These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Melatonin treatment alters glucosensing capacity and mRNA expression levels of peptides related to food intake control in rainbow trout hypothalamus.
    Author: Conde-Sieira M, Librán-Pérez M, López Patiño MA, Soengas JL, Míguez JM.
    Journal: Gen Comp Endocrinol; 2012 Aug 01; 178(1):131-8. PubMed ID: 22569117.
    Abstract:
    As demonstrated in previous studies, the functioning of brain glucosensing systems in rainbow trout is altered under stress conditions in a way that they are unable to respond properly to changes in glucose levels. Melatonin has been postulated as necessary for homeostatic control of energy metabolism in several vertebrate groups, and in fish it has been suggested as an anti-stress molecule. To evaluate the possible effects of melatonin on glucosensing, we have incubated hypothalamus and hindbrains of rainbow trout at different glucose concentrations in the presence of increased doses (0.01, 1, and 100nM) of melatonin assessing whether or not the responses to changes in glucose levels of parameters related to glucosensing (glucose, glycogen and glucose 6-phosphate levels, activities of GK, GSase and PK, and mRNA content of GK, GLUT2, Kir6.x-like, and SUR-like) are modified in the presence of melatonin. While no effects of melatonin were observed in hindbrain, in hypothalamus melatonin treatment up-regulated glucosensing parameters, especially under hypo- and normo-glycaemic conditions. The effects of melatonin in hypothalamus occurred apparently through MT(1) receptors since most effects were counteracted by the presence of luzindole but not by the presence of 4-P-PDOT. Moreover, melatonin treatment induced in hypothalamus increased mRNA expression levels of NPY and decreased mRNA levels of POMC, CART, and CRF. A role of the hormone in daily re-adjustment of hypothalamic glucosensor machinery is discussed.
    [Abstract] [Full Text] [Related] [New Search]