Document Detail


Acute inflammation reduces kisspeptin immunoreactivity at the arcuate nucleus and decreases responsiveness to kisspeptin independently of its anorectic effects.
MedLine Citation:
PMID:  20407007     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Severe inflammatory challenges are frequently coupled to decreased food intake and disruption of reproductive function, the latter via deregulation of different signaling pathways that impinge onto GnRH neurons. Recently, the hypothalamic Kiss1 system, a major gatekeeper of GnRH function, was suggested as potential target for transmitting immune-mediated repression of the gonadotropic axis during acute inflammation, and yet key facets of such a phenomenon remain ill defined. Using lipopolysaccharide S (LPS)-treated male rats as model of inflammation, we document herein the pattern of hypothalamic kisspeptin immunoreactivity (IR) and hormonal responses to kisspeptin during the acute inflammatory phase. LPS injections induced a dramatic but transient drop of serum LH and testosterone levels. Suppression of gonadotropic function was associated with a significant decrease in kisspeptin-IR in the arcuate nucleus (ARC) that was not observed under conditions of metabolic stress induced by 48-h fasting. In addition, absolute responses to kisspeptin-10 (Kp-10), in terms of LH and testosterone secretion, were significantly attenuated in LPS-treated males that also displayed a decrease in food intake and body weight. Yet pair-fed males did not show similar alterations in LH and testosterone secretory responses to Kp-10, whose magnitude was preserved, if not augmented, during food restriction. In summary, our data document the impact of acute inflammation on kisspeptin content at the ARC as key center for the neuroendocrine control of reproduction. Our results also suggest that suppressed gonadotropic function following inflammatory challenges might involve a reduction in absolute responsiveness to kisspeptin that is independent of the anorectic effects of inflammation.
Authors:
J M Castellano; A H Bentsen; M Romero; R Pineda; F Ruiz-Pino; D Garcia-Galiano; M A Sánchez-Garrido; L Pinilla; J D Mikkelsen; M Tena-Sempere
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-20
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  299     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-14     Completed Date:  2010-07-14     Revised Date:  2010-12-09    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E54-61     Citation Subset:  IM    
Affiliation:
Department of Cell Biology, Physiology and Immunology, University of Córdoba, Avenida Menéndez Pidal s/n, Córdoba, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arcuate Nucleus / physiopathology*
Area Under Curve
Eating / physiology
Hypogonadism / physiopathology*
Immunohistochemistry
Inflammation / physiopathology*
Luteinizing Hormone / blood,  physiology*
Male
Oligopeptides / physiology*
Rats
Rats, Wistar
Testosterone / blood,  physiology*
Chemical
Reg. No./Substance:
0/KISS1 protein, human; 0/Oligopeptides; 58-22-0/Testosterone; 9002-67-9/Luteinizing Hormone

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