Fig 1.
(A) Evolution of total body weight on control diet or HFD in WT and PKR-/- mice and body weight gain during diet. Obesity is induced by HFD. Error bars = SEM. (B) Analysis of blood glucose level after 16 weeks of HFD in WT mice and PKR-/- mice showing a significantly increased glucose level in WT mice after HFD treatment (p = 0.0014). Error bars = SEM. (C) Analysis of insulin level after 16 weeks of HFD in WT mice and PKR-/- mice showing a significantly increased insulin level after HFD treatment in PKR -/- mice (p<0.0001). Error bars = SEM. (D) Analysis of triglyceride level after 16 weeks of HFD in WT mice and PKR-/- mice shows no difference of triglyceride level in WT mice and PKR-/- mice after HFD treatment. Error bars = SEM. (E) Analysis of cholesterol level after 16 weeks of HFD in WT mice and PKR-/- mice showing a significant increased cholesterol level in WT HFD and PKR-/- HFD compared to their controls. Error bars = SEM. (F) Analysis of LDL level after 16 weeks of HFD in WT mice and PKR-/- mice showing a significant increased LDL level after HFD in WT mice compared to control diet (p<0.0001). Error bars = SEM. (G) Analysis of HDL level after 16 weeks of HFD in WT mice and PKR-/- mice showing a significant increased HDL level after HFD in WT and PKR-/- mice compared to controls. Error bars = SEM. (H) Analysis of ratio of LDL/HDL after 16 weeks of HFD in WT mice and PKR-/- mice. The results showed a significant difference after HFD treatment in the WT mice (p<0.0027) but not in PKR-/- mice, as well as between WT HFD and PKR-/- HFD mice (p = 0.0405). Error bars = SEM. (I) The oral glucose tolerance test (glucose mg/dl) shows no significant difference between control mice and PKR knockout mice from T0 to T180 minutes. (n = 5).
Fig 2.
(A) Illustration of Iba1 immunostaining in the cortical grey matter in WT and PKR-/- mice control or treated by HFD. Scale bar = 50μm. (B) Histogram of level of Iba1 protein load in the cortical grey matter of WT and PKR-/- mice after 16 weeks of HFD. No significant modification of Iba1 expression is observed in both strains. Error bars = SEM. (C) Histogram of level of TNFalpha in the cortex and serum of WT and PKR-/- mice after 16 weeks of HFD. (n = 5).
Fig 3.
(A) Western blot of PKR showing the absence of PKR in the cortex of PKR-/- mice. (B) Western blot analysis of peIF2alpha and eIF2alpha in cortex of mice. (C) Histogram of the ratio peIF2alpha/eIF2alpha showing a significant increase in the cortex of WT HFD mice (p = 0.0167). Error bars = SEM. (D) Western blot analysis of pJNK and JNK in cortex of mice. (E) Histogram of the ratio pJNK/JNK showing a significant increase in the cortex of WT HFD mice. Error bars = SEM. (F) Immunostaining of pJNK in mice cortex and histogram of level of pJNK in the cortex of mice showing a significant increase of pJNK load in the cortex of WT HFD mice. Error bars = SEM. (n = 5).
Fig 4.
(A) Western blot analysis of pIRS1 and IRS1 in cortex of mice. (B) Histogram of the ratio pIRS1/IRS1 showing a significant increase in the cortex of WT HFD mice. (C) Immunostaining of pIRS in mice cortex and histogram of level of pIRS1 in the cortex of mice did not show any significant change of pIRS1 load in the cortex of both strains. Error bars = SEM. (D) Western blot analysis of pIKKbeta and IKKbeta in cortex of mice. (E) Histogram of the ratio pIKKbeta/ IKKbeta. A significant change was observed between WT HFD and PKR-/- HFD.