Login Register Cart 0
Generic placeholder image

Current Diabetes Reviews

Editor-in-Chief

ISSN (Print): 1573-3998
ISSN (Online): 1875-6417

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
General Review Article

Glycation and HMG-CoA Reductase Inhibitors: Implication in Diabetes and Associated Complications

Author(s): Rabia Nabi, Sahir Sultan Alvi, Mohd. Saeed, Saheem Ahmad and Mohammad Salman Khan*

Volume 15, Issue 3, 2019

Page: [213 - 223] Pages: 11

DOI: 10.2174/1573399814666180924113442

Price: $65

Abstract

Introduction: Diabetes Mellitus (DM) acts as an absolute mediator of cardiovascular risk, prompting the prolonged occurrence, size and intricacy of atherosclerotic plaques via enhanced Advanced Glycation Endproducts (AGEs) formation. Moreover, hyperglycemia is associated with enhanced glyco-oxidized and oxidized Low-Density Lipoprotein (LDL) possessing greater atherogenicity and decreased the ability to regulate HMG-CoA reductase (HMG-R). Although aminoguanidine (AG) prevents the AGE-induced protein cross-linking due to its anti-glycation potential, it exerts several unusual pharmaco-toxicological effects thus restraining its desirable therapeutic effects. HMG-R inhibitors/ statins exhibit a variety of beneficial impacts in addition to the cholesterol-lowering effects.

Objective: Inhibition of AGEs interaction with receptor for AGEs (RAGE) and glyco-oxidized-LDL by HMG-R inhibitors could decrease LDL uptake by LDL-receptor (LDL-R), regulate cholesterol synthesis via HMG-R, decrease oxidative and inflammatory stress to improve the diabetes-associated complications.

Conclusion: Current article appraises the pathological AGE-RAGE concerns in diabetes and its associated complications, mainly focusing on the phenomenon of both circulatory AGEs and those accumulating in tissues in diabetic nephropathy, diabetic neuropathy, and diabetic retinopathy, discussing the potential protective role of HMG-R inhibitors against diabetic complications.

Keywords: Glycation, Advanced Glycation end products (AGEs), HMG-R inhibitors, diabetic complications, Cardiovascular disease (CVD), Receptor for AGEs (RAGE).

