Dietary Resistant Starch Prevents Urinary Excretion of 25-Hydroxycholecalciferol and Vitamin D-Binding Protein in Type 1 Diabetic Rats
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 excr...
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Published in | The Journal of nutrition Vol. 143; no. 7; pp. 1123 - 1128 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
American Society for Nutrition
01.07.2013
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Subjects | |
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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. |
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AbstractList | 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. |
Author | WHITLEY, Elizabeth M ROWLING, Matthew J SMAZAL, Anne L BORCHERDING, Nicholas C ANDEREGG, Alysse S SCHALINSKE, Kevin L |
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Keywords | Endocrinopathy Urine Immunopathology Biological fluid Excretion Nutrition Rat Rodentia Autoimmune disease Resistant starch Micronutrient Binding protein Vertebrata Mammalia Vitamin D Type 1 diabetes Animal |
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SubjectTerms | 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 |
Title | Dietary Resistant Starch Prevents Urinary Excretion of 25-Hydroxycholecalciferol and Vitamin D-Binding Protein in Type 1 Diabetic Rats |
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