Identification of Sucrose Non-Fermenting–Related Kinase (SNRK) as a Suppressor of Adipocyte Inflammation

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FIG. 6.
FIG. 6.

mTOR pathway and adipocyte inflammation. A: SNRK knockdown in 3T3-L1 CAR adipocyte and the effect on raptor and ACC phosphorylation. B: Rapamycin activates IKKβ in 3T3-L1 adipocytes. C: Rapamycin induces lipolysis in 3T3-L1 adipocytes. D: Rapamycin increases expression of proinflammatory factors. *P < 0.05, shSNRK-infected adipocytes vs. shGFP-infected adipocytes or rapamycin (Rapa)-treated adipocytes vs. vehicle (Veh)-treated adipocytes. Duplicate samples were used in Western blots, and triplicate samples were used in gene expression and lipolysis experiments. E: Overexpression of the constitutively active Akt1 (myr-Akt) activates mTOR signaling. F: Overexpression of myr-Akt suppresses lipolysis. G: Overexpression of myr-Akt decreases expression of inflammatory genes. *P < 0.05, cells expressing tTA plus myr-Akt vs. cells expressing tTA alone. Error bars stand for mean ± SE. S, Ser.

This Article

  1. Diabetes vol. 62 no. 7 2396-2409