title: α-Lipoic acid protects 3T3-L1 adipocytes from NYGGF4 (PID1) overexpression-induced insulin resistance through increasing phosphorylation of IRS-1 and Akt.
abstract: NYGGF4 (also called PID1) was demonstrated that it may be related to the development of obesity-related IR. We aimed in the present study to further elucidate the effects of NYGGF4 on IR and the underlying mechanisms through using α-Lipoic acid (LA) treatment, which could facilitate glucose transport and utilization in fully differentiated adipocytes. Our data showed that the LA pretreatment strikingly enhanced insulin-stimulated glucose uptake through increasing GLUT4 translocation to the PM in NYGGF4 overexpression adipocytes. The reactive oxygen species (ROS) levels in NYGGF4 overexpression adipocytes were strikingly enhanced, which could be decreased by the LA pretreatment. NYGGF4 overexpression resulted in significant inhibition of tyrosine phosphorylation of IRS-1 and serine phosphorylation of Akt, whereas incubation with LA strongly activated IRS-1 and Akt phosphorylation in NYGGF4 overexpression adipocytes. These results suggest that LA protects 3T3-L1 adipocytes from NYGGF4-induced IR partially through increasing phosphorylation of IRS-1 and Akt and provide evidence that NYGGF4 may be a potential target for the treatment of obesity and obesity-related IR.
authors.affiliation: Department of Child Health, Huai'an Maternity and Child Health Hospital, Huai'an 223002, China.
authors.forename: Yu-mei
authors.initials: YM
authors.lastname: Wang
authors.forename: Xiao-fei
authors.initials: XF
authors.lastname: Lin
authors.forename: Chun-mei
authors.initials: CM
authors.lastname: Shi
authors.forename: Lan
authors.initials: L
authors.lastname: Lu
authors.forename: Zhen-Ying
authors.initials: ZY
authors.lastname: Qin
authors.forename: Guan-zhong
authors.initials: GZ
authors.lastname: Zhu
authors.forename: Xin-guo
authors.initials: XG
authors.lastname: Cao
authors.forename: Chen-bo
authors.initials: CB
authors.lastname: Ji
authors.forename: Jie
authors.initials: J
authors.lastname: Qiu
authors.forename: Xi-rong
authors.initials: XR
authors.lastname: Guo
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D051379:Mice; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D008063:Thioctic Acid / Q000494:pharmacology*; D014162:Transfection
chemical_list: D002352:Carrier Proteins; D051275:Glucose Transporter Type 4; D055504:Insulin Receptor Substrate Proteins; C556403:NYGGF4 protein, mouse; D017382:Reactive Oxygen Species; C495693:Slc2a4 protein, mouse; D008063:Thioctic Acid; D051057:Proto-Oncogene Proteins c-akt