Evidence map›Paper›PMID 23640535›Full record

ReviewCNS drugs2013

The role of hypothalamic H1 receptor antagonism in antipsychotic-induced weight gain.

Meng He, Chao Deng, Xu-Feng Huang

Abstract readReview
PubMed Publisher
In one paragraph

Review in CNS drugs, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 4 pooled it
5.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 4 syntheses or guidelines pooled it, 118 citations in OpenAlex.

  1. Pooled it
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  5. Trial
  6. Trial
  7. Article
  8. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  9. Article
  10. Review
  11. Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026
    Review
  12. Mirtazapine revisited: new therapeutic perspectives and formulation advances.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Mechanism and treatments of antipsychotic-induced weight gain.International journal of obesity (2005) · 2023
    Review
  18. Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Meng HeCentre for Translational Neuroscience, School of Health Sciences, 32.305, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW 2522, Australia.
Chao Deng
Xu-Feng Huang
Illawarra Health and Medical Research Institute · AUSchizophrenia Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment with second generation antipsychotics (SGAs), notably olanzapine and clozapine, causes severe obesity side effects. Antagonism of histamine H1 receptors has been identified as a main cause of SGA-induced obesity, but the molecular mechanisms associated with this antagonism in different stages of SGA-induced weight gain remain unclear. This review aims to explore the potential role of hypothalamic histamine H1 receptors in different stages of SGA-induced weight gain/obesity and the molecular pathways related to SGA-induced antagonism of these receptors. Initial data have demonstrated the importance of hypothalamic H1 receptors in both short- and long-term SGA-induced obesity. Blocking hypothalamic H1 receptors by SGAs activates AMP-activated protein kinase (AMPK), a well-known feeding regulator. During short-term treatment, hypothalamic H1 receptor antagonism by SGAs may activate the AMPK-carnitine palmitoyltransferase 1 signaling to rapidly increase caloric intake and result in weight gain. During long-term SGA treatment, hypothalamic H1 receptor antagonism can reduce thermogenesis, possibly by inhibiting the sympathetic outflows to the brainstem rostral raphe pallidus and rostral ventrolateral medulla, therefore decreasing brown adipose tissue thermogenesis. Additionally, blocking of hypothalamic H1 receptors by SGAs may also contribute to fat accumulation by decreasing lipolysis but increasing lipogenesis in white adipose tissue. In summary, antagonism of hypothalamic H1 receptors by SGAs may time-dependently affect the hypothalamus-brainstem circuits to cause weight gain by stimulating appetite and fat accumulation but reducing energy expenditure. The H1 receptor and its downstream signaling molecules could be valuable targets for the design of new compounds for treating SGA-induced weight gain/obesity.

Indexed as

AnimalsAntipsychotic AgentsBenzodiazepinesClozapineHistamine H1 AntagonistsHumansHypothalamusObesityOlanzapineReceptors, Histamine H1Weight GainAntipsychotic AgentsBenzodiazepinesClozapineHistamine H1 AntagonistsOlanzapineReceptors, Histamine H1

Identifiers

PMID23640535
OpenAlexW2011700097

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.