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rdf:type |
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lifeskim:mentions |
umls-concept:C0011847,
umls-concept:C0012155,
umls-concept:C0017262,
umls-concept:C0033085,
umls-concept:C0035647,
umls-concept:C0035820,
umls-concept:C0085243,
umls-concept:C0185117,
umls-concept:C0205217,
umls-concept:C0381451,
umls-concept:C0577559,
umls-concept:C1292733,
umls-concept:C2911684
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pubmed:issue |
11
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pubmed:dateCreated |
2001-11-7
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pubmed:abstractText |
We demonstrate that a high-fructose diet reduces the incidence of diabetes in nonobese diabetic (NOD) mice (31.2% v 57.1% on regular chow (RC); P =.009). In a second cohort of mice, we evaluated potential mechanisms for the protective effect of the high-fructose (HF) diet and whether the metabolic changes are strain-specific. Sixty NOD and 60 Balb/c mice were randomized at weaning into HF- and RC-fed groups (30 mice each) and followed for 28 weeks. Glucose tolerance testing demonstrated improved glucose tolerance in HF diet groups (P =.001 in Balb/c; P =.04 in NOD mice at 6 months). beta-cell mass was preserved in NOD mice on the HF diet, but remained unchanged in Balb/c mice. In NOD mice, hepatic insulin receptor substrate (IRS)-2 protein expression increased by 2-fold (P =.01 for 2 v 6 months) in HF-fed mice and was 53% +/- 15% higher (P =.01) in the HF diet versus RC groups at 6 months of age. IRS-2 expression was also increased in skeletal muscle of NOD mice and in both liver and muscle of Balb/c mice. Our data suggest that a HF diet improves glucose tolerance in both NOD and Balb/c mice. The improved glucose tolerance may be related to increased IRS-2 expression and, in NOD mice, preservation of beta-cell mass.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0026-0495
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2001 by W.B. Saunders Company
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pubmed:issnType |
Print
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1369-76
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11699059-Animals,
pubmed-meshheading:11699059-Blood Glucose,
pubmed-meshheading:11699059-Diabetes Mellitus, Experimental,
pubmed-meshheading:11699059-Dietary Carbohydrates,
pubmed-meshheading:11699059-Female,
pubmed-meshheading:11699059-Food, Formulated,
pubmed-meshheading:11699059-Fructose,
pubmed-meshheading:11699059-Glucose Tolerance Test,
pubmed-meshheading:11699059-Incidence,
pubmed-meshheading:11699059-Insulin,
pubmed-meshheading:11699059-Insulin Receptor Substrate Proteins,
pubmed-meshheading:11699059-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:11699059-Islets of Langerhans,
pubmed-meshheading:11699059-Liver,
pubmed-meshheading:11699059-Mice,
pubmed-meshheading:11699059-Mice, Inbred BALB C,
pubmed-meshheading:11699059-Mice, Inbred NOD,
pubmed-meshheading:11699059-Models, Animal,
pubmed-meshheading:11699059-Muscle, Skeletal,
pubmed-meshheading:11699059-Phosphoproteins,
pubmed-meshheading:11699059-Triglycerides
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pubmed:year |
2001
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pubmed:articleTitle |
High-fructose diet preserves beta-cell mass and prevents diabetes in nonobese diabetic mice: A potential role for increased insulin receptor substrate-2 expression.
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pubmed:affiliation |
Section on Immunology, Joslin Diabetes Center, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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