[1]
Kumar A, Goel MK, Jain RB, Khanna P, Chaudhary V. India towards diabetes control: Key issues. Australas Med J 2013; 6(10): 524-31.
[2]
Whiting DR, Guariguata L, Weil C, Shaw J. IDF Diabetes atlas: Global estimates of the prevalence of diabetes for 2011 and 2030. Diabetes Res Clin Pract 2011; 94(3): 311-21.
[3]
Kaveeshwar SA, Cornwall J. The current state of diabetes mellitus in India. Australas Med J 2014; 7(1): 45-8.
[4]
Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract 2010; 87(1): 4-14.
[5]
Negre-Salvayre A, Salvayre R, Augé N, Paplona R, Portero-Otín M. Hyperglycemia and glycation in diabetic complications. Antioxid Redox Signal 2009; 11(12): 3071-109.
[6]
Akhter F, Khan MS, Alatar AA, Faisal M, Ahmad S. Antigenic role of the adaptive immune response to D-ribose glycated LDL in diabetes, atherosclerosis and diabetes atherosclerotic patients. Life Sci 2016; 15(151): 139-46.
[7]
Vlassara H, Uribarri J, Cai W, et al. Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease. Clin J Am Soc Nephrol 2012; 7(6): 934-42.
[8]
Guimaraes EL, Empsen C, Geerts A, Van Grunsven LA. Advanced glycation end products induce production of reactive oxygen species via the activation of NADPH oxidase in murine hepatic stellate cells. J Hepatol 2010; 52(3): 389-97.
[9]
Bharti AK, Agrawal A, Agrawal S. Advanced glycation end products in progressive course of diabetic nephropathy: Exploring interactive associations. Int J Pharm Sci Res 2015; 6(2): 521-8.
[10]
Tabrez S, Al-Shali KZ, Ahmad S. Lycopene powers the inhibition of glycation-induced diabetic nephropathy: A novel approach to halt the AGE-RAGE axis menace. Biofactors 2015; 41(5): 372-81.
[11]
Singh P, Ramesha H. Jayaramaiah, et al Potential dual role of eugenol in inhibiting advanced glycation end products in diabetes. Proteomic and mechanistic insights. Sci Rep 2016; 7(6): 18798.
[http://dx.doi.org/doi:10.1038/srep18798]
[12]
Voziyan PA, Hudson BG. Pyridoxamine as a multifunctional pharmaceutical: Targeting pathogenic glycation and oxidative damage. Cell Mol Life Sci 2005; 62(15): 1671-81.
[13]
American Diabetes Association.Diagnosis and classification of diabetes mellitus. Diabetes Care 2010; 33(1): S62-9.
[14]
Rizvi AA. Type 2 diabetes: Epidemiologic trends, evolving pathogenetic concepts, and recent changes in therapeutic approach. South Med J 2004; 97(11): 1079-87.
[15]
Nabi R, Alvi SS, Khan RH, Ahmad S, Ahmad S, Khan MS. Antiglycation study of HMG-R inhibitors and tocotrienol against glycated BSA and LDL: A comparative study. Int J Biol Macromol 2018; 116: 983-92.
[16]
Lin S, Huang K, Weng C, Shiuan D. Exploration of natural product ingredients as inhibitors of human HMG-CoA reductase through structure-based virtual screening. Drug Des Devel Ther 2015; 9: 3313-24.
[17]
Jasiñska M, Owczarek J, Orszulak-Michalak D. Statins: A new insight into their mechanisms of action and consequent pleiotropic effects. Pharmacol Rep 2007; 59(5): 483-99.
[18]
Kavalipati N, Shah J, Ramakrishan A, Vasnawala H. Pleiotropic effects of statins. Indian J Endocrinol Metab 2015; 19(5): 554-62.
[19]
Maillard LC. Action des acides amines sur les sucres; formation des melanoidines par voie methodique. C R Hebd Seances Acad Sci 1912; 154: 66-8.
[20]
Ahmad S, Shahab U, Baig MH, et al. Inhibitory effect of metformin and pyridoxamine in the formation of early, intermediate and advanced glycation end-products. PLoS One 2013; 8: e72128.
[21]
Yamagishi S, Nakamura N, Suematsu M, Kaseda K, Matsui T. Advanced glycation end products: A molecular target for vascular complications in diabetes. Mol Med 2015; 21: S32-40.
[22]
Lin JA, Wu CH, Lu CC, Hsia SM, Yen GC. Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression. Mol Nutr Food Res 2016; 60(8): 1850-64.
[23]
