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 inThe 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
LanguageEnglish
Published Bethesda, MD American Society for Nutrition 01.07.2013
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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.
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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Issue 7
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
URI https://www.ncbi.nlm.nih.gov/pubmed/23677864
Volume 143
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