Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes

Abstract

Insulin resistance is a hallmark of the metabolic syndrome and type 2 diabetes. Dysfunction of PI-3K/Akt signaling was involved in insulin resistance. Glucose transporter 4 (GLUT4) is a key factor for glucose uptake in muscle and adipose tissues, which is closely regulated by PI-3K/Akt signaling in response to insulin treatment. Low-power laser irradiation (LPLI) has been shown to regulate various physiological processes and induce the synthesis or release of multiple molecules such as growth factors, which (especially red and near infrared light) is mainly through the activation of mitochondrial respiratory chain and the initiation of intracellular signaling pathways. Nevertheless, it is unclear whether LPLI could promote glucose uptake through activation of PI-3K/Akt/GLUT4 signaling in 3T3L-1 adipocytes. In this study, we investigated how LPLI promoted glucose uptake through activation of PI-3K/Akt/GLUT4 signaling pathway. Here, we showed that GLUT4 was localized to the Golgi apparatus and translocated from cytoplasm to cytomembrane upon LPLI treatment in 3T3L-1 adipocytes, which enhanced glucose uptake. Moreover, we found that glucose uptake was mediated by the PI3-K/Akt2 signaling, but not Akt1 upon LPLI treatment with Akt isoforms gene silence and PI3-K/Akt inhibitors. Collectively, our results indicate that PI3-K/Akt2/GLUT4 signaling act as the key regulators for improvement of glucose uptake under LPLI treatment in 3T3L-1 adipocytes. More importantly, our¯ndings suggest that activation of PI3-K/Akt2/GLUT4 signaling by LPLI may provide guidance in practical applications for promotion of glucose uptake in insulin-resistant adipose tissue.

Photoactivation of Dok1/ERK/PPARγ signaling axis inhibits excessive lipolysis in insulin-resistant adipocytes

“…Kenji Ryotokuji et al [39] have shown that pinpoint plantar longwavelength infrared light irradiation (PP-LILI) can normalize blood glucose levels by reducing stress hormones and by improving insulin sensitivity. Our recent study confirmed that He-Ne laser can promote glucose uptake of 3T3-L1 adipocytes through activating PI3-K/Akt/ GLUT4 pathway [24]. Nevertheless, whether LPLI could ameliorate lipid metabolic disorders remains unclear.…”

“…In addition, growing evidences have shown that LPLI activates RTKs and triggers its downstream effectors, such as Ras, PKC, and PI3-K/Akt [19,23]. Recent study has demonstrated that LPLI promotes glucose uptake through activation of PI-3K/Akt2/GLUT4 pathway in 3T3-L1 adipocytes [24]. The effects of LPLI on energy expenditure in adipocytes may provide potential for improving metabolic disorders in insulin-resistant condition.…”