Articles

Hyperglycemia induced generation of ADTIQ and dopamine metabolism imbalance

  • XIE Bingjie ,
  • WU Hanyan ,
  • DENG Yulin
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  • School of Life Science, Beijing Institute of Technology, Beijing 100081, China

Received date: 2015-07-02

  Revised date: 2015-07-31

  Online published: 2015-09-12

Abstract

Recent studies show that for the type 2 diabetes the Parkinson's disease is more likely to be developed than for normal diabetes, and the 1-acetyl-6, 7-dihydroxyl-1, 2, 3, 4-tetrahydroisoquinoline (ADTIQ) could be a key factor associated with the diabetes and the PD. In the present study, the SH-SY5Y cells are used as a model to investigate the ADTIQ generated conditions. It is found that the hyperglycemia could induce the increase of the endogenous methylglyoxal, which might react with the dopamine to generate the ADTIQ. Again, the hyperglycemia leads to a reduction of the dopamine in the SH-SY5Y cells and the plasma of the type 2 diabetic rats, and an increase of the tyrosine hydroxylase (TH) and the dopamine transporter (DAT). So, the hyperglycemia induces the generation of the ADTIQ and the dopamine metabolism imbalance. The generation of the ADTIQ could play a key role in increasing the risk of the PD in patients with diabetes.

Cite this article

XIE Bingjie , WU Hanyan , DENG Yulin . Hyperglycemia induced generation of ADTIQ and dopamine metabolism imbalance[J]. Science & Technology Review, 2015 , 33(17) : 90 -95 . DOI: 10.3981/j.issn.1000-7857.2015.17.010

References

1] Shastry B S. Parkinson disease:Etiology, pathogenesis and future of gene therapy[J]. Neuroscience Research, 2001, 41(1):5-12.
[2] Chase T N, Oh J D, Blanchet P J. Neostriatal mechanisms in parkinson's disease[J]. Neurology, 1998, 51(Suppl 2):S30-35.
[3] Hu G, Jousilahti P, Bidel S, et al. Type 2 diabetes and the risk of parkinson's disease[J]. Diabetes Care, 2007, 30(4):842-847.
[4] Driver J A, Smith A, Buring J E, et al. Prospective cohort study of type 2 diabetes and the risk of parkinson's disease[J]. Diabetes Care, 2008, 31 (10):2003-2005.
[5] Xu Q, Park Y, Huang X, et al. Diabetes and risk of parkinson's disease[J]. Diabetes Care, 2011, 34(4):910-915.
[6] Cereda E, Barichella M, Pedrolli C, et al. Diabetes and risk of parkinson's disease[J]. Movement Disorders, 2013, 28(2):257.
[7] Cereda E, Barichella M, Pedrolli C, et al. Diabetes and risk of parkinson's disease:A systematic review and meta-analysis[J]. Diabetes Care, 2011, 34(12):2614-2623.
[8] Choi J Y, Jang E H, Park C S, et al. Enhanced susceptibility to 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine neurotoxicity in high-fat dietinduced obesity[J]. Free Radical Biology and Medicine, 2005, 38(6):806-816.
[9] Morris J K, Bomhoff G L, Stanford J A, et al. Neurodegeneration in an animal model of parkinson's disease is exacerbated by a high-fat diet[J]. American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2010, 299(4):1082-1090.
[10] Santiago J A, Potashkin J A. Sha red dysregulated pathways lead to parkinson's disease and diabetes[J]. Trends in Molecular Medicine, 2013, 19(3):176-186.
[11] Palacios N, Ascherio A. Reply to:Diabetes and risk of parkinson's disease[J]. Movement Disorders, 2013, 28(2):258.
[12] Deng Y, Zhang Y, Li Y, et al. Occurrence and distribution of salsolinollike compound, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (adtiq) in parkinsonian brains[J]. Journal of Neural Transmission, 2012, 119(4):435-441.
[13] Xie B, Lin F, Ullah K, et al. A newly discovered neurotoxin adtiq associated with hyperglycemia and parkinson's disease[J]. Biochemical and Biophysical Research Communications, 2015, 459(3):361-366.
[14] Kikuchi S, Shinpo K, Moriwaka F, et al. Neurotoxicity of methylglyoxal and 3-deoxyglucosone on cultured cortical neurons:Synergism between glycation and oxidative stress, possibly involved in neurodegenerative diseases[J]. Journal of Neuroscience Research, 1999, 57(2):280-289.
[15] Shinpo K, Kikuchi S, Sasaki H, et al. Selective vulnerability of spinal motor neurons to reactive dicarbonyl compounds, intermediate products of glycation, in vitro:Implication of inefficient glutathione system in spinal motor neurons[J]. Brain Research, 2000, 861(1):151-159.
[16] Lu J, Randell E, Han Y, et al. Increased plasma methylglyoxal level, inflammation, and vascular endothelial dysfunction in diabetic nephropathy[J]. Clinical Biochemistry, 2011, 44(4):307-311.
[17] Vander D L. Methylglyoxal, diabetes mellitus and diabetic complications[J]. Drug Metabolism and Drug Interactions, 2008, 23(1/2):93-124.
[18] Turk Z, Nemet I, Varga L, et al. Elevated level of methylglyoxal during diabetic ketoacidosis and its recovery phase[J]. Diabetes & Metabolism, 2006, 32(2):176-180.
[19] Hipkiss A R. Aging risk factors and parkinson's disease:Contrasting roles of common dietary constituents[J]. Neurobiology of Aging, 2014, 35 (6):1469-1472.
[20] Alan R. Parkinson's disease and type-2 diabetes:Methylglyoxal may be a common causal agent; carnosine could be protective[J/OL]. Molecular Medicine & Therapeutics[2015-07-02]. http://mattitolonen.fi/files/pdf/Hipkiss_2013.pdf.
[21] Burke W J, Li S W, Chung H D, et al. Neurotoxicity of mao metabolites of catecholamine neurotransmitters:Role in neurodegenerative diseases[J]. Neurotoxicology, 2004, 25(1/2):101-115.
[22] Stokes A H, Hastings T G, Vrana K E. Cytotoxic and genotoxic potential of dopamine[J]. Journal of Neuroscience Research, 1999, 55(6):659-665.
[23] Kitayama S, Wang J B, Uhl G R. Dopamine transporter mutants selectively enhance mpp+ transport[J]. Synapse, 1993, 15(1):58-62.
[24] Boada J, Cutillas B, Roig T, et al. Mpp(+)-induced mitochondrial dysfunction is potentiated by dopamine[J]. Biochemical and Biophysical Research Communications, 2000, 268(3):916-920.
[25] Song D W, Xin N, Xie B J, et al. Formation of a salsolinol-like compound, theneurotoxin,1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in a cellular model of hyperglycemia and a rat model of diabetes[J]. International Journal of Molecular Medicine, 2014, 33(3):736-742.
[26] Morris J K, Bomhoff G L, Gorres B K, et al. Insulin resistance impairs nigrostriatal dopamine function[J]. Experimental Neurology, 2011, 231 (1):171-180.
[27] Schultz W. Getting formal with dopamine and reward[J]. Neuron, 2002, 36(2):241-263.
[28] Xie B, Lin F, Peng L, et al. Methylglyoxal increased dopamine level and led to oxidative stress in sh-sy5y cells[J]. Acta Biochimica et Biophysica Sinica, 2014, 46(11):950-956.
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