Location: Reproduction ResearchTitle: Effects of nesfatin-1 on food intake and LH secretion in prepubertal gilts and genomic association of the porcine NUCB2 gene with growth traits Author
|Nonneman, Danny - Dan|
Submitted to: Domestic Animal Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/6/2013
Publication Date: 8/1/2013
Publication URL: http://handle.nal.usda.gov/10113/59675
Citation: Lents, C.A., Barb, C.R., Hausman, G.J., Nonneman, D., Heidorn, N.L., Cisse, R.S., Azain, M.J. 2013. Effects of nesfatin-1 on food intake and LH secretion in prepubertal gilts and genomic association of the porcine NUCB2 gene with growth traits. Domestic Animal Endocrinology. 45(2):89-97. Interpretive Summary: Adipose tissue is not simply a storage depot for energy in the form of lipid. Fat tissue also acts as the largest endocrine organ of the body by secreting biologically active molecules called adipokines that play important roles in regulating economically important traits such as feed intake, tissue growth, and reproduction. Identifying new adipokines and defining their biological role in livestock is an important area of research. Scientists studied a newly discovered adipokine called nesfatin-1 and found that it is expressed in adipose tissue of pigs and that it appears to play a role in controlling energy balance. They found that nesfatin-1 acts in the brain to suppress appetite, causing pigs to eat less. Nesfatin-1 was also found to stimulate the secretion of reproductive hormone from the pituitary gland that is necessary to initiate puberty and maintain normal reproductive function, indicating that nesfatin-1 plays an important role in the metabolic regulation of reproduction. Genetic variation in the nesfatin-1 gene is associated with differences in body weight during growth and at puberty. Further understanding how nesfatin-1 contributes to variation in growth and reproduction will be critical to continue to improve efficiency and profitability of swine production.
Technical Abstract: Nesfatin-1, a product of the nucleobindin 2 (NUCB2) gene, purportedly plays important roles in whole-body energy homeostasis. Experiments were conducted to determine how NUCB2 expression in fat depots may be controlled in the pig and to test the hypothesis that nesfatin-1 regulates appetite and LH secretion in the gilt. Prepubertal gilts were used to study expression of NUCB2 in fat and the effects of intracerebroventricular (i.c.v.) injection of nesfatin-1 on food intake and pituitary hormone secretion. Growing pigs (gilts and barrows at 22 wk of age, n = 1,145) or sexually mature gilts (n = 439) were used to test association of SNP in the NUCB2 gene with growth traits. The expression of NUCB2 was similar for subcutaneous fat compared with perirenal fat. An i.c.v. injection of the melanocortin-4 receptor agonist [Nle**4, d-Phe**7]-alpha-melanocyte-stimulating hormone did not alter expression of NUCB2 mRNA in the hypothalamus but reduced (P = 0.056) NUCB2 mRNA expression in subcutaneous fat. Short-term (7 d) submaintenance feeding reduced (P < 0.05) BW and did not alter expression of mRNA for NUCB2, visfatin, or leptin but increased (P < 0.05) expression of adiponectin mRNA in fat. Central injection of nesfatin-1 suppressed (P < 0.001) feed intake. Secretion of LH was greater (P < 0.01) after i.c.v. injection of nesfatin-1 than after saline. Single nucleotide polymorphisms in the porcine NUCB2 gene were not associated with adiposity of growing pigs or age at puberty in gilts but were associated (P < 0.05) with BW at puberty. These data indicate that NUCB2 is expressed in fat depots of the pig and that the level of expression is sensitive to stimulation of appetite-regulating pathways in the hypothalamus. It is confirmed herein that nesfatin-1 can regulate appetite in the pig and affect the gonadotropic axis of the prepubertal pig. Association of SNP in the porcine NUCB2 gene with BWat puberty suggests that regulation of appetite by nesfatin-1 in the pig affects growth, which may have important consequences for adult phenotypes.