Alterations in Acylcarnitines, Amines, and Lipids Inform about the Mechanism of Action of Citalopram/Escitalopram in Major Depression
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Abstract
Abstract Selective serotonin reuptake inhibitors (SSRIs) are the first-line treatment for major depressive disorder (MDD), yet their mechanisms of action are not fully understood and their therapeutic benefit varies among individuals. We used a targeted metabolomics approach utilizing a panel of 180 metabolites to gain insights into mechanisms of action and response to citalopram/escitalopram. Plasma samples from 136 participants with MDD enrolled into the Mayo Pharmacogenomics Research Network Antidepressant Medication Pharmacogenomic Study (PGRN-AMPS) were profiled at baseline and after 8 weeks of treatment. After treatment, we saw increased levels of short-chain acylcarnitines and decreased levels of medium-chain and long-chain acylcarnitines, suggesting an SSRI effect on β-oxidation and mitochondrial function. Amines—including arginine, proline, and methionine sulfoxide—were upregulated while serotonin and sarcosine were downregulated, suggesting an SSRI effect on urea cycle, one-carbon metabolism, and serotonin uptake. Eighteen lipids within the phosphatidylcholine (PC aa and ae) classes were upregulated. Changes in several lipid and amine levels correlated with changes in 17-item Hamilton Rating Scale for Depression scores (HRSD 17 ). Differences in metabolic profiles at baseline and post-treatment were noted between participants who remitted (HRSD 17 ≤ 7) and those who gained no meaningful benefits (<30% reduction in HRSD 17 ). Remitters exhibited (a) higher baseline levels of C3, C5, alpha-aminoadipic acid, sarcosine, and serotonin; and (b) higher week-8 levels of PC aa C34:1, PC aa C34:2, PC aa C36:2, and PC aa C36:4. These findings suggest that mitochondrial energetics—including acylcarnitine metabolism, transport, and its link to β-oxidation—and lipid membrane remodeling may play roles in SSRI treatment response.
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Analyses of plasma lipid profile following citalopram and escitalopram administration reveal changes in several types of PC, including increases in PC (36:2), PC (30:0), PC (34:3), PC-O (34:2), PC-O (36:3), LPC (24:0), and SM (24:0) and decreases in PC (36:4), PC (38:6), LPC (20:4), and SM (18:1).
“Analyses of the plasma lipid profile following citalopram and escitalopram administration revealed changes in several types of PC, namely alkyl-PC, lysopPC, and SM (e.g., increases in PC (36:2), PC (30:0), PC (34:3), PC-O (34:2), PC-O (36:3), LPC (24:0), and SM (24:0) and decreases in PC (36:4), PC (38:6), LPC (20:4), and SM (18:1)) [157,158,159].”
From Lipids in Psychiatric Disorders: Functional and Potential Diagnostic Role as Blood Biomarkers (2024) · cites this paper as [159]
The increase in PC may be associated with an increase in the activity of membrane proteins such as carnitine palmitoyltransferase 1, which is involved in fatty acid beta-oxidation.
“In view of the fact that phosphatidylcholines are involved in membrane construction and remodeling, the increase in PC may be associated with an increase in the activity of membrane proteins, such as carnitine palmitoyltransferase 1, which is involved in fatty acid beta-oxidation [159].”
From Lipids in Psychiatric Disorders: Functional and Potential Diagnostic Role as Blood Biomarkers (2024) · cites this paper as [159]
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- Authors
- MahmoudianDehkordi, S., Ahmed, A. T., Bhattacharyya, S., Han, X., Baillie, R. A., Arnold, M., Skime, M. K., John-Williams, L. S., Moseley, M. A., Thompson, J. W., Louie, G., Riva-Posse, P., Craighead, W. E., McDonald, W., Krishnan, R., Rush, A. J., Frye, M. A., Dunlop, B. W., Weinshilboum, R. M., Kaddurah-Daouk, R., The Mood Disorders Precision Medicine Consortium (MDPMC), Kaddurah-Daouk, R., Rush, J., Tenenbaum, J., Moseley, A., Thompson, W., Louie, G., Blach, C., Mahmoudiandehkhordi, S., Baillie, R., Han, X., Bhattacharyya, S., Frye, M., Weinshilboum, R., Ahmed, A., Neavin, D., Liu, D., Skime, M., Rinaldo, P., Fiehn, O., Brydges, C., Mayberg, H., Choi, K. S., Cha, J., Kastenmüller, G., Arnold, M., Binder, E., Knauer-Arloth, J., Nevado-Holgado, A., Shi, L., Dunlop, B., Craighead, E., McDonald, W., Posse, P. R., Penninx, B., Milaneschi, Y., Jansen, R., & Krishnan, R.
- Affiliations
- Duke University (US)
- Mayo Clinic (US)
- Emory University (US)
- Duke Medical Center (US)
- University of California, Davis (US)
- Helmholtz Munich (DE)
- Max Planck Society (DE)
- University of Oxford (GB)
- University of Amsterdam (NL)
- ORCID
- MahmoudianDehkordi, Siamak
- Ahmed, Ahmed T.
- Baillie, Rebecca A.
- Craighead, W. Edward
- Rush, A. John
- Dunlop, Boadie W.
- Weinshilboum, Richard M.
- Tenenbaum, Jessica
- Blach, Colette
- Ahmed, Ahmed
- Neavin, Drew
- Liu, Duan
- Fiehn, Oliver
- Brydges, Christopher
- Mayberg, Helen
- Choi, Ki Sueng
- Cha, Jungho
- Kastenmüller, Gabi
- Binder, Elisabeth
- Shi, Liu
- Penninx, Brenda
- Milaneschi, Yuri
- Jansen, Rick
- Venue
- Translational Psychiatry
- Published
- 2021-03-02
- Volume
- 11
- Issue
- 1
- Pages
- 153-153
- ISSN
- 2158-3188 (ISSN-L)
- PMC
- PMC7925685
- OpenAlex
- W3135759638
- Cited by
- 95
- References
- 90
- Citations by year
- 2026: 13 · 2025: 21 · 2024: 20 · 2023: 14 · 2022: 17 · 2021: 10
- FWCI
- 9.04
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Translational Psychiatry (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion, other-oa)
- Pure Amsterdam UMC (submittedVersion, cc-by)
- MPG.PuRe (Max Planck Society) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Site cant be reached (submittedVersion, cc-by)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion, cc-by)
- ThinkTech (Texas Tech University) (submittedVersion, cc-by)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Mental Health (R01MH108348)
- U.S. Department of Health & Human Services | NIH | National Institute on Aging (R01AG046171, U01AG061359, RF1AG051550)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolomics and Mass Spectrometry Studies
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- citalopram, escitalopram, major depressive disorder, selective serotonin reuptake inhibitors, antidepressant response, acylcarnitines, short-chain acylcarnitines, fatty acid beta-oxidation, mitochondrial function, amines, methionine sulfoxide, urea cycle, one-carbon metabolism, phosphatidylcholine, serotonin, sarcosine, alpha-aminoadipic acid, plasma metabolomics
- MeSH terms
- Amines, Antidepressive Agents, Carnitine, Depression, Major Depressive Disorder, Humans, Lipids, Citalopram, Selective Serotonin Reuptake Inhibitors
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