Key result
Asymmetric dimethylarginine significantly impaired basal and insulin-stimulated glucose transport in 3T3-L1 adipocytes, an effect that was prevented by Vitamin E via the ROS/TLR4 pathway.
ADMA impairs glucose transport in adipocytes via the ROS/TLR4 pathway, an effect that can be prevented by Vitamin E.
May link ADMA to adipocyte insulin resistance; hypothesis-generating and requires human validation before any clinical consideration.
BACKGROUND: Asymmetric dimethylarginine (ADMA), the inhibitor of nitric oxide synthase (NOS), has been reported to be associated with glucose metabolism, but its mechanisms remain unknown. METHODS: In 3T3-L1 adipocytes, we measured the effects of ADMA on glucose transport process under basal or insulin-induced condition, and examined the production of nitric oxide (NO), reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-alpha), and the expression of toll-like receptor 4 (TLR4). RESULTS: ADMA significantly impaired basal or insulin-stimulated 2-deoxy- [3H] glucose uptake, and decreased the expression of insulin receptor substrate-1 (IRS-1) and glucose transporter-4 (GLUT4). Phosphorylated protein of IRS-1 and translocation of GLUT4 with insulin-stimulation were also inhibited by ADMA. NO decreased, while production of ROS and TNF-alpha, and expression of TLR4 increased after ADMA treatment. Vitamin E reduced the effects of ADMA on glucose transport system, and on NO, ROS and TLR4. Moreover, vitamin E decreased ADMA contents by up-regulating dimethylarginine dimethylaminohydrolase (DDAH) activity in adipocytes. Though L-arginine also increased NO level, but failed to reduce the effects of ADMA. CONCLUSION: ADMA significantly impairs both basal and insulin-stimulated glucose transport in adipocytes, which may relate to activation of the ROS/TLR4 pathway.
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Yang et al. (2009) studied Glucose metabolism in adipocytes. Asymmetric dimethylarginine (ADMA) and Vitamin E vs. Basal or insulin-induced condition without ADMA/Vitamin E was evaluated on Glucose transport process (2-deoxy-[3H] glucose uptake). Asymmetric dimethylarginine significantly impaired basal and insulin-stimulated glucose transport in 3T3-L1 adipocytes, an effect that was prevented by Vitamin E via the ROS/TLR4 pathway.
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