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United States Department of Agriculture

Agricultural Research Service

Research Project: GENOMIC REGULATION OF SEASONAL INFERTILITY IN SWINE

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Title: Evidence that nesfatin-1 is a satiety factor in the pig and that the hypothalamus controls its expression in adipose tissue

Authors
item Lents, Clay -
item Barb, Claude
item Hausman, Gary
item LEE-RUTHERFORD, LAURA
item Rogers, C -
item Heidorn, R -
item Cisse, R -
item Azain, M -

Submitted to: American Society of Animal Science Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: May 3, 2010
Publication Date: June 24, 2010
Citation: Lents, C.A., Barb, C.R., Hausman, G.J., Lee Rutherford, L., Rogers, C.J., Heidorn, R.S., Cisse, R.S., Azain, M.J. 2010. Evidence that nesfatin-1 is a satiety factor in the pig and that the hypothalamus controls its expression in adipose tissue [abstract]. American Society of Animal Science Annual Meeting. V.88E(Suppl.2) p.867

Technical Abstract: Two experiments (Exp) were conducted to test if nesfatin-1 is part of the adipose tissue-hypothalamic loop regulating appetite and energy balance of the pig. In Exp 1, prepuberal gilts were adapted to a twice-daily feeding schedule (0800 and 1600 h) and received intracerebroventricular (i.c.v.) injection of 100 µg of either recombinant human leptin or nesfatin-1 in 0.9% saline. Control animals received 0.9% saline alone (n = 4/group). Four hours after i.c.v. injection, feeders were placed in all pens (1600 h) for determination of cumulative intake at 4, 20, 44, and 68 h after feed presentation. Food consumption of nesfatin-1 treated pigs was suppressed (P < 0.01) during the first 20 h compared with saline controls (0.54 ± 0.3 and 3.15 ± 0.3 kg, respectively), but was not different from leptin treated pigs (1.04 ± 0.3 kg). Although food intake of leptin and nesfatin-1 treated pigs increased (P < 0.05) after 20 h, it was still less (P < 0.001) at 68 h than that observed for saline treated animals (4.50, 4.04, and 8.76 ± 0.31 kg for leptin, nesfatin-1, and saline, respectively). Subcutaneous (SC) adipose in the pig is innervated by hypothalamic neurons that are sensitive to secreted adipokines. Nesfatin-1 is proposed to work through the melanocortin 3/4 receptor (MC3/4R) pathway, which when activated alters gene expression in fat. In Exp II, gilts received i.c.v. injection of 10 µg of the MC3/4R agonist NDP-MSH or 0.9% saline alone (n= 9/group). Pigs were sacrificed 24 h later and SC adipose tissue was collected for isolation of RNA. Abundance of mRNA for nesfatin was quantified with real-time RT-PCR. Relative differences in expression were calculated by the REST© procedure with 18S rRNA as the reference control. mRNA for nesfatin in SC adipose tissue of NDP-MSH treated pigs was reduced 1.7 fold (P = 0.05) compared with saline treated pigs. We conclude that nesfatin-1 is a satiety factor in the pig and that activation of the MC3/4R pathway suppresses expression of nesfatin-1, which may be mediated by sympathetic neuronal outflow to adipose tissue. swine, nesfatin-1, feed intake, gene expression To italicize a P: <i>P</i> µg is coded as: $\mu#$g ± is coded as: $\plusmn#$ © is codes as: ^{$\copy#$}^ Two experiments (Exp) were conducted to test if nesfatin-1 is part of the adipose tissue-hypothalamic loop regulating appetite and energy balance of the pig. In Exp 1, prepuberal gilts were adapted to a twice-daily feeding schedule (0800 and 1600 h) and received intracerebroventricular (i.c.v.) injection of 100 $\mu#$g of either recombinant human leptin or nesfatin-1 in 0.9% saline. Control animals received 0.9% saline alone (n = 4/group). Four hours after i.c.v. injection, feeders were placed in all pens (1600 h) for determination of cumulative intake at 4, 20, 44, and 68 h after feed presentation. Food consumption of nesfatin-1 treated pigs was suppressed (<i>P</i> < 0.01) during the first 20 h compared with saline controls (0.54 $\plusmn#$ 0.3 and 3.15 $\plusmn#$ 0.3 kg, respectively), but was not different from leptin treated pigs (1.04 $\plusmn#$ 0.3 kg). Although food intake of leptin and nesfatin-1 treated pigs was increasing (<i>P</i> < 0.05) after 20 h, it was still less (<i>P</i> < 0.001) at 68 h than that observed for saline treated pigs (4.50, 4.04, and 8.76 $\plusmn#$ 0.31 kg for leptin, nesfatin-1, and saline, respectively). Subcutaneous (SC) adipose in the pig is innervated by hypothalamic neurons that are sensitive to secreted adipokines. Nesfatin-1 is proposed to work through the melanocortin 3/4 receptor (MC3/4R) pathway, which when activated alters gene expression in fat. In Exp II, gilts received i.c.v. injection of 10 $\mu#$g of the MC3/4R agonist NDP-MSH or 0.9% saline alone (n= 9/group). Pigs were sacrificed 24 h later and SC adipose tissue was collected for isolation of RNA. Abundance of mRNA for nesfatin was quantified with real-time RT-PCR. Relative differences in expression were calculated by the REST^{$\copy#$}^ procedure with 18S rRNA as the reference control. mRNA for nesfatin in SC adipose tissue of NDP-MSH treated pigs was reduced 1.7 fold (<i>P</i> = 0.05) compared with saline treated pigs. We conclude that nesfatin-1 is a satiety factor in the pig and that activation of the MC3/4R pathway suppresses expression of nesfatin-1, which may be mediated by sympathetic neuronal outflow to adipose tissue.

Last Modified: 9/10/2014
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