American Journal of Life Sciences

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Effects of Neurotensin and LANT-6 on Food Intake in Chicks

Received: 20 March 2015    Accepted: 24 March 2015    Published: 06 May 2015
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Abstract

Neurotensin (NT) and an NT-related peptide (Lys, Asn, NT8–13; LANT-6) are produced in the chicken brain and intestine, and these peptides are encoded by the same precursor gene (NT/LANT-6 precursor). Although it has been reported that the central administration of NT suppresses food intake in mammals, the effect of NT and LANT-6 on feeding behavior in birds has not yet been investigated. In this paper, we analyzed the expression levels of NT/LANT-6 precursor and the NT receptor (NTR1) mRNAs in the hypothalamic infundibulum, an important region for regulating feeding behaviors. We also examined the effects of NT and LANT-6 administration on food intake in chicks. Real-time PCR analysis showed that NT/LANT-6 precursor and NTR1 mRNAs had moderately high expression in the hypothalamic infundibulum. Further, in the hypothalamic infundibulum, the mRNA level of NT/LANT-6 precursor showed a trend toward increasing during postnatal development and increased 2.9-fold after a 48 hour fast, although the NTR1 mRNA level was not changed in both analyses. Contrary to our expectations, central administration of NT or LANT-6 had no effect on food intake in chicks.

DOI 10.11648/j.ajls.s.2015030302.14
Published in American Journal of Life Sciences (Volume 3, Issue 3-2, May 2015)

This article belongs to the Special Issue Biology and Medicine of Peptide and Steroid Hormones

Page(s) 17-23
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Brain, Chicken, Food Intake, Hypothalamic Infundibulum, LANT-6, mRNA, Neurotensin

