Impaired brain glucose consumption is a possible trigger of Alzheimer’s disease (AD). Animal models can help characterize each contributor to the cascade independently. Here we use the intracerebroventricular-streptozotocin rat model of AD in a first-time longitudinal study of white matter degeneration using diffusion MRI. Diffusion and kurtosis tensor metrics reveal alterations in the cingulum, fimbria and fornix. The two-compartment WMTI-Watson biophysical model further characterizes the cingulum damage as axonal injury and loss - consistent with previous histopathological studies. White matter degeneration induced by brain glucose metabolism disruption can bring further insight into the role of this mechanism in AD.