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Stephan Wueest, Reto A. Rapold, Desiree M. Schumann, Julia M. Rytka, Anita Schildknecht, Ori Nov, Alexander V. Chervonsky, Assaf Rudich, Eugen J. Schoenle, Marc Y. Donath, Daniel Konrad
Published in Volume 120, Issue 1
J Clin Invest. 2010; 120(1):191–202 doi:10.1172/JCI38388
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Figure 2
Fas-def mice are protected from HFD-induced changes in adipose tissue and glucose homeostasis.

(A) Weight gain was analyzed in HFD-fed WT and Fas-def mice. Results are mean ± SEM of 10 animals per group. (B) Perigonadal fat pads were harvested and weighed. Results are expressed relative to total body weight and represent mean ± SEM of 10–15 mice group. *P < 0.05 (Student’s t test). (C) Left: Relative size distribution of adipocyte diameter after 6 weeks of HFD. Results represent mean ± SEM of 6 mice per group. Right: Mean adipocyte diameter of chow- or HFD-fed Fas-def and WT mice. Results represent mean ± SEM of 6 mice per group. *P < 0.05 (Student’s t test). (D) Intraperitoneal glucose tolerance tests in WT (left) and Fas-def (right) mice. Results are mean ± SEM of 12–18 animals per group. *P < 0.05, **P < 0.01 (Student’s t test). (E) Fasting insulin levels were determined in WT (left) and Fas-def (right) mice after 8 hours of food withdrawal. Results are mean ± SEM of 4–5 animals per group. *P < 0.05 (Student’s t test). (F) 14C-d-glucose incorporation into isolated adipocytes from chow- and HFD-fed mice was determined in the absence or presence of insulin. Left: Fold glucose incorporation in WT mice. Right: Fold glucose incorporation in Fas-def mice. Results represent mean ± SEM of 6 experiments. **P < 0.01 (Student’s t test).