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Ketamine in Diabetes Care: Metabolic Insights and Clinical Applications.

Shiryn D. Sukhram, Majandra Sanchez, Ayotunde Anidugbe, Bora Kupa, Vincent P Edwards, Muhammad Zia, Grozdena Yilmaz

Pharmaceutics January 8, 2026 DOI: 10.3390/pharmaceutics18010081 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Scoping review Randomized Peer reviewed
Sample size 11
Population Human and animal studies evaluating ketamine, esketamine, or norketamine in the context of diabetes or diabetic neuropathy
Topics Esketamine Ketamine
Keywords Cyp2b6 Cyp3a4 Pk-pd Diabetes mellitus Diabetic neuropathy Exposure–response Model-informed precision dosing Population pharmacokinetics
Key findings Short-term improvements were reported for treatment-resistant depression and neuropathic pain, but glycemic effects varied and drug-disease-drug interactions remain insufficiently studied.

Abstract

Background: Depression and diabetic neuropathy (DN) commonly complicate diabetes and impair glycemic control and quality of life. Ketamine and its S-enantiomer, esketamine, provide rapid antidepressant and analgesic effects, yet diabetes-related pathophysiology and co-therapies may modify exposure, response, and safety.

Methods: We conducted a scoping review following PRISMA-ScR. MEDLINE/PubMed, CINAHL, and APA PsycInfo were searched (January 2020-31 May 2025). Eligible human and animal studies evaluated ketamine, esketamine, or norketamine in the context of diabetes (type 1 [T1DM], type 2 [T2DM], gestational [GDM]), or DN, and reported psychiatric, analgesic, metabolic, or mechanistic outcomes. Two reviewers independently screened and charted data; no formal risk-of-bias assessment was performed.

Results: Eleven studies met inclusion criteria: four human case reports/series (three T1DM, one T2DM), one randomized trial in GDM, two narrative reviews of topical ketamine for DN, and four preclinical rodent studies using streptozotocin- or diet-induced diabetes models. Short-term improvements were reported for treatment-resistant depression and neuropathic pain, including opioid-sparing postoperative analgesia in GDM. Glycemic effects varied across settings, with both hyperglycemia and hypoglycemia reported. Mechanistic and clinical drug-drug and drug-disease interactions (particularly involving metformin, GLP-1 receptor agonists, SGLT2 inhibitors, and CYP3A4/CYP2B6 modulators) remain insufficiently studied. We outline a forward-looking population pharmacokinetic (popPK) and pharmacokinetic-pharmacodynamic (PK-PD) research agenda, including priority covariates (eGFR, hepatic function, inflammatory status, HbA1c, genotype, co-medications) and sparse-sampling windows for future model-informed precision dosing.

Conclusions: Current evidence supports cautious, selective use of ketamine for refractory depression and DN within multidisciplinary diabetes care. Purpose-built popPK/PK-PD studies in both human and preclinical diabetic models cohorts are needed to quantify variability, define drug-disease-drug interactions and glycemic risk, and inform individualized dosing strategies.

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