Purpose: The eye is a rhythmic organ specifically evolved to function around the light cycle via functional circadian clocks. Diseases such as diabetes have been reported to disrupt circadian rhythms and circadian disruption emerges as an important factor in the prognosis of disease outcomes and treatment success. Herein we mapped the rhythmic transcriptome in the mouse retina to understand the extent of circadian disruption due to diabetes. Methods: Healthy control and Ins2Akita/J diabetic mice were kept under a physiological 12h:12h light-dark cycle until 4 months of age. Retinas were collected from 4-5 mice every 4 hrs around the day/night cycle. Deep mRNA sequencing was conducted and trascripts were identified. Computational approaches were used for detection of rhythmicity (empirical JTK_Cycle, emp p 1.2), acrophase prediction (Harmonic Regression with a set period of 24 hrs and normalization set to false), differential rhythmic patterns (DORD anlaysis BH corrected p < 0.05), phase set enrichment analysis (PSEA, BH corrected p-value < 0.01) and upstream regulator predictions (IPA, p<0.05). Animal studies were carried out at the institutional animal care facilities at the Indiana University School of Medicine in accordance with institutional and national guidelines for the care and use of laboratory animals (IACUC #10604 and #11167) Results: Almost 10% of the retinal transcriptome was identified as rhythmic with a clear 12hr axis of transcriptional activity, peaking at midday and midnight. Although the 12-hour transcriptional axis is retained in the diabetic retina, it was phase advanced by approximately 1-3 hours. Interestingly, only mild changes in the circadian rhythms were observed, as those were entrained by the light cycle. However, oxidative phosphorylation and HIF1A and NUPR1 were identified as the major upstream regulators for the phase shifts. An altered peak in daily glucose levels in diabetic mice may drive the phase shifts in the retina.  Conclusions: To our knowledge this is the first study mapping the effects of diabetes in the rhythmic output in the retina. Importantly, we identified that many of the daily rhythmicity in the retina is altered and the source of this shift is more related to abnormal metabolic adaptation rather than circadian disruption.