pubmed-article:16985262 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16985262 | lifeskim:mentions | umls-concept:C1333572 | lld:lifeskim |
pubmed-article:16985262 | lifeskim:mentions | umls-concept:C0166418 | lld:lifeskim |
pubmed-article:16985262 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
pubmed-article:16985262 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
pubmed-article:16985262 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
pubmed-article:16985262 | lifeskim:mentions | umls-concept:C1449704 | lld:lifeskim |
pubmed-article:16985262 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:16985262 | pubmed:dateCreated | 2007-2-6 | lld:pubmed |
pubmed-article:16985262 | pubmed:abstractText | High-fructose consumption is associated with insulin resistance and diabetic dyslipidemia, but the underlying mechanism is unclear. We show in hamsters that high-fructose feeding stimulated forkhead box O1 (FoxO1) production and promoted its nuclear redistribution in liver, correlating with augmented apolipoprotein C-III (apoC-III) production and impaired triglyceride metabolism. High-fructose feeding upregulated peroxisome proliferator-activated receptor-gamma coactivator-1beta and sterol regulatory element binding protein-1c expression, accounting for increased fat infiltration in liver. High-fructose-fed hamsters developed hypertriglyceridemia, accompanied by hyperinsulinemia and glucose intolerance. These metabolic aberrations were reversible by fenofibrate, a commonly used anti-hypertriglyceridemia agent that is known to bind and activate peroxisome proliferator-activated receptor-alpha (PPARalpha). PPARalpha physically interacted with, but functionally antagonized, FoxO1 in hepatic apoC-III expression. These data underscore the importance of FoxO1 deregulation in the pathogenesis of hypertriglyceridemia in high-fructose-fed hamsters. Counterregulation of hepatic FoxO1 activity by PPARalpha constitutes an important mechanism by which fibrates act to curb apoC-III overproduction and ameliorate hypertriglyceridemia. | lld:pubmed |
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pubmed-article:16985262 | pubmed:language | eng | lld:pubmed |
pubmed-article:16985262 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16985262 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16985262 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16985262 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16985262 | pubmed:month | Feb | lld:pubmed |
pubmed-article:16985262 | pubmed:issn | 0193-1849 | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:HausE MEM | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:AltomonteJenn... | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:KamagateAdama... | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:YuJiangJ | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:QuShenS | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:PerdomoGerman... | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:SuDongmingD | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:TseToniaT | lld:pubmed |
pubmed-article:16985262 | pubmed:author | pubmed-author:DongH HenryHH | lld:pubmed |
pubmed-article:16985262 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16985262 | pubmed:volume | 292 | lld:pubmed |
pubmed-article:16985262 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16985262 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16985262 | pubmed:pagination | E421-34 | lld:pubmed |
pubmed-article:16985262 | pubmed:dateRevised | 2011-5-6 | lld:pubmed |
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