Lankin V, Konovalova G, Tikhaze A, Shumaev K, Kumskova E. Viigimaa. The initiation of free radical peroxidation of low-density lipoproteins by glucose and its metabolite methylglyoxal: A common molecular mechanism of vascular wall injure in atherosclerosis and diabetes. Mol Cell Biochem 2014; 395(1-2): 241-52.
[24]
Thornalley PJ, Battah S, Ahmed N, et al. Quantitative screening of advanced glycation end-products in cellular and extra- cellular proteins by tandem mass spectrometry. Biochem J 2003; 375(Pt 3): 581-92.
[25]
Akhter F, Khan MS, Shahab U. Moinuddin, Ahmad S. Bio-physical characterization of ribose induced glycation: A mechanistic study on DNA perturbations. Int J Biol Macromol 2013; 58: 206-10.
[26]
Mustafa I, Ahmad S, Dixit K. Moinuddin, Ahmad J, Ali A. Glycated human DNA is a preferred antigen for anti-DNA antibodies in diabetic patients. Diabetes Res Clin Pract 2012; 95(1): 98-104.
[27]
Bucala R, Vlassara H. Advanced glycation end-products in diabetic renal and vascular disease. Am J Kidney Dis 1995; 26(6): 875-88.
[28]
Ramasamy R, Yan SF, Herold K, Clynes R, Schmidt AM. Receptor for advanced glycation end products fundamental roles in the inflammatory response: winding the way to the pathogenesis of endothelial dysfunction and atherosclerosis. Ann N Y Acad Sci 2008; 1126: 7-13.
[29]
Baynes JW. Chemical modification of proteins by lipids in diabetes. Clin Chem Lab Med 2003; 41(9): 1159-65.
[30]
Gugliucci A, Menini T. The axis AGE-RAGE-soluble RAGE and oxidative stress in chronic kidney disease. Adv Exp Med Biol 2014; 824: 191-208.
[31]
Quade-Lyssy P, Kanarek AM, Baiersdörfer M, Postina R, Kojro E. Statins stimulate the production of a soluble form of the receptor for advanced glycation end products. J Lipid Res 2013; 54(11): 3052-61.
[32]
Yamagishi S, Nakamura K, Matsui T. Regulation of advanced glycation end product (AGE)-receptor (RAGE) system by PPAR gamma agonists and its implication in cardiovascular disease. Pharmacol Res 2009; 60(3): 174-8.
[33]
Pathania M, Rathaur VK, Yadav N, Jayara A, Chaturvedi A. Quantitative micro-albuminuria assessment from ‘random voided urinary albumin: Creatinine ratio’ versus ‘24 hours urinary albumin concentration’ for screening of diabetic nephropathy. J Clin Diagn Res 2013; 7(12): 2828-31.
[34]
Fukami K, Yamagishi S, Ueda S, Okuda S. Role of AGEs in diabetic nephropathy. Curr Pharm Des 2008; 14(10): 946-52.
[35]
Zhuang A, Forbes JM. Diabetic kidney disease: A role for advanced glycation end-product receptor 1 (AGE-R1)? Glycoconj J 2016; 33(4): 645-52.
[36]
Bohlender JM, Franke S, Stein G, Wolf G. Advanced glycation end products and the kidney. Am J Physiol Renal Physiol 2005; 289(4): 645-59.
[37]
McNulty M, Mahmud A, Feely J. Advanced glycation end-products and arterial stiffness in hypertension. Am J Hypertens 2007; 20(3): 242-07.
[38]
Yamamoto Y, Miura J, Sakurai S, et al. Assaying soluble forms of receptor for advanced glycation end products. Arterioscler Thromb Vasc Biol 2007; 27: e33-4.
[39]
Yamagishi S, Inagaki Y, Okamoto T, Amano S, Koga K, Takeuchi M. Advanced glycation end products inhibit de novo protein synthesis and induce TGF beta overexpression in proximal tubular cells. Kidney Int 2003; 63(2): 464-73.
[40]
Ahmad N. Advanced glycation end-products role in pathology of diabetic complications. Diabetes Res Clin Pract 2005; 67(1): 3-21.
[41]
Mao Y, Ootaka T, Saito T, Sato T, Ito S. The involvement of advanced glycation end-products (AGEs) in renal injury of diabetic glomerulosclerosis: Association with phenotypic change in renal cells and infiltration of immune cells. Clin Exp Nephrol 2003; 7(3): 3201-9.
[42]
Hanewinckel R, Drenthen J, van Oijen M, Hofman A, van Doorn PA, Ikram MA. Prevalence of polyneuropathy in the general middle-aged and elderly population. Neurology 2016; 87(18): 1892-8.
[43]
Sugimoto K, Yasujima M, Yagihashi S. Role of advanced glycation end products in diabetic neuropathy. Curr Pharm Des 2008; 14(10): 953-61.
[44]
