title: Dietary resistant starch prevents urinary excretion of 25-hydroxycholecalciferol and vitamin D-binding protein in type 1 diabetic rats.
abstract: Diabetes is a rapidly growing epidemic affecting millions of Americans and has been implicated in a number of devastating secondary complications. We previously demonstrated that type 2 diabetic rats exhibit vitamin D deficiency due to aberrant megalin-mediated endocytosis and excessive urinary excretion of 25-hydroxycholecalciferol (25D3) and vitamin D-binding protein (DBP). Here, we examined whether a model of type 1 diabetes [T1D; streptozotocin (STZ)-treated Sprague-Dawley rats] would similarly excrete abnormally high concentrations of 25D3 and DBP due to renal damage and compromised expression of megalin and its endocytic partner, disabled-2 (Dab2). Moreover, we tested whether feeding diabetic rats starch that is resistant to digestion could alleviate these abnormalities. Control (n = 12) rats were fed a standard, semipurified diet (AIN-93G) containing 55% total dietary starch and STZ-treated rats were fed the AIN-93G diet (n = 12) or a diet containing 55% high-amylose maize that is partially resistant to digestion [20% total dietary resistant starch (RS); n = 12] for 2 and 5 wk. The RS diet attenuated weight loss and polyuria in STZ-treated rats. Histology and immunohistochemistry revealed that dietary RS also attenuated the loss of Dab2 expression in renal proximal tubules. Moreover, urinary concentrations of both 25D3 and DBP were elevated ∼10-fold in STZ-treated rats (5 wk post STZ injection), which was virtually prevented by the RS. We also observed a ∼1.5-fold increase in megalin mRNA expression in STZ-treated rats, which was attenuated by feeding rats the RS diet for 2 wk. Taken together, these studies indicate that consumption of low-glycemic carbohydrates can attenuate disruption of vitamin D homeostasis in T1D through the rescue of megalin-mediated endocytosis in the kidney.
authors.affiliation: Department of Food Science and Human Nutrition, College of Veterinary Medicine, Iowa State University, Ames, IA, USA.
authors.forename: Anne L
authors.initials: AL
authors.lastname: Smazal
authors.forename: Nicholas C
authors.initials: NC
authors.lastname: Borcherding
authors.forename: Alysse S
authors.initials: AS
authors.lastname: Anderegg
authors.forename: Kevin L
authors.initials: KL
authors.lastname: Schalinske
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Whitley
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Rowling
mesh_terms: D033942:Adaptor Proteins, Vesicular Transport / Q000235:genetics / Q000378:metabolism; D000688:Amylose / Q000008:administration & dosage; D000818:Animals; D001786:Blood Glucose / Q000032:analysis / Q000378:metabolism; D002112:Calcifediol / Q000652:urine*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy*; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy*; D004032:Diet; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D004063:Digestion; D006706:Homeostasis / Q000187:drug effects; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D026561:Low Density Lipoprotein Receptor-Related Protein-2 / Q000235:genetics / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D013213:Starch / Q000008:administration & dosage*; D013311:Streptozocin / Q000009:adverse effects / Q000378:metabolism; D014809:Vitamin D-Binding Protein / Q000652:urine*; D003313:Zea mays / Q000737:chemistry
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D001786:Blood Glucose; C501404:Dab2 protein, rat; D004040:Dietary Carbohydrates; D026561:Low Density Lipoprotein Receptor-Related Protein-2; D012333:RNA, Messenger; D014809:Vitamin D-Binding Protein; D013311:Streptozocin; D013213:Starch; D000688:Amylose; D002112:Calcifediol