title: Curcumin improves high glucose-induced INS-1 cell insulin resistance via activation of insulin signaling.
abstract: Curcumin is a yellow pigment isolated from Corcuma longan. This research investigates the improvement of curcumin on INS-1 cells with insulin resistance induced by high glucose. INS-1 cells were treated with high glucose (30 mmol L(-1)) for 48 h. Subsequently, the medium was replaced with curcumin for 24 h. Curcumin effectively increased insulin gene expression and glucose stimulated insulin secretion (GSIS) in a dose-dependent manner. Furthermore, the molecular mechanism of curcumin-induced insulin expression and secretion in high glucose-induced INS-1 cells was investigated in this study. Curcumin increased the expression of glucose transporter 2 (GLUT2) and phosphorylation of insulin receptor (IR), insulin receptor substrate-1 (IRS1), phosphatidylinositol-3-kinase (PI3K) and AKT in the INS-1 cells. Moreover, curcumin stimulation increased the expression of PDX-1 and GCK. This investigation suggests that curcumin prevented high glucose-reduced insulin expression and secretion through activation of the PI3K/Akt/GLUT2 pathway in INS-1 cells.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, 157 Baojian Road, Nangang District, 150086, Harbin, People's Republic of China. wenying_alice@163.com hongfengyer7@126.com wanghuan662@163.com zhulin121@sina.cn xuejiegod1@163.com 302503168@qq.com duyu820113@126.com.
authors.forename: Zhenfeng
authors.initials: Z
authors.lastname: Song
authors.forename: Huan
authors.initials: H
authors.lastname: Wang
authors.forename: Lin
authors.initials: L
authors.lastname: Zhu
authors.forename: Mingbao
authors.initials: M
authors.lastname: Han
authors.forename: Yuan
authors.initials: Y
authors.lastname: Gao
authors.forename: Yu
authors.initials: Y
authors.lastname: Du
authors.forename: Ying
authors.initials: Y
authors.lastname: Wen
mesh_terms: D000818:Animals; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D003474:Curcumin / Q000494:pharmacology*; D005941:Glucokinase / Q000235:genetics / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage / Q000009:adverse effects* / Q000032:analysis; D051273:Glucose Transporter Type 2 / Q000235:genetics / Q000378:metabolism; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D051273:Glucose Transporter Type 2; D018398:Homeodomain Proteins; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D012333:RNA, Messenger; C495683:Slc2a2 protein, rat; D015534:Trans-Activators; C084010:pancreatic and duodenal homeobox 1 protein; D019869:Phosphatidylinositol 3-Kinases; D005941:Glucokinase; D011972:Receptor, Insulin; D051057:Proto-Oncogene Proteins c-akt; D003474:Curcumin; D005947:Glucose