NDLI: Growth receptor binding protein 10 inhibits glucose-stimulated insulin release from pancreatic ß-cells associated with suppression of the insulin/insulin-like growth factor-1 signalling pathway.

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Growth receptor binding protein 10 inhibits glucose-stimulated insulin release from pancreatic ß-cells associated with suppression of the insulin/insulin-like growth factor-1 signalling pathway.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Ling Li, Xiaowen Zhu, Yunxia Zhang, Mingliang Yin, Dechao Lu, Junxi Liu, Feng Wang, Chen Jia, Weiping
Description	Country affiliation: China Author Affiliation: Li L ( Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China)
Abstract	Growth receptor binding protein 10 (Grb10) is an adaptor protein that interacts with the insulin receptor and insulin-like growth factor (IGF)-1 receptor. Overexpression of Grb10 in muscle cells and adipocytes inhibits insulin signalling, and transgenic mice overexpressing Grb10 exhibit impaired glucose tolerance. However, the roles of Grb10 in ß-cells remain unknown. The aim of the present study was to explore the effect of Grb10 on ß-cell function. The effects of Grb10 on glucose-stimulated insulin secretion (GSIS) and the insulin/IGF-1 signalling pathway were investigated in rat islets and/or dispersed islet cells with Grb10 overexpresion by adenovirus transfection. Protein expression was detected by western blot analysis. We found that Grb10 was expressed in both human and rat pancreas. Expression of Grb10 was increased in islets isolated from rats fed a high-fat plus high-sugar diet compared with islets isolated from rats fed normal chow diet, as well as in INS 832/13 cells exposed to high levels of glucose (20 mmol/L), palmitate (1 mmol/L) and interleukin-1ß (50 U/mL). Overexpression of Grb10 in INS 832/13 cells or rat islets impaired GSIS compared with the respective control (all P < 0.05). Moreover, inhibition of GSIS by Grb10 overexpression was associated with a decrease in insulin- and IGF-1-induced Akt and extracellular signal-regulated kinase 1/2 phosphorylation. The results of the present study demonstrate that Grb10 is an important negative regulator of insulin/IGF-1 signalling in pancreatic ß-cells and a potential target to improve ß-cell function.
File Format	HTM / HTML
ISSN	03051870
Issue Number	12
Volume Number	40
e-ISSN	14401681
Journal	Clinical and Experimental Pharmacology and Physiology
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2013-12-01
Publisher Place	Australia
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Physiology Discipline Pharmacology Grb10 Adaptor Protein Physiology Glucose Pharmacology Insulin-like Growth Factor I Antagonists & Inhibitors Insulin-secreting Cells Drug Effects Insulin Secretion Signal Transduction Animals Cell Culture Techniques Cells, Cultured Diet, High-fat Biosynthesis Humans Insulin Resistance Metabolism Interleukin-1beta Map Kinase Signaling System Male Organ Specificity Palmitates Phosphorylation Proto-oncogene Proteins C-akt Rats Rats, Sprague-dawley Transfection Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Pharmacology

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