NDLI: 3-Deoxyglucosone induces insulin resistance by impairing insulin signaling in HepG2 cells.

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3-Deoxyglucosone induces insulin resistance by impairing insulin signaling in HepG2 cells.

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3-Deoxyglucosone induces insulin resistance by impairing insulin signaling in HepG2 cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Qian, Zhen Song, Xiudao Wang, Fei Zhang, Lurong Liang, Guoqiang Jiang, Guorong
Description	Author Affiliation: Liang G ( Basic Research Laboratory, Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, Suzhou, Jiangsu 215003, P.R. China.); Wang F ( Basic Research Laboratory, Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, Suzhou, Jiangsu 215003, P.R. China.); Song X ( Basic Research Laboratory, Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, Suzhou, Jiangsu 215003, P.R. China.); Zhang L ( Basic Research Laboratory, Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, Suzhou, Jiangsu 215003, P.R. China.); Qian Z ( Basic Research Laboratory, Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, Suzhou, Jiangsu 215003, P.R. China.); Jiang G ( Basic Research Laboratory, Suzhou Academy of Wumen Chinese Medicine, Suzhou Hospital of Traditional Chinese Medicine, Suzhou, Jiangsu 215003, P.R. China.)
Abstract	3-Deoxyglucosone (3DG), a highly reactive dicarbonyl intermediate generated during glycation, has been confirmed to be markedly elevated in the plasma of patients with diabetes. Our previous study found that there is an association between increasing accumulation of plasma 3DG and impaired glucose regulation in non-diabetic seniors (females, >50 years old; males, >55 years old). It was also found that 3DG led to impaired plasma glucose homeostasis in healthy mice, however, the mechanisms underlying the deleterious effect of 3DG in diabetes remain to be fully elucidated. The present study aimed to investigate the ability of 3DG to cause hepatic insulin resistance in a cell model by assessing glucose uptake and glycogen content. In addition, the molecular signaling events, including the phosphoinositide 3kinase (PI3K)/AKT/glucose transporter 2 (GLUT2) and PI3K/AKT/glycogen synthase kinase3 (GSK3) pathways, which affect hepatic insulin resistance, were further investigated using Western blot analysis. The results showed that 3DG (10300 ng/ml) had no significant effect on HepG2 cell viability, however, the viability of the HepG2 cells decreased with exposure to concentrations of 500 and 1,000 ng/ml. Treatment with noncytotoxic 3DG concentrations resulted in decreased uptake of glucose and glycogen content with insulin stimulation, but not under basal conditions. The insulininduced expression of GLUT2 and pGSK3 were eliminated by 3DG (80 and 300 ng/ml), in addition to inhibiting the phosphorylation of downstream effectors of the insulin signaling pathway, including insulin receptor substrate 1, PI3K and AKT. In conclusion, the findings of the present study indicated that the addition of exogenous 3DG directly contributed to the induction of insulin resistance by impairing insulin signaling in the HepG2 cells, which suggested that 3DG may be involved in worsening of the diabetic condition.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	13
Language	English
Publisher	Spandidos Publications
Publisher Date	2016-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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