References
[1] Carraway R, Leeman SE, “The isolation of a new hypotensive peptide, neurotensin, from bovine hypothalami,” J Biol Chem, 1973, 248, pp. 6854-6861.
[2] Minamino N, Kangawa K, Matsuo H, “Neuromedin N: a novel neurotensin-like peptide identified in porcine spinal cord,” Biochem Biophys Res Commun, 1984, 122, pp. 542-549.
[3] Dobner PR, Barber DL, Villa-Komaroff L, McKiernan C, “Cloning and sequence analysis of cDNA for the canine neurotensin/neuromedin N precursor,” Proc Natl Acad Sci U S A, 1987, 84, pp. 3516-3520.
[4] Tanaka K, Masu M, Nakanishi S, “Structure and functional expression of the cloned rat neurotensin receptor,” Neuron, 1990, 4, pp. 847-854.
[5] Chalon P, Vita N, Kaghad M, Guillemot M, Bonnin J, Delpech B, Le Fur G, Ferrara P, Caput D, “Molecular cloning of a levocabastine-sensitive neurotensin binding site,” FEBS Lett, 1996, 386, pp. 91-94.
[6] Mazella J, Botto JM, Guillemare E, Coppola T, Sarret P, Vincent JP, “Structure, functional expression, and cerebral localization of the levocabastine-sensitive neurotensin/neuromedin N receptor from mouse brain,” J Neurosci, 1996, 16, pp. 5613-5620.
[7] Mazella J, Zsürger N, Navarro V, Chabry J, Kaghad M, Caput D, Ferrara P, Vita N, Gully D, Maffrand JP, Vincent JP, “The 100-kDa neurotensin receptor is gp95/sortilin, a non-G-protein-coupled receptor,” J Biol Chem, 1998, 273, pp. 26273-26276.
[8] Kalafatakis K, Triantafyllou K, “Contribution of neurotensin in the immune and neuroendocrine modulation of normal and abnormal enteric function,” Regul Pept, 2011, 170, pp. 7-17.
[9] Tyler-McMahon BM, Boules M, Richelson E, “Neurotensin: peptide for the next millennium,” Regul Pept, 2000, 93, pp. 125-136.
[10] Luttinger D, King RA, Sheppard D, Strupp J, Nemeroff CB, Prange AJ Jr, “The effect of neurotensin on food consumption in the rat,” Eur J Pharmacol, 1982, 81, pp. 499-503.
[11] Levine AS, Kneip J, Grace M, Morley JE, “Effect of centrally administered neurotensin on multiple feeding paradigms,” Pharmacol Biochem Behav, 1983, 18, pp. 19-23.
[12] Cooke JH, Patterson M, Patel SR, Smith KL, Ghatei MA, Bloom SR, Murphy KG, “Peripheral and central administration of xenin and neurotensin suppress food intake in rodents,” Obesity (Silver Spring), 2009, 17, pp. 1135-1143.
[13] Carraway R, Bhatnagar YM, “Isolation, structure and biologic activity of chicken intestinal neurotensin,” Peptides, 1980, 1, pp. 167-174.
[14] Carraway RE, Ferris CF, “Isolation, biological and chemical characterization, and synthesis of a neurotensin-related hexapeptide from chicken intestine,” J Biol Chem, 1983, 258, pp. 2475-2479.
[15] Tanaka M, Nakao N, Yamamoto I, Tsushima N, Ohta Y, “Changes in expression levels of neurotensin precursor and receptor mRNA in chicken intestinal tissues and liver during late embryonic and early posthatching development,” Poult Sci, 2013, 92, pp. 2765-2771.
[16] Numao M, Sudo H, Yamamoto I, Nakao N, Kaiya H, Miyazato M, Tsushima N, Tanaka M, “Molecular characterization of structure and tissue distribution of chicken neurotensin receptor,” Gen Comp Endocrinol, 2011, 171, pp. 33-38.
[17] Masuda K, Iwakoshi-Ukena E, Bessho Y, Taniuchi S, Maejima S, Shikano K, Kondo K, Furumitsu M, Ukena K, “Identification of neurotensin and LANT-6 and localization of mRNA encoding their precursor in the chicken brain,” Zoolog Sci, 2014, 31, pp. 353-359.
[18] Williams G, Cai XJ, Elliott JC, Harrold JA, “Anabolic neuropeptides,” Physiol Behav, 2004, 81, pp. 211-222.
[19] Kameda Y, Miura M, Nishimaki T, “Localization of neuropeptide Y mRNA and peptide in the chicken hypothalamus and their alterations after food deprivation, dehydration, and castration,” J Comp Neurol, 2001, 436, pp. 376-388.
[20] Kuenzel WJ, Douglass LW, Davison BA, “Robust feeding following central administration of neuropeptide Y or peptide YY in chicks, Gallus domesticus,” Peptides, 1987, 8, pp. 823-828.
[21] Tachibana T, Sato M, Oikawa D, Takahashi H, Boswell T, Furuse M, “Intracerebroventricular injection of neuropeptide Y modifies carbohydrate and lipid metabolism in chicks,” Regul Pept, 2006, 136, pp. 1-8.
[22] Saneyasu T, Honda K, Kamisoyama H, Ikura A, Nakayama Y, Hasegawa S, “Neuropeptide Y effect on food intake in broiler and layer chicks,” Comp Biochem Physiol A Mol Integr Physiol, 2011, 159, pp. 422-426.
[23] National Research Council. “Guide for the care and use of laboratory animals,” Washington, D.C: National Academy Press, 1996.
[24] Davis JL, Masuoka DT, Gerbrandt LK, Cherkin A, “Autoradiographic distribution of L-proline in chicks after intracerebral injection,” Physiol Behav, 1979, 22, pp. 693-695.
[25] Furuse M, Ando R, Bungo T, Ao R, Shimojo M, Masuda Y, “Intracerebroventricular injection of orexins does not stimulate food intake in neonatal chicks,” Br Poult Sci, 1999, 40, pp. 698-700.
