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  High-fat diet-induced hyperinsulinemia and tissue-specific insulin resistance in Cry-deficient mice.

Barclay, J. L., Shostak, A., Leliavski, A., Tsang, A. H., Jöhren, O., Müller-Fielitz, H., et al. (2013). High-fat diet-induced hyperinsulinemia and tissue-specific insulin resistance in Cry-deficient mice. American Journal of Physiology-Endocrinology and Metabolism, 304(10), E1053-E1063. doi:10.1152/ajpendo.00512.2012.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0013-B208-6 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0027-C7E1-3
Genre: Journal Article

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1795436l.pdf (Publisher version), 468KB
 
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Barclay, J. L.1, Author              
Shostak, A.1, Author              
Leliavski, A.1, Author              
Tsang, A. H.1, Author              
Jöhren, O., Author
Müller-Fielitz, H., Author
Landgraf, D.1, Author              
Naujokat, N.1, Author              
van der Horst, G., Author
Oster, H.1, Author              
Affiliations:
1Research Group of Circadian Rhythms, MPI for biophysical chemistry, Max Planck Society, ou_578594              

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 Abstract: Perturbation of circadian rhythmicity in mammals, either by environmental influences such as shiftwork or by genetic manipulation, has been associated with metabolic disturbance and the development of obesity and diabetes. Circadian clocks are based on transcriptional/translational feedback loops, comprising positive and negative components. Whereas the metabolic effects of deletion of the positive arm of the clock gene machinery, as in Clock- or Bmal1-deficient mice, have been well characterized, inactivation of Period genes (Per1-3) as components of the negative arm have more complex, sometimes contradictory effects on energy homeostasis. The CRYPTOCHROMEs are critical interaction partners of PERs, and simultaneous deletion of Cry1 and -2 results in behavioral and molecular circadian arrhythmicity. We show that, when challenged with a high-fat diet, Cry1/2(-/-) mice rapidly gain weight and surpass that of wild-type mice, despite displaying hypophagia. Transcript analysis of white adipose tissue reveals up-regulated expression of lipogenic genes, many of which are insulin targets. High-fat diet-induced hyperinsulinemia, as a result of potentiated insulin secretion, coupled with selective insulin sensitivity in adipose tissue of Cry1/2(-/-) mice, correlates with increased lipid uptake. Collectively, these data indicate that Cry deficiency results in an increased vulnerability to high-fat diet-induced obesity that might be mediated by increased insulin secretion and lipid storage in adipose tissues.

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Language(s): eng - English
 Dates: 2013-03-262013-05-15
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1152/ajpendo.00512.2012
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Title: American Journal of Physiology-Endocrinology and Metabolism
Source Genre: Journal
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Pages: - Volume / Issue: 304 (10) Sequence Number: - Start / End Page: E1053 - E1063 Identifier: -