Show/Hide Menu
Hide/Show Apps
anonymousUser
Logout
Türkçe
Türkçe
Search
Search
Login
Login
OpenMETU
OpenMETU
About
About
Open Science Policy
Open Science Policy
Frequently Asked Questions
Frequently Asked Questions
Communities & Collections
Communities & Collections
Dysregulation of hypothalamic modulation in olanzapine treated male rats
Date
2016-11-03
Author
Sezlev-Bilecen, Deniz
AK, MEHMET
Yanık, Tülin
Metadata
Show full item record
This work is licensed under a
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License
.
Item Usage Stats
9
views
0
downloads
The mechanism of weight gain through application of olanzapine, a serotonin and dopamine receptor antagonist has not been fully understood. Weight gain and food intake are under the control of various neurohormones; POMC (proopiomelanocortin), CART (cocaine and amphetamine regulated transcript), AgRP (Agouti-related peptide) and NPY (neuropeptide Y) that are majorly synthesized and secreted from the arcuate nucleus (ARC) of hypothalamus. In this study, the alteration of the ARC neurohormone levels in rats were determined as one of the weight gain mechanisms. To understand the underlying mechanism of olanzapine-induced weight gain, the drug was orally administrated to healthy male Wistar rats for analysis of both the hypothalamic gene expression and peripheral levels of those candidate neuropeptides. In rats hypothalamic mRNA levels of NPY, AgRP and POMC decreased while CART levels did not show any alteration. Consistently, circulating levels of NPY, AgRP and alpha-MSH decreased significantly yet CART levels were also reduced. In conclusion, it may be presumed that the antagonistic effect of olanzapine on the ARC neurons might be the onset for a dysregulation of the neurohormones secretion which may cause weight gain during treatment.
Subject Keywords
Biological Psychiatry
,
Pharmacology
URI
https://hdl.handle.net/11511/38621
Journal
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
DOI
https://doi.org/10.1016/j.pnpbp.2016.06.012
Collections
Department of Biology, Article