Case Report | Vol. 7, Issue 2 | Journal of Dermatology Research | Open Access |
Anna Bowling1*, Christina M Bear1, Joshua R Cook2, Lindsey A Bordone3
1Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA
2Diabetes and Endocrinology Research Center, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA
3Columbia University Irving Medical Center, Department of Dermatology, New York, NY, USA
*Correspondence author: Anna Bowling, BS, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA;
Email: [email protected]
Citation: Bowling A, et al. Psoriasis Remission in an Obese, Non-Diabetic Patient with Hyperinsulinemia Treated with GLP-1 Receptor Agonist Therapy. J Dermatol Res. 2026;7(2):1-5.
Copyright: © 2026 The Authors. Published by Athenaeum Scientific Publishers.
This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
License URL: https://creativecommons.org/licenses/by/4.0/
| Received 08 June, 2026 | Accepted 06 July, 2026 | Published 13 July, 2026 |
Psoriasis is a chronic immune-mediated inflammatory skin disease increasingly linked to metabolic dysfunction, including obesity and insulin resistance. While Glucagon-Like Peptide-1 (GLP-1) receptor agonists are approved for the treatment of type 2 diabetes mellitus and obesity, emerging evidence suggests they may also improve psoriasis, primarily in patients with diabetes. Their role in non-diabetic individuals remains unclear. We report a case of a 36-year-old man with obesity and chronic plaque psoriasis who achieved marked and reproducible disease improvement with semaglutide therapy despite normal glycemic indices. The patient had a history of psoriasis previously controlled on biologic therapy but sought alternative treatment due to concerns about long-term immunosuppression. Laboratory evaluation demonstrated hyperinsulinemia and features of metabolic syndrome in the absence of diabetes. Following initiation and titration of semaglutide, the patient experienced significant weight loss and near complete clearance of psoriatic plaques off of biologic therapy. Notably, psoriasis flared during periods of treatment interruption and improved again upon reinitiation of therapy, suggesting a reproducible pharmacologic effect. Reduction in fasting insulin levels paralleled clinical improvement, while glycemic parameters remained largely unchanged. This case highlights insulin resistance and metabolic inflammation as potentially modifiable drivers of psoriasis independent of glycemic control. GLP-1 receptor agonists may offer a novel therapeutic approach in select patients by addressing both metabolic dysfunction and cutaneous disease. Further investigation is warranted to define the mechanisms underlying these effects and to identify patient populations most likely to benefit.
Keywords: Psoriasis; Obesity; Metabolic syndrome; Hyperinsulinemia; Semaglutide; Glucagon-like Peptide-1 Receptor Agonist
TNF-α: Tumor Necrosis Factor Alpha; IL-6: Interleukin-6; T2DM: Type 2 Diabetes Mellitus; GLP-1: Glucagon-Like Peptide-1; SC: Subcutaneous; BSA: Body Surface Area; BMI: Body Mass Index; HbA1c: Hemoglobin A1c; HDL: High-Density Lipoprotein; LDL: Low-Density Lipoprotein; NF-κB: Nuclear Factor Kappa-Light-Chain-Enhancer of Activated B Cells
Psoriasis is a chronic immune-mediated inflammatory skin disease strongly influenced by metabolic dysfunction. Specifically, obesity has been suggested to exacerbate disease severity and impair treatment response through adipokine-driven inflammation, including elevations in Tumor Necrosis Factor Alpha (TNF-α) and Interleukin 6 (IL-6) [1]. Beyond adiposity, hyperinsulinemia and insulin resistance are increasingly recognized as contributors to psoriasis pathogenesis, even among euglycemic individuals who do not meet criteria for pre-diabetes or Type 2 Diabetes Mellitus (T2DM) [2,3]. Glucagon-Like Peptide-1 (GLP-1) receptor agonists are approved for diabetes and obesity treatment. Beyond their acute insulin-secretagogue effect, they reduce fasting hyperinsulinemia over time by improving insulin sensitivity through weight loss and its associated decrease in systemic inflammation [4-6]. All existing reports of psoriasis improvement with GLP-1 therapy are limited to patients with concurrent T2DM, leaving it unknown whether GLP-1 therapy can improve psoriasis through mechanisms independent of glycemic correction [7-9]. We present a case of plaque psoriasis in a patient with euglycemic obesity who achieved durable disease clearance on GLP-1 therapy, with reproducible flares upon interruption and resolution with reinitiation, suggesting a direct pharmacologic effect on psoriatic inflammation.
A 36-year-old man with a history of frontal fibrosing alopecia (treated with hydroxychloroquine), BRCA1 positivity and class I obesity presented for management of chronic plaque psoriasis. He had previously achieved clearance on Subcutaneous (SC) ustekinumab but lost access to this medication during the COVID-19 pandemic. On exam, psoriatic plaques covered ~30% of his Body Surface Area (BSA). Ustekinumab was restarted, leading to durable control (<5% BSA) for two years.
