Type 2 diabetes (T2D) is an epidemic that is a leading cause of disease or damage to the kidneys in the United States. Renal complications of T2D diabetes include proteinuria and suboptimal 25-hydroxycholecalciferol (25D) concentrations in the blood. 25D is the major circulating form of vitamin D and can be converted to 1,25-dihydroxycholecalciferol (1,25D), the active form of vitamin D. Absorption factors in the kidneys determine whether 25D can be activated to 1,25D or returned to circulation. In this study, we utilized Zucker diabetic fatty rats, a model of obesity-related T2D, to determine whether feeding resistant starch (RS) could prevent loss of vitamin D and maintain 25D concentrations in the blood. Non-diabetic control rats were fed a cornstarch control diet and diabetic fatty rats were fed either the control diet or one in which cornstarch was replaced with RS for 6 weeks. RS reduced hyperglycemia by 41% and prevented urinary excretion of vitamin D binding protein and albumin, which were elevated in control diet-fed diabetic fatty rats. Additionally, urinary excretion of 25D and 1,25D was higher and 25D concentrations in the blood were lower in diabetic fatty rats fed the control diet compared to those on RS diet. These data provide evidence that suggests vitamin D balance is dependent on the absence of proteinuria, which can be prevented by dietary RS in T2D independent of vitamin D supplementation