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Dokumenttyp:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Article
Autor(en):
Kirchner, H; Hofmann, SM; Fischer-Rosinsky, A; Hembree, J; Abplanalp, W; Ottaway, N; Donelan, E; Krishna, R; Woods, SC; Müller, TD; Spranger, J; Perez-Tilve, D; Pfluger, PT; Tschöp, MH; Habegger, KM
Titel:
Caloric restriction chronically impairs metabolic programming in mice.
Abstract:
Although obesity rates are rapidly rising, caloric restriction remains one of the few safe therapies. Here we tested the hypothesis that obesity-associated disorders are caused by increased adipose tissue as opposed to excess dietary lipids. Fat mass (FM) of lean C57B6 mice fed a high-fat diet (HFD; FMC mice) was "clamped" to match the FM of mice maintained on a low-fat diet (standard diet [SD] mice). FMC mice displayed improved glucose and insulin tolerance as compared with ad libitum HFD mice (P < 0.001) or SD mice (P < 0.05). These improvements were associated with fewer signs of inflammation, consistent with the less-impaired metabolism. In follow-up studies, diet-induced obese mice were food restricted for 5 weeks to achieve FM levels identical with those of age-matched SD mice. Previously, obese mice exhibited improved glucose and insulin tolerance but showed markedly increased fasting-induced hyperphagia (P < 0.001). When mice were given ad libitum access to the HFD, the hyperphagia of these mice led to accelerated body weight gain as compared with otherwise matched controls without a history of obesity. These results suggest that although caloric restriction on a HFD provides metabolic benefits, maintaining those benefits may require lifelong continuation, at least in individuals with a history of obesity.
Zeitschriftentitel:
Diabetes
Jahr:
2012
Band / Volume:
61
Heft / Issue:
11
Seitenangaben Beitrag:
2734-42
Volltext / DOI:
doi:10.2337/db11-1621
PubMed:
http://view.ncbi.nlm.nih.gov/pubmed/22787140
Print-ISSN:
0012-1797
TUM Einrichtung:
Kliniken und Institute
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