Intracerebroventricular administration of C-type natriuretic peptide suppresses food intake via activation of the melanocortin system in mice

Nobuko Goto, Goro Katsuura, Ken Ebihara, Megumi Inuzuka, Yukari Ochi, Yui Yamashita, Toru Kusakabe, Akihiro Yasoda, Noriko Satoh-Asahara, Hiroyuki Ariyasu, Kiminori Hosoda, Kazuwa Nakao

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

C-type natriuretic peptide (CNP) and its receptor are abundantly distributed in the brain, especially in the arcuate nucleus (ARC) of the hypothalamus associated with regulating energy homeostasis. To elucidate the possible involvement of CNP in energy regulation, we examined the effects of intracerebroventricular administration of CNP on food intake in mice. The intracerebroventricular administration of CNP-22 and CNP-53 significantly suppressed food intake on 4-h refeeding after 48-h fasting. Next, intracerebroventricular administration of CNP-22 and CNP-53 significantly decreased nocturnal food intake. The increment of food intake induced by neuropeptide Y and ghrelin was markedly suppressed by intracerebroventricular administration of CNP-22 and CNP-53. When SHU9119, an antagonist for melanocortin-3 and melanocortin-4 receptors, was coadministered with CNP-53, the suppressive effect of CNP-53 on refeeding after 48-h fasting was significantly attenuated by SHU9119. Immunohistochemical analysis revealed that intracerebroventricular administration of CNP-53 markedly increased the number of c-Fos - positive cells in the ARC, paraventricular nucleus, dorsomedial hypothalamus, ventromedial hypothalamic nucleus, and lateral hypothalamus. In particular, c-Fos-positive cells in the ARC after intracerebroventricular administration of CNP-53 were coexpressed with α-melanocyte-stimulating hormone immunoreactivity. These results indicated that intracerebroventricular administration of CNP induces an anorexigenic action, in part, via activation of the melanocortin system.

Original languageEnglish
Pages (from-to)1500-1504
Number of pages5
JournalDiabetes
Volume62
Issue number5
DOIs
Publication statusPublished - 2013 May 1
Externally publishedYes

Fingerprint

C-Type Natriuretic Peptide
Melanocortins
Eating
Arcuate Nucleus of Hypothalamus
Fasting
Ventromedial Hypothalamic Nucleus
Receptor, Melanocortin, Type 4
Lateral Hypothalamic Area
Melanocyte-Stimulating Hormones
Ghrelin
Paraventricular Hypothalamic Nucleus
Neuropeptide Y

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Intracerebroventricular administration of C-type natriuretic peptide suppresses food intake via activation of the melanocortin system in mice. / Goto, Nobuko; Katsuura, Goro; Ebihara, Ken; Inuzuka, Megumi; Ochi, Yukari; Yamashita, Yui; Kusakabe, Toru; Yasoda, Akihiro; Satoh-Asahara, Noriko; Ariyasu, Hiroyuki; Hosoda, Kiminori; Nakao, Kazuwa.

In: Diabetes, Vol. 62, No. 5, 01.05.2013, p. 1500-1504.

Research output: Contribution to journalArticle

Goto, N, Katsuura, G, Ebihara, K, Inuzuka, M, Ochi, Y, Yamashita, Y, Kusakabe, T, Yasoda, A, Satoh-Asahara, N, Ariyasu, H, Hosoda, K & Nakao, K 2013, 'Intracerebroventricular administration of C-type natriuretic peptide suppresses food intake via activation of the melanocortin system in mice', Diabetes, vol. 62, no. 5, pp. 1500-1504. https://doi.org/10.2337/db12-0718
Goto, Nobuko ; Katsuura, Goro ; Ebihara, Ken ; Inuzuka, Megumi ; Ochi, Yukari ; Yamashita, Yui ; Kusakabe, Toru ; Yasoda, Akihiro ; Satoh-Asahara, Noriko ; Ariyasu, Hiroyuki ; Hosoda, Kiminori ; Nakao, Kazuwa. / Intracerebroventricular administration of C-type natriuretic peptide suppresses food intake via activation of the melanocortin system in mice. In: Diabetes. 2013 ; Vol. 62, No. 5. pp. 1500-1504.
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AU - Ochi, Yukari

AU - Yamashita, Yui

AU - Kusakabe, Toru

AU - Yasoda, Akihiro

AU - Satoh-Asahara, Noriko

AU - Ariyasu, Hiroyuki

AU - Hosoda, Kiminori

AU - Nakao, Kazuwa

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AB - C-type natriuretic peptide (CNP) and its receptor are abundantly distributed in the brain, especially in the arcuate nucleus (ARC) of the hypothalamus associated with regulating energy homeostasis. To elucidate the possible involvement of CNP in energy regulation, we examined the effects of intracerebroventricular administration of CNP on food intake in mice. The intracerebroventricular administration of CNP-22 and CNP-53 significantly suppressed food intake on 4-h refeeding after 48-h fasting. Next, intracerebroventricular administration of CNP-22 and CNP-53 significantly decreased nocturnal food intake. The increment of food intake induced by neuropeptide Y and ghrelin was markedly suppressed by intracerebroventricular administration of CNP-22 and CNP-53. When SHU9119, an antagonist for melanocortin-3 and melanocortin-4 receptors, was coadministered with CNP-53, the suppressive effect of CNP-53 on refeeding after 48-h fasting was significantly attenuated by SHU9119. Immunohistochemical analysis revealed that intracerebroventricular administration of CNP-53 markedly increased the number of c-Fos - positive cells in the ARC, paraventricular nucleus, dorsomedial hypothalamus, ventromedial hypothalamic nucleus, and lateral hypothalamus. In particular, c-Fos-positive cells in the ARC after intracerebroventricular administration of CNP-53 were coexpressed with α-melanocyte-stimulating hormone immunoreactivity. These results indicated that intracerebroventricular administration of CNP induces an anorexigenic action, in part, via activation of the melanocortin system.

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