[26] Saito ES, Kaiya H, Tachibana T, Tomonaga S, Denbow DM, Kangawa K, Furuse M, “Inhibitory effect of ghrelin on food intake is mediated by the corticotropin-releasing factor system in neonatal chicks,” Regul Pept, 2005, 125, pp. 201-208.
[27] Ohinata K, Shimano T, Yamauchi R, Sakurada S, Yanai K, Yoshikawa M, “The anorectic effect of neurotensin is mediated via a histamine H1 receptor in mice,” Peptides, 2004 , 25, pp. 2135-2138.
[28] Furuse M, “Central regulation of food intake in the neonatal chick,” Animal Science Journal, 2002, 73, pp. 83-94.
[29] Vaccarino FJ, Bloom FE, Rivier J, Vale W, Koob GF, “Stimulation of food intake in rats by centrally administered hypothalamic growth hormone-releasing factor,” Nature, 1985, 314, pp. 167-168.
[30] Vaccarino FJ, “Growth hormone-releasing factor and feeding. Behavioral evidence for direct central actions,” Ann N Y Acad Sci, 1990, 579, pp. 227-232.
[31] Tachibana T, Sugimoto I, Ogino M, Sakirul Islam Khan M, Masuda K, Ukena K, Wang Y, “Central administration of chicken growth hormone-releasing hormone decreases food intake in chicks,” Physiol Behav, 2015, 139, pp. 195-201.
[32] Lawrence CB, Celsi F, Brennand J, Luckman SM, “Alternative role for prolactin-releasing peptide in the regulation of food intake,” Nat Neurosci, 2000, 3, pp. 645-646.
[33] Lawrence CB, Ellacott KL, Luckman SM, “PRL-releasing peptide reduces food intake and may mediate satiety signaling,” Endocrinology, 2002, 143, pp. 360-367.
[34] Tachibana T, Moriyama S, Takahashi A, Tsukada A, Oda A, Takeuchi S, Sakamoto T, “Isolation and characterisation of prolactin-releasing peptide in chicks and its effect on prolactin release and feeding behavior,” J Neuroendocrinol, 2011, 23, pp. 74-81.
[35] Friedman JM, Halaas JL, “Leptin and the regulation of body weight in mammals,” Nature, 1998, 395, pp. 763-770.
[36] Hâkansson ML, Brown H, Ghilardi N, Skoda RC, Meister B, “Leptin receptor immunoreactivity in chemically defined target neurons of the hypothalamus,” J Neurosci, 1998, 18, pp. 559-572.
[37] Sahu A, “Evidence suggesting that galanin (GAL), melanin-concentrating hormone (MCH), neurotensin (NT), proopiomelanocortin (POMC) and neuropeptide Y (NPY) are targets of leptin signaling in the hypothalamus,” Endocrinology, 1998, 139, pp. 795-798.
[38] Sahu A, Carraway RE, Wang YP, “Evidence that neurotensin mediates the central effect of leptin on food intake in rat,” Brain Res, 2001, 888, pp. 343-347.
[39] Prokop JW, Schmidt C, Gasper D, Duff RJ, Milsted A, Ohkubo T, Ball HC, Shawkey MD, Mays HL Jr, Cogburn LA, Londraville RL, “Discovery of the elusive leptin in birds: identification of several 'missing links' in the evolution of leptin and its receptor,” PLoS One, 2014, 9, e92751.
[40] Friedman-Einat M, Cogburn LA, Yosefi S, Hen G, Shinder D, Shirak A, Seroussi E, “Discovery and characterization of the first genuine avian leptin gene in the rock dove (Columba livia),” Endocrinology, 2014, 155, pp. 3376-3384.
[41] Huang G, Li J, Wang H, Lan X, Wang Y, “Discovery of a novel functional leptin protein (LEP) in zebra finches: evidence for the existence of an authentic avian leptin gene predominantly expressed in the brain and pituitary,” Endocrinology, 2014, 155, pp. 3385-3396.
[42] Denbow DM, Meade S, Robertson A, McMurtry JP, Richards M, Ashwell C, “Leptin-induced decrease in food intake in chickens,” Physiol Behav, 2000, 69, pp. 359-362.
[43] Bungo T, Shimojo M, Masuda Y, Tachibana T, Tanaka S, Sugahara K, Furuse M, “Intracerebroventricular administration of mouse leptin does not reduce food intake in the chicken,” Brain Res, 1999, 817, pp. 196-198.
[44] Machidori H, Sakata T, Yoshimatsu H, Ookuma K, Fujimoto K, Kurokawa M, Yamatodani A, Wada H, “Zucker obese rats: defect in brain histamine control of feeding,” Brain Res, 1992, 590, pp. 180-186.
[45] Lecklin A, Etu-Seppälä P, Stark H, Tuomisto L, “Effects of intracerebroventricularly infused histamine and selective H1, H2 and H3 agonists on food and water intake and urine flow in Wistar rats,” Brain Res, 1998, 793, pp. 279-288.
[46] Bessho Y, Iwakoshi-Ukena E, Tachibana T, Maejima S, Taniuchi S, Masuda K, Shikano K, Kondo K, Furumitsu M, Ukena K, “Characterization of an avian histidine decarboxylase and localization of histaminergic neurons in the chicken brain,” Neurosci Lett, 2014, 578, pp. 106-110.
[47] Kawakami S, Bungo T, Ohgushi A, Ando R, Shimojo M, Masuda Y, Denbow DM, Furuse M, “Brain-derived mast cells could mediate histamine-induced inhibition of food intake in neonatal chicks,” Brain Res, 2000, 857, pp. 313-316.
Author Information
  • Graduate School of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima, Japan

