Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes
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...
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| Format: | Article |
| Language: | English |
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World Scientific Publishing
2014-05-01
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| Series: | Journal of Innovative Optical Health Sciences |
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| Online Access: | http://www.worldscientific.com/doi/pdf/10.1142/S1793545813500673 |
| _version_ | 1818290220226838528 |
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| author | Lei Huang Longlong Gong Xiaoxiao Jiang Da Xing |
| author_facet | Lei Huang Longlong Gong Xiaoxiao Jiang Da Xing |
| author_sort | Lei Huang |
| collection | DOAJ |
| description | 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 findings 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. |
| first_indexed | 2024-12-13T02:24:42Z |
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| id | doaj.art-06b758e4345a4bed9d8f7aa7a1744a5f |
| institution | Directory Open Access Journal |
| issn | 1793-5458 1793-7205 |
| language | English |
| last_indexed | 2024-12-13T02:24:42Z |
| publishDate | 2014-05-01 |
| publisher | World Scientific Publishing |
| record_format | Article |
| series | Journal of Innovative Optical Health Sciences |
| spelling | doaj.art-06b758e4345a4bed9d8f7aa7a1744a5f2022-12-22T00:02:39ZengWorld Scientific PublishingJournal of Innovative Optical Health Sciences1793-54581793-72052014-05-01731350067-11350067-1010.1142/S179354581350067310.1142/S1793545813500673Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytesLei Huang0Longlong Gong1Xiaoxiao Jiang2Da Xing3MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, P. R. ChinaMOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, P. R. ChinaMOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, P. R. ChinaMOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, P. R. ChinaInsulin 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 findings 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.http://www.worldscientific.com/doi/pdf/10.1142/S1793545813500673Glucose transporter 4PI-3K/Aktlow-power laser irradiationinsulin resistance3T3-L1 adipocytestype 2 diabetes |
| spellingShingle | Lei Huang Longlong Gong Xiaoxiao Jiang Da Xing Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes Journal of Innovative Optical Health Sciences Glucose transporter 4 PI-3K/Akt low-power laser irradiation insulin resistance 3T3-L1 adipocytes type 2 diabetes |
| title | Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes |
| title_full | Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes |
| title_fullStr | Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes |
| title_full_unstemmed | Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes |
| title_short | Photoactivation of GLUT4 translocation promotes glucose uptake via PI3-K/Akt2 signaling in 3T3-L1 adipocytes |
| title_sort | photoactivation of glut4 translocation promotes glucose uptake via pi3 k akt2 signaling in 3t3 l1 adipocytes |
| topic | Glucose transporter 4 PI-3K/Akt low-power laser irradiation insulin resistance 3T3-L1 adipocytes type 2 diabetes |
| url | http://www.worldscientific.com/doi/pdf/10.1142/S1793545813500673 |
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