesfatin-1 was detected in the circulation of female rainbow trout (Caldwell et al, 2014).…”

Nucleobindin-1 encodes a nesfatin-1-like peptide that stimulates insulin secretion

“…Nesfatin-1 increases glucose-stimulated insulin secretion from b cells by direct action involving Ca 2+ influx through L-type calcium channels (Nakata et al, 2011). Nesfatin-1 was also identified in zebrafish (Hatef et al, 2014), Ya fish (Lin et al, 2014), trout (Caldwell et al, 2014) and frogs (Senejani et al, 2014). Nesfatin-1 suppresses feeding (Gonzalez et al, 2010;Kerbel and Unniappan, 2012), and reproductive hormone secretion in goldfish (Gonzalez et al, 2012b).…”