The effect of betahistine, a histamine H1 receptor agonist/H3 antagonist, on olanzapine-induced weight gain in first-episode schizophrenia patients

2005 ◽  
Vol 20 (2) ◽  
pp. 101-103 ◽  
Author(s):  
Michael Poyurovsky ◽  
Artashes Pashinian ◽  
Aya Levi ◽  
Ronit Weizman ◽  
Abraham Weizman
Endocrinology ◽  
2014 ◽  
Vol 155 (12) ◽  
pp. 4895-4904 ◽  
Author(s):  
Meng He ◽  
Qingsheng Zhang ◽  
Chao Deng ◽  
Hongqin Wang ◽  
Xu-Feng Huang

Weight gain and its related metabolic disorders are major side effects associated with second generation antipsychotic drug treatment. The dorsal vagal complex (DVC) and AMP-activated protein kinase (AMPK) are implicated in the regulation of food intake and body weight. Blocking the histamine H1 receptor contributes to antipsychotic-induced weight gain. The present study investigated the time-dependent effect of olanzapine treatment (8, 16, and 36 d) on DVC AMPK signaling in olanzapine-induced weight gain and whether these changes are associated with olanzapine-induced H1 receptor antagonism. During the 8-day olanzapine treatment, the rats were hyperphagic and rapidly gained weight. The phosphorylation of AMPK (pAMPK) (activated AMPK) as well as its directly downstream phospho-acetyl-coenzyme A carboxylase was significantly increased. The pAMPK/AMPK ratio, an indicator of AMPK activity, was significantly positively correlated with feeding efficiency and weight gain. As treatment was prolonged (16 and 36 d of olanzapine treatment), the rats were no longer hyperphagic, and there were no longer any changes in DVC AMPK signaling. Although the DVC H1 receptor protein expression was not significantly altered by olanzapine, the pAMPK expression was significantly positively correlated with the H1 receptor level after the 8-, 16-, and 36-day olanzapine treatments. Moreover, we showed that an H1 receptor agonist, 2-(3-trifluoromethylphenyl) histamine, significantly inhibited the olanzapine-induced hyperphagia and DVC AMPK activation in a dose-dependent manner. These results suggest a time-dependent role of DVC AMPK in olanzapine-induced obesity. Thus, olanzapine-induced DVC AMPK activation may be at least partially related to olanzapine’s antagonistic effect on the H1 receptor.


2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S114-S115
Author(s):  
Stéfan Du Plessis ◽  
Hilmar Luckhoff ◽  
Sanja Kilian ◽  
Laila Asmal ◽  
Frederika Scheffler ◽  
...  

Abstract Background In this study, we explored the relationship between hippocampal subfield volumes and change in body mass over 12 months of treatment in 90 first-episode schizophrenia spectrum disorder patients (66 males, 24 females; mean age= 24.7±6.8 years). Methods Body mass index was assessed in patients at baseline, and at months 3, 6, 9 and 12. Hippocampal subfields of interest were assessed using a segmentation algorithm included in the FreeSurfer 6.0 software program. Results Linear regression analysis showed a significant interactive effect between sex and anterior hippocampus size as a predictor of change in body mass over 12 months, adjusting for age, substance use, treatment duration, and posterior hippocampal volumes. In an exploratory sub-analysis, partial correlations revealed a significant association between weight gain and smaller CA1, CA3 and subiculum volumes in females, but not males, adjusting for age and substance use, with similar trends evident for the CA4 and presubiculum subfields. Discussion In conclusion, our findings suggest that smaller anterior hippocampal subfields are associated with the development of weight gain over the course of treatment in first-episode schizophrenia spectrum disorders in a sex-specific fashion, and may partly explain the more severe and ongoing increase in body mass evident for female patients.


Author(s):  
Emad Khalilzadeh ◽  
Farzin Azarpey ◽  
Reza Hazrati

ABSTRACTObjective: In this study, the effect of different classes of histamine H receptor antagonists (chlorpheniramine, cetirizine, and fexofenadine), µopioid receptor agonist (morphine), and opioid receptor antagonist (naloxone) in separate and combined treatments were investigated on the acutetrigeminal model of pain in rats.1Methods: Eye wiping test used for induction of acute trigeminal pain by putting a drop of NaCl, 5 M solution (40 µl) on the corneal surface of the eye,and the number of eye wipes counted during the first 30 seconds.Results: Intraperitoneal injection of both chlorpheniramine and cetirizine at doses of 10 and 20 mg/kg significantly inhibited the acute trigeminal pain.However, fexofenadine did not change corneal pain response. Morphine at doses of 1.25, 2.5, and 5 mg/kg reduced eye wipe responses. Administrationof both chlorpheniramine and cetirizine but not fexofenadine before morphine-enhanced morphine analgesic activity, also pretreatment of animalswith naloxone inhibited morphine, chlorpheniramine, and cetirizine-induced analgesia in the acute corneal pain.Conclusion: Our results showed that chlorpheniramine as a histamine H antagonist that efficiently Penetrates blood-brain barrier (BBB) andcetirizine with less penetration of BBB but not fexofenadine (an H11 receptor antagonist with a negligible brain-accessibility) could induce analgesiain the acute corneal pain via opioidergic mechanism. Coadministration of morphine with chlorpheniramine or cetirizine could enhance its analgesicactivity in the acute trigeminal model of pain in rats.Keywords: Trigeminal pain, Morphine, Histamine H1 receptor antagonists, Naloxone, Rats.


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