Dietary Resistant Starch Prevents Urinary Excretion of 25-Hydroxycholecalciferol and Vitamin D-Binding Protein in Type 1 Diabetic Rats

• Published in: The Journal of nutrition Vol. 143; no. 7; pp. 1123 - 1128
• Main Authors: SMAZAL, Anne L, BORCHERDING, Nicholas C, ANDEREGG, Alysse S, SCHALINSKE, Kevin L, WHITLEY, Elizabeth M, ROWLING, Matthew J
• Format: Journal Article
• Language: English
• Published: Bethesda, MD American Society for Nutrition 01.07.2013
• Subjects: Adaptor Proteins, Vesicular Transport - genetics; Adaptor Proteins, Vesicular Transport - metabolism; Amylose - administration & dosage; Animals; Biological and medical sciences; Blood Glucose - analysis; Blood Glucose - metabolism; Calcifediol - urine; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Type 1 - drug therapy; Diabetes. Impaired glucose tolerance; Diet; Dietary Carbohydrates - administration & dosage; Digestion; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Homeostasis - drug effects; Immunohistochemistry; Kidney - drug effects; Kidney - metabolism; Low Density Lipoprotein Receptor-Related Protein-2 - genetics; Low Density Lipoprotein Receptor-Related Protein-2 - metabolism; Male; Medical sciences; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Starch - administration & dosage; Streptozocin - adverse effects; Streptozocin - metabolism; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Vitamin D-Binding Protein - urine; Zea mays - chemistry; Endocrinopathy; Urine; Immunopathology; Biological fluid; Excretion; Nutrition; Rat; Rodentia; Autoimmune disease; Resistant starch; Micronutrient; Binding protein; Vertebrata; Mammalia; Vitamin D; Type 1 diabetes; Animal
• ISSN: 0022-3166; 1541-6100
• DOI: 10.3945/jn.112.173278

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.