| Dietary fructose causes tubulointerstitial injury in the normal rat kidney. | |
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MedLine Citation:
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PMID: 20071464 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Recent studies suggest that the metabolic syndrome is associated with renal disease. We previously reported that a high-fructose diet, but not a high-glucose diet, can induce metabolic syndrome and accelerate chronic renal disease in rats. We now examined the effects of a high-fructose diet on normal rat kidneys. Three groups of Sprague-Dawley rats were pair fed a special diet containing 60% fructose, 60% glucose, or control standard rat chow for 6 wk, and then histological studies were performed. The effect of fructose to induce cell proliferation in cultured proximal tubular cells was also performed. Fructose diet, but not glucose diet, significantly increased kidney weight by 6 wk. The primary finding was tubular hyperplasia and proliferation involving all segments of the proximal tubules while glomerular changes were not observed. This is the same site where the fructose transporters (GLUT2 and -5) as well as the key enzyme in fructose metabolism (ketohexokinase) were expressed. Consistently, fructose also induced proliferation of rat proximal tubular cells in culture. In vivo, tubular proliferation was also associated with focal tubular injury, with type III collagen deposition in the interstitium, an increase in alpha-smooth muscle actin positive myofibroblasts, and an increase in macrophage infiltration. In conclusion, a high-fructose diet induces cell proliferation and hyperplasia in proximal tubules, perhaps via a direct metabolic effect. The effect is independent of total energy intake and is associated with focal tubulointerstitial injury. These studies may provide a mechanism by which metabolic syndrome causes renal disease. |
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Authors:
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Takahiro Nakayama; Tomoki Kosugi; Michael Gersch; Thomas Connor; Laura Gabriela Sanchez-Lozada; Miguel A Lanaspa; Carlos Roncal; Santos E Perez-Pozo; Richard J Johnson; Takahiko Nakagawa |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural Date: 2010-01-13 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 298 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-02-25 Completed Date: 2010-03-19 Revised Date: 2011-07-25 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F712-20 Citation Subset: IM |
Affiliation:
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Division of Nephrology, University of Florida, Gainesville, Florida, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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metabolism Animals Cell Proliferation / drug effects* Cells, Cultured Collagen / metabolism Dietary Sucrose / metabolism, toxicity* Fibroblasts / drug effects, metabolism, pathology Fructokinases / metabolism Fructose / metabolism, toxicity* Glucose / pharmacology* Glucose Transporter Type 2 / metabolism Glucose Transporter Type 5 / metabolism Hyperplasia Kidney Diseases / etiology*, metabolism, pathology Kidney Tubules, Proximal / drug effects*, metabolism, pathology Macrophages / drug effects, pathology Male Organ Size Rats Rats, Sprague-Dawley Severity of Illness Index Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL-68607-01/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Dietary Sucrose; 0/Glucose Transporter Type 2; 0/Glucose Transporter Type 5; 0/Slc2a2 protein, rat; 0/Slc2a5 protein, rat; 0/smooth muscle actin, rat; 30237-26-4/Fructose; 50-99-7/Glucose; 9007-34-5/Collagen; EC 2.7.1.-/Fructokinases; EC 2.7.1.3/ketohexokinase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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