Although his psoriasis remained well-controlled on ustekinumab, the patient expressed concern about the long-term oncologic risk of biologic immunosuppression in the context of his BRCA1 positivity. Given his Body Mass Index (BMI) remained >30 kg/m2 and the biological plausibility of GLP-1 therapy as a non-immunomodulatory approach to psoriasis, the patient was referred to endocrinology for evaluation. Labs at that time showed normal fasting glucose (91 mg/dL) and Hemoglobin A1c (HbA1c) (5.4%) but suggested underlying insulin resistance, with fasting hyperinsulinemia (30.7 µIU/mL), hypertriglyceridemia (230 mg/dL) and low HDL cholesterol (36 mg/dL), consistent with metabolic syndrome. Two months of lifestyle modification did not result in weight loss and so semaglutide 0.25 mg SC was initiated and titrated to 1 mg weekly over the course of two months, resulting in loss of 11 kg (Fig. 1). Despite self-discontinuation of ustekinumab after one month on semaglutide, the patient exhibited sustained control of his psoriatic plaques to <5% BSA involvement for four months on weekly semaglutide treatment. Unfortunately, his psoriasis flared after regaining 2.25 kg (self-reported weights) during interruption of semaglutide treatment due to drug shortages, prompting the care team to prescribe a single dose of risankizumab 150 mg SC. After resumption and up-titration of semaglutide to the maximum dose of 2.4 mg SC weekly, the patient lost 6 kg and his skin cleared again without further biologic intervention. However, he then self-discontinued semaglutide a second time after rapid weight loss in the setting of bereavement associated hypophagia, causing a subjective psoriasis flare (reported in phone call to care team) after being off GLP-1 agonist therapy for ~four weeks. Once the patient’s appetite had returned to baseline, his skin flare was again mitigated by resumption of semaglutide at 0.5 mg SC weekly. He was able to titrate up to 2.4 mg SC weekly over the course of 3 months. Around this time, repeat labs were drawn, showing a marked reduction in his insulin level to 6 µIU/mL with minimal change in fasting glucose and HbA1c. His skin remained clear on semaglutide for 19 months after his last risankizumab injection.
Figure 1: Clinical timeline showing psoriasis disease course, metabolic parameters and treatment history in relation to GLP-1 therapy.
We present for the first time a case of durable psoriasis clearance in a euglycemic, insulin-resistant patient treated with semaglutide, with flares occurring only during treatment interruptions and resolving upon reinitiation. This repeated positive re-challenge represents strong observational evidence of a causal drug effect.
Obesity is a recognized risk factor for psoriasis severity and biologic treatment resistance, partly through adipokine-driven inflammation, including elevated TNF-α and IL-6 [1]. Separately, insulin resistance and its accompanying compensatory hyperinsulinemia may drive psoriatic inflammation through a distinct pathway, even in patients who remain euglycemic [2,3]. Patients with psoriasis are more insulin resistant than controls otherwise matched for age, sex, body mass index, body composition and glycemic parameters, even in the absence of overt diabetes [2]. Additionally, while directionality cannot be established in this case, prospective cohort data link insulin resistance to psoriasis incidence and severity, suggesting a complex relationship between metabolic and cutaneous inflammation [3]. Mechanistically, the hyperinsulinemia needed to overcome insulin resistance in order to maintain euglycemia may promote keratinocyte proliferation and amplify proinflammatory cytokine production. We are currently conducting an observational study of insulin signaling in psoriatic and non-lesional human skin to test this hypothesis (NCT06242847).
GLP-1 receptor agonists directly address both obesity and insulin resistance. Clinical trials of incretin-based treatments for obesity have shown improvements in indices of insulin sensitivity, including reduced hyperinsulinemia [4,5,10]. Prior reports of semaglutide treatment in psoriasis have been limited to patients with both obesity and T2DM, in whom improvements in skin severity may have been attributable primarily to improved glycemic control [7-9]. To our knowledge, this is the first reported case of reproducible semaglutide-associated psoriasis clearance in a euglycemic patient, in whom an 80% reduction in fasting insulin (from 30.7 to 6 µIU/mL) occurred without meaningful change in fasting glucose or HbA1c. This dissociation implicates insulin resistance and hyperinsulinemia, rather than glycemic correction, as relevant therapeutic targets, suggesting a novel mechanism for psoriasis treatment. Although semaglutide does not directly target the IL-23/IL-17 axis, the 19-month remission following a single risankizumab dose indicates that metabolic correction alone was sufficient to sustain disease control in this patient.
This case suggests that metabolic phenotyping, including fasting insulin and markers of insulin resistance, may identify a subset of patient with obesity-associated psoriasis who are candidates for GLP-1 therapy as an alternative or adjunct to immunomodulatory treatment. GLP-1 receptor agonists may offer a dual benefit in select patients, such as those with obesity, fasting hyperinsulinemia, metabolic syndrome features and psoriasis who either cannot tolerate or wish to avoid long-term biologic therapy. An industry-sponsored clinical trial of tirzepatide (NCT06588283) for psoriasis in obese patients without diabetes mellitus is currently underway. If this trial demonstrates efficacy of incretin-based treatment of obesity-associated psoriasis, much work will remain to define the mechanisms and specific patient subgroups that would most benefit from this therapeutic strategy. This case argues for routine metabolic phenotyping in psoriasis clinical trials and practice and raises the possibility that fasting insulin, rather than BMI or glycemic status alone, may be the most informative biomarker for identifying patients likely to benefit from incretin-based therapy.
The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.
This research did not receive any specific grant from funding agencies in the public, commercial or non-profit sectors.
The authors have no acknowledgments to declare.
The data supporting the findings of this study are available from the corresponding author upon reasonable request.
The project did not meet the definition of human subject research under the preview of the IRB according to federal regulations and therefore was exempt.
Informed consent was obtained from all participants included in the study.
All authors contributed equally to this paper.
Anna Bowling1*, Christina M Bear1, Joshua R Cook2, Lindsey A Bordone3
1Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA
2Diabetes and Endocrinology Research Center, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA
3Columbia University Irving Medical Center, Department of Dermatology, New York, NY, USA
*Correspondence author: Anna Bowling, BS, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA;
Email: [email protected]
Copyright: © 2026 The Authors. Published by Athenaeum Scientific Publishers.
This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
License URL: https://creativecommons.org/licenses/by/4.0/
Citation: Bowling A, et al. Psoriasis Remission in an Obese, Non-Diabetic Patient with Hyperinsulinemia Treated with GLP-1 Receptor Agonist Therapy. J Dermatol Res. 2026;7(2):1-5.
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