Association of antipsychotic drugs on type 2 diabetes mellitus risk in patients with schizophrenia: a population-based cohort and in vitro glucose homeostasis-related gene expression study.
Antipsychotic medications
Cohort study
Glucose homeostasis
Schizophrenia
Type 2 diabetes mellitus
Journal
BMC psychiatry
ISSN: 1471-244X
Titre abrégé: BMC Psychiatry
Pays: England
ID NLM: 100968559
Informations de publication
Date de publication:
30 Oct 2024
30 Oct 2024
Historique:
received:
22
07
2024
accepted:
25
10
2024
medline:
30
10
2024
pubmed:
30
10
2024
entrez:
30
10
2024
Statut:
epublish
Résumé
Type 2 diabetes mellitus (T2DM) and its related complications are associated with schizophrenia. However, the relationship between antipsychotic medications (APs) and T2DM risk remains unclear. In this population-based, retrospective cohort study across the country, we investigated schizophrenia and the effect of APs on the risk of T2DM, and glucose homeostasis-related gene expression. We used information from the Longitudinal Health Insurance Database of Taiwan for individuals newly diagnosed with schizophrenia (N = 4,606) and a disease-free control cohort (N = 4,606). The differences in rates of development of T2DM between the two cohorts were assessed using a Cox proportional hazards regression model. The effects of APs on the expression of glucose homeostasis-related genes in liver and muscle cell lines were assessed using quantitative real-time PCR. After controlling potential associated confounding factors, the risk of T2DM was higher in the case group than that in the control group [adjusted hazard ratio (aHR), 1.80, p < 0.001]. Moreover, the likelihood of T2DM incidence in patients with schizophrenia without AP treatment (aHR, 2.83) was significantly higher than that in non-schizophrenia controls and those treated with APs (aHR ≤ 0.60). In an in vitro model, most APs did not affect the expression of hepatic gluconeogenesis genes but upregulated those beneficial for glucose homeostasis in muscle cells. This study demonstrates the impact of schizophrenia and APs and the risk of developing T2DM in Asian populations. Unmeasured confounding risk factors for T2DM may not have been included in the study. These findings may help psychiatric practitioners identify patients at risk of developing T2DM.
Sections du résumé
BACKGROUND
BACKGROUND
Type 2 diabetes mellitus (T2DM) and its related complications are associated with schizophrenia. However, the relationship between antipsychotic medications (APs) and T2DM risk remains unclear. In this population-based, retrospective cohort study across the country, we investigated schizophrenia and the effect of APs on the risk of T2DM, and glucose homeostasis-related gene expression.
METHODS
METHODS
We used information from the Longitudinal Health Insurance Database of Taiwan for individuals newly diagnosed with schizophrenia (N = 4,606) and a disease-free control cohort (N = 4,606). The differences in rates of development of T2DM between the two cohorts were assessed using a Cox proportional hazards regression model. The effects of APs on the expression of glucose homeostasis-related genes in liver and muscle cell lines were assessed using quantitative real-time PCR.
RESULTS
RESULTS
After controlling potential associated confounding factors, the risk of T2DM was higher in the case group than that in the control group [adjusted hazard ratio (aHR), 1.80, p < 0.001]. Moreover, the likelihood of T2DM incidence in patients with schizophrenia without AP treatment (aHR, 2.83) was significantly higher than that in non-schizophrenia controls and those treated with APs (aHR ≤ 0.60). In an in vitro model, most APs did not affect the expression of hepatic gluconeogenesis genes but upregulated those beneficial for glucose homeostasis in muscle cells.
CONCLUSION
CONCLUSIONS
This study demonstrates the impact of schizophrenia and APs and the risk of developing T2DM in Asian populations. Unmeasured confounding risk factors for T2DM may not have been included in the study. These findings may help psychiatric practitioners identify patients at risk of developing T2DM.