  • Graduate School of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima, Japan

  • Faculty of Agriculture, Department of Agrobiological Science, Ehime University, Matsuyama, Japan

  • Graduate School of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima, Japan

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    Keiko Masuda, Eiko Iwakoshi-Ukena, Tetsuya Tachibana, Kazuyoshi Ukena. (2015). Effects of Neurotensin and LANT-6 on Food Intake in Chicks. American Journal of Life Sciences, 3(3-2), 17-23. https://doi.org/10.11648/j.ajls.s.2015030302.14

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    Keiko Masuda; Eiko Iwakoshi-Ukena; Tetsuya Tachibana; Kazuyoshi Ukena. Effects of Neurotensin and LANT-6 on Food Intake in Chicks. Am. J. Life Sci. 2015, 3(3-2), 17-23. doi: 10.11648/j.ajls.s.2015030302.14

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    AMA Style

    Keiko Masuda, Eiko Iwakoshi-Ukena, Tetsuya Tachibana, Kazuyoshi Ukena. Effects of Neurotensin and LANT-6 on Food Intake in Chicks. Am J Life Sci. 2015;3(3-2):17-23. doi: 10.11648/j.ajls.s.2015030302.14

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  • @article{10.11648/j.ajls.s.2015030302.14,
      author = {Keiko Masuda and Eiko Iwakoshi-Ukena and Tetsuya Tachibana and Kazuyoshi Ukena},
      title = {Effects of Neurotensin and LANT-6 on Food Intake in Chicks},
      journal = {American Journal of Life Sciences},
      volume = {3},
      number = {3-2},
      pages = {17-23},
      doi = {10.11648/j.ajls.s.2015030302.14},
      url = {https://doi.org/10.11648/j.ajls.s.2015030302.14},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.ajls.s.2015030302.14},
      abstract = {Neurotensin (NT) and an NT-related peptide (Lys, Asn, NT8–13; LANT-6) are produced in the chicken brain and intestine, and these peptides are encoded by the same precursor gene (NT/LANT-6 precursor). Although it has been reported that the central administration of NT suppresses food intake in mammals, the effect of NT and LANT-6 on feeding behavior in birds has not yet been investigated. In this paper, we analyzed the expression levels of NT/LANT-6 precursor and the NT receptor (NTR1) mRNAs in the hypothalamic infundibulum, an important region for regulating feeding behaviors. We also examined the effects of NT and LANT-6 administration on food intake in chicks. Real-time PCR analysis showed that NT/LANT-6 precursor and NTR1 mRNAs had moderately high expression in the hypothalamic infundibulum. Further, in the hypothalamic infundibulum, the mRNA level of NT/LANT-6 precursor showed a trend toward increasing during postnatal development and increased 2.9-fold after a 48 hour fast, although the NTR1 mRNA level was not changed in both analyses. Contrary to our expectations, central administration of NT or LANT-6 had no effect on food intake in chicks.},
     year = {2015}
    }
    

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  • TY  - JOUR
    T1  - Effects of Neurotensin and LANT-6 on Food Intake in Chicks
    AU  - Keiko Masuda
    AU  - Eiko Iwakoshi-Ukena
    AU  - Tetsuya Tachibana
    AU  - Kazuyoshi Ukena
    Y1  - 2015/05/06
    PY  - 2015
    N1  - https://doi.org/10.11648/j.ajls.s.2015030302.14
    DO  - 10.11648/j.ajls.s.2015030302.14
    T2  - American Journal of Life Sciences
    JF  - American Journal of Life Sciences
    JO  - American Journal of Life Sciences
    SP  - 17
    EP  - 23
    PB  - Science Publishing Group
    SN  - 2328-5737
    UR  - https://doi.org/10.11648/j.ajls.s.2015030302.14
    AB  - Neurotensin (NT) and an NT-related peptide (Lys, Asn, NT8–13; LANT-6) are produced in the chicken brain and intestine, and these peptides are encoded by the same precursor gene (NT/LANT-6 precursor). Although it has been reported that the central administration of NT suppresses food intake in mammals, the effect of NT and LANT-6 on feeding behavior in birds has not yet been investigated. In this paper, we analyzed the expression levels of NT/LANT-6 precursor and the NT receptor (NTR1) mRNAs in the hypothalamic infundibulum, an important region for regulating feeding behaviors. We also examined the effects of NT and LANT-6 administration on food intake in chicks. Real-time PCR analysis showed that NT/LANT-6 precursor and NTR1 mRNAs had moderately high expression in the hypothalamic infundibulum. Further, in the hypothalamic infundibulum, the mRNA level of NT/LANT-6 precursor showed a trend toward increasing during postnatal development and increased 2.9-fold after a 48 hour fast, although the NTR1 mRNA level was not changed in both analyses. Contrary to our expectations, central administration of NT or LANT-6 had no effect on food intake in chicks.
    VL  - 3
    IS  - 3-2
    ER  - 

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