NOS activation could be modulated by HDL through Akt, which is initiated through the binding of HDL to SR-BI. Activation of PI3K/Akt and NOS promotes translocation of GLUT4 vesicle to plasma membrane. Therefore, it is reasonable to think that PI3K-Akt-NOS works as one pathway to regulate glucose uptake. Meanwhile, HDL prompted translocation of GLUT4 to plasma membrane from intracellular storage organelles. Any approach to expand retention of GLUT4 in plasma membrane would lead to enhancement of glucose uptake by peripheral tissues, especially skeletal muscle and adipose tissue. PI3K/Akt and AMPK signaling pathways have been showed to participate in GLUT4 exocytosis and activation. GLUT4 translocation rather than its total amount variation plays a crucial role under diabetic conditions. The present study demonstrated that HDL prompted GLUT4 exocytosis in parallel with activating both PI3K/Akt and AMPK signaling pathways. Meanwhile, glucose transport in 3T3-L1 adipocytes with HDL stimulation was disturbed in the presence of LY294002, consistent with the results obtained in muscle cells infected with AMPK-DN virus. Moreover, GLUT4 endocytosis followed by its dysfunction could be regulated through changing cholesterol contents in plasma membrane. Both Chromium and methyl-bcyclodextrin are suggested to induce GLUT4 endocytosis coupled to membrane cholesterol loss that leads to insulin sensitizing in 3T3-L1 adipocytes.Although infliximab has attracted attention for its curative effect on moderate/severe UC and CD, there are problems of resistance and side effects upon long term dosage. Thus, novel therapeutic drugs with better efficacy and side effects profiles are needed. Both DSS and TNBS-induced colitis are considered useful experimental models for IBD. BTZO15 significantly suppressed the typical symptoms of DSS-induced colitis in rats: large intestine shortening, rectum weight gain, diarrhea, and bleeding. BTZO-15 also suppressed an increase in rectal MPO activity, which is an index of tissue-associated neutrophil accumulation. In contrast, TNBS-induced colitis is believed to induce a T-cell-mediated response against haptenmodified autologous proteins/luminal antigens similar to a Th1 immune response and comparable to the inflammatory processes present in human CD. BTZO-15 significantly decreased the ulcer-affected area with suppression of rectal MPO activity in rats with TNBS-induced colitis. Interestingly, BTZO-15 did not affect the rectal TNF-a level. These results indicate that BTZO-15 has potential as a novel therapeutic drug for both UC and CD. BTZO-15 induced expression of HO-1 and suppressed NOinduced cell death in a rat intestinal epithelial cell line. Reactive oxygen species, such as NO, play an important role in the pathogenesis of various.