Diabetic retinopathy (DR) is one of the most feared complications of diabetes and a leading cause of visual impairment. One of the common causes of vision loss with DR is diabetic macular edema (DME), characterised by swelling within the central macula. Müller cells, specialised macroglia within the retina, regulate ions and subsequent water movement via the inwardly rectifying potassium channel 4.1 (Kir4.1) and aquaporin 4 (AQP4). Here, we evaluated the role of Müller cells in the development of swelling in a mouse model of type I diabetes. Müller cell-specific nestin-cre transgenic mice were rendered diabetic after injection of streptozotocin (STZ group, n = 6, 50 mg/kg, blood glucose: >15mmol/L) or citrate buffer (control group, n = 6). Following 12 weeks of diabetes, retinas were imaged, and Müller cell volume was quantified using Imaris. Changes in the gene expression of Kcnj10 (Kir4.1) and Aqp4 were quantified using qPCR. The effect of BaCl₂ (100 μmol/l), VU0134992 (2 μmol/l) and inflammatory mediators on Müller cell volume was also quantified using ex vivo retinal explants. We observed a significantly increased soma volume in the retinae of 12-week STZ mice compared to the control groups, however, gene expressions of Kcnj10 and Aqp4 were unchanged. An increase in Müller cell soma volume was observed in ex vivo retinas incubated with BaCl₂, VU0134992, and inflammatory molecules, including LPS and TNF-α. These results suggest that diabetes is associated with increased swelling of Müller cells and that inflammatory mediators may be important regulators of this effect.