Identifiants
pubmed: 39472855
doi: 10.1186/s12888-024-06222-z
pii: 10.1186/s12888-024-06222-z
doi:
Substances chimiques
Antipsychotic Agents
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
751Subventions
Organisme : Chang Bing Show Chwan Memorial Hospital
ID : SRD-112040
Organisme : Chang Bing Show Chwan Memorial Hospital
ID : SRD-112040
Organisme : Buddhist Tzu Chi Medical Foundation
ID : TTCRD113-30
Organisme : Buddhist Tzu Chi Medical Foundation
ID : TTCRD113-30
Organisme : Buddhist Tzu Chi Medical Foundation
ID : TTCRD113-30
Organisme : Buddhist Tzu Chi Medical Foundation
ID : TTCRD113-30
Organisme : China Medical University, Taiwan
ID : CMU112-MF-29
Organisme : China Medical University, Taiwan
ID : CMU112-MF-29
Organisme : China Medical University, Taiwan
ID : CMU112-MF-29
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST110-2320-B-039-016-MY3
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST110-2320-B-039-016-MY3
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST110-2320-B-039-016-MY3
Organisme : Taiwan Ministry of Health and Welfare Clinical Trial Center
ID : MOHW110-TDU-B-212-124004
Organisme : Taiwan Ministry of Health and Welfare Clinical Trial Center
ID : MOHW110-TDU-B-212-124004
Organisme : Taiwan Ministry of Health and Welfare Clinical Trial Center
ID : MOHW110-TDU-B-212-124004
Informations de copyright
© 2024. The Author(s).
Références
Diabetes. 1993 May;42(5):675-81
pubmed: 7683288
J Biol Chem. 2004 Nov 19;279(47):48941-9
pubmed: 15347677
World Psychiatry. 2014 Jun;13(2):176-83
pubmed: 24890070
Proc Natl Acad Sci U S A. 2005 Apr 26;102(17):6086-91
pubmed: 15837923
Schizophr Bull. 2013 Mar;39(2):295-305
pubmed: 22927670
Diabetes. 2009 Mar;58(3):579-89
pubmed: 19074989
Annu Rev Clin Psychol. 2008;4:189-216
pubmed: 18370616
Curr Diab Rep. 2016 Feb;16(2):16
pubmed: 26803652
Braz J Psychiatry. 2022 Nov 24;44(6):664-673
pubmed: 36709510
Front Psychiatry. 2018 Dec 05;9:622
pubmed: 30568606
Front Med (Lausanne). 2023 Jun 22;10:1137977
pubmed: 37425327
Mol Cell Biol. 2000 Jul;20(14):5343-9
pubmed: 10866690
Psychiatriki. 2018 Jan-Mar;29(1):64-73
pubmed: 29754122
J Psychopharmacol. 2010 Nov;24(4 Suppl):91-118
pubmed: 20923924
PLoS One. 2016 Nov 17;11(11):e0166429
pubmed: 27855222
J Diabetes Res. 2017;2017:1403206
pubmed: 29201918
Front Neurosci. 2015 Sep 03;9:297
pubmed: 26388714
Diabetologia. 2022 Mar;65(3):440-456
pubmed: 34841451
J Clin Endocrinol Metab. 1996 Apr;81(4):1552-6
pubmed: 8636366
Br J Psychiatry Suppl. 2004 Apr;47:S87-93
pubmed: 15056600
J Clin Psychopharmacol. 2022 Sep-Oct 01;42(5):440-444
pubmed: 35730552
Arch Gen Psychiatry. 2011 Jun;68(6):609-16
pubmed: 21300937
Biochem Biophys Res Commun. 1991 Dec 31;181(3):1419-24
pubmed: 1764093
Psychiatry Res. 2017 May;251:131-136
pubmed: 28199911
Ann Neurosci. 2016 Mar;23(1):3-5
pubmed: 27536015
JAMA Psychiatry. 2017 Mar 01;74(3):261-269
pubmed: 28097367
Int J Neuropsychopharmacol. 2023 Apr 17;26(4):249-258
pubmed: 36721972
Neuropsychiatr Dis Treat. 2021 Feb 11;17:453-469
pubmed: 33603382
Neuropsychopharmacology. 2010 Aug;35(9):1997-2004
pubmed: 20520598
Schizophr Res. 2011 Mar;126(1-3):110-6
pubmed: 21216567
Schizophr Bull. 2013 Mar;39(2):306-18
pubmed: 22207632
Diabetes. 2005 May;54(5):1552-8
pubmed: 15855345
JAMA Psychiatry. 2014 Dec 1;71(12):1350-63
pubmed: 25321337
Focus (Am Psychiatr Publ). 2020 Oct;18(4):482-492
pubmed: 33343261
Diabetes. 2001 Jun;50(6):1324-9
pubmed: 11375332
Br J Psychiatry. 2008 Jun;192(6):406-11
pubmed: 18515889
J Biosci. 2010 Sep;35(3):473-84
pubmed: 20826956
Am J Psychiatry. 2002 Apr;159(4):561-6
pubmed: 11925293
Lancet Psychiatry. 2015 May;2(5):431-451
pubmed: 26360287