Evidence map›Paper›PMID 36168413›Full record

ArticleExperimental and therapeutic medicine2022

Olanzapine enhances adipogenesis and suppresses lipolysis in 3T3‑L1 adipocytes under low‑glucose and weak differentiation/maturation conditions.

Taisuke Matsuo, Yuzuki Omori, Takashi Tomita, Yasuyuki Sadzuka

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Pharmaceuticals (Basel, Switzerland) · 2026
    Article
  2. Article
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

4 authors.

Taisuke MatsuoDivision of Advanced Pharmaceutics, Department of Clinical Pharmaceutical Sciences, School of Pharmacy, Iwate Medical University, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.
Yuzuki OmoriDivision of Advanced Pharmaceutics, Department of Clinical Pharmaceutical Sciences, School of Pharmacy, Iwate Medical University, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.
Takashi TomitaDepartment of Pharmaceutical Sciences, Faculty of Pharmaceutical Sciences, Teikyo Heisei University, Nakano-ku, Tokyo 164-8530, Japan.
Yasuyuki SadzukaDivision of Advanced Pharmaceutics, Department of Clinical Pharmaceutical Sciences, School of Pharmacy, Iwate Medical University, Yahaba-cho, Shiwa-gun, Iwate 028-3694, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Olanzapine, a second-generation antipsychotic used in the treatment of schizophrenia, is classified as a multi-acting receptor-targeted antipsychotic. Abnormal weight gain is one of the most common side effects of this drug, along with an increased appetite and food intake. However, weight gain has also been reported in patients taking olanzapine without an increase in appetite. Olanzapine has been reported to be directly associated with enhanced adipogenesis; however, whether olanzapine increases lipid content in adipocytes under weak stimulus conditions, such as low glucose concentrations and weak differentiation and/or maturation conditions, is poorly understood. The present study examined the stimulatory effect of olanzapine during the differentiation and maturation of 3T3-L1 pre-adipocytes under low-glucose and weak stimulation conditions by evaluating the expression levels of PPARγ by western blotting and oil red O staining. Western blotting revealed that olanzapine suppressed perilipin phosphorylation, which is an important lipolysis step in adipocytes. The findings of the present study provide novel insights to explain weight gain in patients taking olanzapine but not presenting with increased food intake.

Indexed as

3T3-L1 cellsadipogenesisglucose concentrationlipolysisolanzapineperilipin

Identifiers

PMID36168413
PMCPMC9475343

What OpenQuestion holds

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Registered trials

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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.