Lukic IK, Humpert PM, Nawroth PP, Bierhaus A. The RAGE pathway: Activation and perpetuation in the pathogenesis of diabetic neuropathy. Ann N Y Acad Sci 2008; 1126: 76-80.
[45]
Feldman EL, Nave KA, Jensen TS, Bennett DLH. New horizons in diabetic neuropathy: mechanisms, Bioenergetics and Pain. Neuron 2017; 93(6): 1296-313.
[46]
Furukawa K, Fuse I, Iwakura Y, et al. Advanced glycation end products induce brain-derived neurotrophic factor release from human platelets through the Src-family kinase activation. Cardiovasc Diabetol 2017; 16(1): 1-9.
[47]
Boulton AJM, Malik RA. Diabetes mellitus: neuropathy.In:Jameson JL, De Groot LJ, de, Eds. Endocrinology: Adult and pediatric. Philadelphia, PA: Elsevier Saunders, In: 2016.
[48]
Frank RN. Diabetic retinopathy. N Engl J Med 2004; 350(1): 48-58.
[49]
Chen M, Curtis TM, Stitt AW. Advanced glycation end products and diabetic retinopathy. Curr Med Chem 2013; 20(26): 3234-340.
[50]
Stitt AW. Advanced glycation: an important pathological event in diabetic and age related ocular disease. Br J Ophthalmol 2001; 85(6): 746-53.
[51]
Fokkens BT, Mulder DJ, Schalkwijk CG, Scheijen JL, Smit AJ, Los LI. Vitreous advanced glycation end-products and α-dicarbonyls in retinal detachment patients with type 2 diabetes mellitus and non-diabetic controls. PLoS One 2017; 12(3): 1-11.
[52]
Kleina BEK, Horaka KL, Maynard JD, Leea KE, Klein R. Association of skin intrinsic fluorescence with retinal microvascular complications of long term type 1 diabetes in the wisconsin epidemiologic study of diabetic retinopathy. Ophthalmic Epidemiol 2017; 24(2)
[http://dx.doi.org/10.1080/09286586.2016.1269934]
[53]
Pollreisz A, Schmidt-Erfurth U. Diabetic cataract-pathogenesis, epidemiology and treatment. J Ophthalmol 2010; 2010: 1-8.
[54]
Singh VP, Bali A, Singh N, Jaggi AS. Advanced glycation end products and diabetic complications. Korean J Physiol Pharmacol 2014; 18(1): 1-14.
[55]
Nin JW, Jorsal A, Ferreira I, et al. Higher plasma levels of advanced glycation end products are associated with incident cardiovascular disease and all-cause mortality in type 1 diabetes: a 12-year follow-up study. Diabetes Care 2011; 34(2): 442-7.
[56]
Yamagishi S, Matsui T. Pathological role of dietary advanced glycation end products in cardiometabolic disorders and the therapeutic intervention. Nutrition 2016; 32(2): 157-65.
[57]
Falcone C, Bozzini S, D’Angelo A, et al. Plasma levels of soluble receptor for advanced glycation end products and coronary atherosclerosis: possible correlation with clinical presentation. Dis Markers 2013; 35(3): 135-40.
[58]
Akhter F, Khan MS, Singh S, Ahmad S. An Immunohistochemical analysis to validate the rationale behind the enhanced immunogenicity of D-ribosylated low density lipo-protein. PLoS One 2014; 9(11): 1-8.
[59]
Daiji K, Keiichiro M, Kazunori U. Dyslipidemia in diabetic nephropathy. Ren Repl Ther 2016; 2(16)
[http://dx.doi.org/10.1186/s41100-016-0028-0]
[60]
Oshaghi EA, Khodadadi I, Mirzaei F, Khazaei M, Tavilani H, Goodarzi MT. Methanolic extract of dill leaves inhibits AGEs formation and shows potential hepatoprotective effects in CCl4 induced liver toxicity in rat. J Pharm (Cairo) 2017; 2017: 1-9.
[61]
Lewis BS, Harding JJ. The effects of aminoguanidine on the glycation (non-enzymic glycosylation) of lens protein. Exp Eye Res 1990; 50: 463-7.
[62]
Edelstein D, Brownlee M. Mechanistic studies of advanced glycosylation endproduct inhibition by aminoguanidine. Diabetes 1992; 41: 26-9.
[63]
Ou P, Wolff SP. Aminoguanidine: A drug proposed for prophylaxis in diabetes inhibits catalase and generates hydrogen peroxide in vitro. Biochem Pharmacol 1993; 46: 1139-44.
[64]
Freedman BI, Wuerth JP, Cartwright K, et al. Design and baseline characteristics for the aminoguanidine clinical trial in overt type 2 diabetic nephropathy (ACTION II). Control Clin Trials 1999; 20(5): 493-510.
[65]
Oturai PS, Rasch R, Haselager E, et al. