title: Photoactivation of Dok1/ERK/PPARγ signaling axis inhibits excessive lipolysis in insulin-resistant adipocytes.
abstract: Insulin resistance is a hallmark of the metabolic syndrome and type 2 diabetes. Increased plasma FFA level is an important cause of obesity-associated insulin resistance. Over-activated ERK is closely related with FFA release from adipose tissues in patients with type 2 diabetes. Nevertheless, there are no effective strategies to lower plasma FFA level. Low-power laser irradiation (LPLI) has been reported to regulate multiple biological processes. However, whether LPLI could ameliorate metabolic disorders and the molecular mechanisms involved remain unknown. In this study, we first demonstrated that LPLI suppresses excessive lipolysis of insulin-resistant adipocytes by activating tyrosine kinases-1(Dok1)/ERK/PPARγ pathway. Our data showed that LPLI inhibits ERK phosphorylation through the activation of Dok1, resulting in decreased phospho-PPARγ level. Non-phosphorylated PPARγ maintains in nucleus to promote the expression of adipogenic genes, reversing excessive lipolysis in insulin-resistant adipocytes. In summary, the present research highlights the important roles of Dok1/ERK/PPARγ pathway in lowering FFA release from adipocytes, and our research extends the knowledge of the biological effects induced by LPLI.
authors: MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.
authors: Xiaoxiao
authors: X
authors: Jiang
authors: MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.
authors: Lei
authors: L
authors: Huang
authors: MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China. Electronic address: xingda@scnu.edu.cn.
authors: Da
authors: D
authors: Xing
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects; D000818:Animals; D004268:DNA-Binding Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000032:analysis / Q000378:metabolism; D007333:Insulin Resistance; D007834:Lasers; D008066:Lipolysis / Q000528:radiation effects*; D051379:Mice; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D010750:Phosphoproteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000528:radiation effects; D014158:Transcription, Genetic / Q000187:drug effects; D014280:Triglycerides / Q000032:analysis
chemical_list: D004268:DNA-Binding Proteins; C489561:Dok1 protein, mouse; D005230:Fatty Acids, Nonesterified; D047495:PPAR gamma; D010750:Phosphoproteins; D034741:RNA, Small Interfering; D016601:RNA-Binding Proteins; D014280:Triglycerides; D048049:Extracellular Signal-Regulated MAP Kinases
keywords: Dok1; ERK; Excessive lipolysis; Insulin resistance; LPLI