rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2010-9-27
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pubmed:abstractText |
The C57BL/6J (B6/J) male mouse represents a standard for diet-induced obesity (DIO) and is unique in expressing a loss-of-function nicotinamide nucleotide transhydrogenase (Nnt) gene. This mutation was associated with a marked reduction in glucose-stimulated insulin secretion from B6/J islets in vitro and moderately impaired glucose clearance in vivo. To assess the contribution of this Nnt mutation, we compared DIO responsiveness of Nnt-mutant B6/J males to Nnt wild-type C57BL/6NJ (B6/NJ) males over a 14-week period of feeding a high-fat (60% of calories) diet. Initial mean body weights at 6 weeks did not distinguish the substrains and both substrains were DIO-sensitive. However, B6/J males outgained the B6/NJ males, with a significant 3 g higher mean body weight at 20 weeks accompanied by significant increases in both lean and fat mass. Mean nonfasting serum glucose over time was also significantly higher in B6/J males, as was impairment of glucose tolerance assessed at 8 and 20 weeks of age. Serum leptin, but not insulin, was significantly higher in B6/J males over time. Potential contributions of the wild-type Nnt gene were demonstrable on a lower fat diet (10% of calories) where a significantly greater weight gain over time by B6/NJ males was correlated with a significantly higher serum insulin. In conclusion, DIO developed in response to 60% fat feeding regardless of Nnt allele status. Contribution of the B6/J-unique Nnt mutation was most evident in response to 10% fat feeding that resulted in reduced serum insulin and weight gain compared to B6/NJ males.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1930-7381
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
18
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1902-5
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:20057372-Adipose Tissue,
pubmed-meshheading:20057372-Animals,
pubmed-meshheading:20057372-Blood Glucose,
pubmed-meshheading:20057372-Body Fluid Compartments,
pubmed-meshheading:20057372-Body Weight,
pubmed-meshheading:20057372-Diet,
pubmed-meshheading:20057372-Dietary Fats,
pubmed-meshheading:20057372-Glucose Intolerance,
pubmed-meshheading:20057372-Insulin,
pubmed-meshheading:20057372-Leptin,
pubmed-meshheading:20057372-Male,
pubmed-meshheading:20057372-Mice,
pubmed-meshheading:20057372-Mice, Inbred C57BL,
pubmed-meshheading:20057372-Mice, Mutant Strains,
pubmed-meshheading:20057372-Mutation,
pubmed-meshheading:20057372-NADP Transhydrogenases,
pubmed-meshheading:20057372-Obesity,
pubmed-meshheading:20057372-Weight Gain
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pubmed:year |
2010
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pubmed:articleTitle |
Diet-induced obesity in two C57BL/6 substrains with intact or mutant nicotinamide nucleotide transhydrogenase (Nnt) gene.
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pubmed:affiliation |
The Jackson Laboratory, Bar Harbor, Maine, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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