Dietary Resistant Starch Prevents Urinary Excretion of Vitamin D Metabolites and Maintains Circulating 25-Hydroxycholecalciferol Concentrations in Zucker Diabetic Fatty Rats. Issue 11 (27th August 2014)

• Record Type: Journal Article
• Authors: Koh, Gar Yee; Whitley, Elizabeth M.; Mancosky, Kirsten; Loo, Yi Ting; Grapentine, Kelly; Bowers, Emily; Schalinske, Kevin L.; Rowling, Matthew J.
• Is Part Of: Journal of nutrition. Volume 144:Issue 11(2014)
• Page Start: 1667
• Page End: 1673
• Publication Date: 2014-08-27
• Subjects: Nutrition -- Periodicals; Diet -- Periodicals; 613.205
• DOI: 10.3945/jn.114.198200
• Languages: English
• ISSNs: 0022-3166

Abstract

Abstract: Background: Type 2 diabetes (T2D) is the leading cause of nephropathy in the United States. Renal complications of T2D include proteinuria and suboptimal serum 25-hydroxycholecalciferol (25D) concentrations. 25D is the major circulating form of vitamin D and renal reabsorption of the 25D–vitamin D–binding protein (DBP) complex via megalin-mediated endocytosis is believed to determine whether 25D can be activated to 1, 25-dihydroxycholecalciferol (1, 25D) or returned to circulation. We previously demonstrated that excessive urinary excretion of 25D–DBP and albuminuria occurred in rats with type 1 diabetes (T1D) and T2D. Moreover, feeding rats with T1D high-amylose maize partially resistant to digestion [resistant starch (RS)] prevented excretion of 25D–DBP without significantly affecting hyperglycemia. Objective: We used Zucker diabetic fatty (ZDF) rats, a model of obesity-related T2D, to determine whether feeding RS could similarly prevent loss of vitamin D and maintain serum 25D concentrations. Methods: Lean control Zucker rats ( n = 8) were fed a standard semi-purified diet (AIN-93G) and ZDF rats were fed either the AIN-93G diet ( n = 8) or the AIN-93G diet in which cornstarch was replaced with RS (550 g/kg diet; 35% resistant to digestion) ( n = 8) for 6 wk. Results: RS attenuated hyperglycemia by 41% ( P < 0.01) and prevented urinary DBP excretion and albuminuria, which were elevated 3.0- ( P < 0.01) and 3.6-fold ( P < 0.01), respectively, in control diet–fed ZDF rats. Additionally, urinary excretion of 25D ( P = 0.01) and 1, 25D ( P = 0.03) was higher (89% and 97%, respectively), whereas serum 25D concentrations were 31% lower ( P < 0.001) in ZDF rats fed the control diet compared with RS-fed ZDF rats. Histopathologic scoring of the kidney revealed that RS attenuated diabetes-mediated damage by 21% ( P = 0.12) despite an ∼50% decrease in megalin protein abundance. Conclusions: Taken together, these data provide evidence that suggests vitamin D balance can be maintained by dietary RS through nephroprotective actions in T2D, which are independent of vitamin D supplementation and renal expression of megalin.