2026-07-01 | Association of Eosinophilic Esophagitis and Type 1 Diabetes: A Case Report

Association of Type 1 Diabetes Mellitus and Eosinophilic Esophagitis Introduction Eosinophilic esophagitis (EoE) is a rare chronic immune-mediated disorder characterized by eosinophilic infiltration of the esophageal mucosa. We report the case of a child with type 1 diabetes mellitus (T1DM) who presented with dysphagia and was subsequently diagnosed with EoE. Case Report An 11-year-old boy with a 6-year history of well-controlled type 1 diabetes mellitus on insulin therapy and known celiac disease managed with a gluten-free diet was admitted for progressive dysphagia. Symptoms initially involved solid foods and subsequently progressed to both solids and liquids over a one-month period. Physical examination revealed mild growth retardation (−1.5 SD) and conjunctival pallor. Upper gastrointestinal endoscopy demonstrated ulcerative esophagitis extending over 5 cm. Histopathological examination of esophageal biopsies confirmed eosinophilic esophagitis. Duodenal biopsies showed subtotal villous atrophy consistent with celiac disease. The patient was treated with proton pump inhibitors (PPIs) and topical corticosteroid therapy. Due to the unavailability of commercially prepared topical budesonide formulations (oral viscous suspension or spray), an alternative preparation combining injectable budesonide with stevia was administered. A marked clinical improvement was observed within 48 hours. Discussion The coexistence of eosinophilic esophagitis and type1 diabetes mellitus is uncommon. Previous studies have reported a predominance among male patients. Diagnosis relies on upper gastrointestinal endoscopy with systematic esophageal biopsies. The current standard treatment consists of proton pump inhibitors combined with topical corticosteroids. Conclusion Eosinophilic esophagitis remains a rare condition with incompletely understood pathogenesis and natural history. It may present with a wide spectrum of gastrointestinal symptoms and has been associated with connective tissue disorders and several autoimmune diseases. However, its association with type 1 diabetes mellitus remains exceptionally rare.

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2026-06-22 | β-Hydroxybutyrate Improves Glucose Metabolism in Streptozotocin-Induced Type 1 Diabetes by Inhibiting Gut and Liver Glucose Transporters via GPR109A.

Ketone bodies, particularly β-hydroxybutyrate (3HB), are often elevated in type 1 diabetes (T1D); however, their physiological roles remain unclear. In a low-carbohydrate diet study, patients with insulin-deficient diabetes exhibited reduced fasting blood glucose and increased fasting blood ketone levels, negatively correlated. Another clinical study using continuous glucose and ketone monitoring confirmed inverse glucose-ketone fluctuations. To test causality, we conducted animal and cellular studies. In streptozotocin-induced T1D mice, 7-week oral 3HB administration improved glucose metabolism and alleviated glycogenic hepatopathy. Imaging with 2-deoxy-2-[18F]-fluoro-d-glucose positron emission tomography/computed tomography demonstrated reduced hepatic and intestinal glucose uptake. Western blotting confirmed 3HB suppressed glucose transporter (sodium-glucose cotransporter 1, GLUT2, GLUT5) overexpression and normalized glycogen metabolism. In vitro, 3HB dose-dependently inhibited glucose transporter expression and glucose uptake in primary hepatocytes and IEC-6 cells. G protein-coupled receptor 109A (GPR109A) serves as the primary receptor for 3HB. Mechanistic studies using the GPR109A inhibitor mepenzolate bromide, the mTOR inhibitor rapamycin, and siRNA-mediated gene silencing revealed that these effects were GPR109A dependent and linked to inhibition of the PI3K/AKT/mTOR pathway. Overall, this study provides new insights into the role of ketone bodies in T1D, establishing 3HB as a modulator of glucose homeostasis through GPR109A-mediated suppression of glucose transporters in the liver and intestine.

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2026-06-08 | DIABETES MELLITUS IN WOLFRAM SYNDROME 1: CHARACTERISTICS AND PERSPECTIVES IN TREATMENT

Wolfram syndrome 1 is a rare autosomal recessive disorder caused by mutations in the WFS1 gene related to endoplasmic reticulum (ER) function. The course of the disease most often begins with diagnosis of insulin-dependent non-autoimmune diabetes mellitus with an early onset. Its clinical character is presented with an acronym DIDMOAD: diabetes insipidus (DI), diabetes mellitus (DM), optic atrophy (OA) and deafness (D). This article focuses on the clinical features of diabetes mellitus in Wolfram syndrome. We also describe current approach to its therapy and discuss possible treatment options placing the main emphasis on the GLP1 receptor agonists and cell regenerative therapy. Methods and materials: A qualitative synthesis of the data focusing on GLP-1 agonists, cell regenerative therapy and diabetes mellitus in Wolfram syndrome was performed. This literature review of GLP-1 receptor agonists and cell regenerative therapy effect on metabolic control, and current perspectives of treatment in patients with Wolfram syndrome, a monogenic type of diabetes, included recent publications, primarily from the past 10 years, and was conducted from November 2025 to April 2026 using the PubMed database. A systematic search was performed using specific keywords and medical subject headings (MeSH terms) related to GLP-1 agonists and Wolfram syndrome. The primary search terms included: “diabetes mellitus”, “GLP-1 agonists”, “Wolfram syndrome”, “WFS1”, “monogenic diabetes”, “islet transplantation”, and “cell regenerative therapy”. The criteria for inclusion of articles were as follows: published before April 2026, written in English, peer-reviewed original research articles. Exclusion criteria included publications not available in full text, articles in languages other than English. Editorials, commentaries, and conference abstracts without full data were also excluded. Titles and abstracts of the retrieved articles were screened to determine eligibility based on the inclusion and exclusion criteria.

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