Dietary resistant starch prevents urinary excretion of vitamin D metabolites and restores circulating 25‐hydroxycholecalciferol concentrations in the Zucker diabetic fatty rat (1041.3)

Abstract

Type 2 diabetes (T2D) is an epidemic that leads to renal disease if left untreated. Compromised renal function has been implicated in vitamin D deficiency as the renal proximal tubule maintains circulating 25‐hydroxycholecalciferol (25D) concentrations as well as its activation to 1,25‐dihydroxycholecalciferol (1,25D). We previously showed that feeding high‐amylose maize that is partially resistant to digestion (RS) prevented excretion of 25D‐vitamin D‐binding protein (DBP) and albumin in T1D rats. Here, we utilized Zucker diabetic fatty rats (ZDF) to determine whether dietary RS could prevent excessive excretion of vitamin D metabolites and maintain serum 25D level. Lean control Zucker (n=8) rats were fed a control diet (AIN‐93G) and ZDF were fed either the AIN‐93G diet (n=8) or the AIN‐93G diet in which cornstarch was replaced by RS (n=8) for 6 week. RS attenuated hyperglycemia by 41% and prevented excretion of DBP and albumin. Urinary 25D and 1,25D concentrations were 89% and 97% lower, respectively, while serum 25D levels were 40% higher in RS‐fed ZDF compared to ZDF fed the control diet. mRNA expression of CYP27B1 and CYP24A1, which are essential in vitamin D metabolism, were not affected by diabetes or RS. Collectively, these data suggested that vitamin D balance is dependent on the absence of proteinuria, which can be prevented by dietary RS in T2D independent of vitamin D supplementation.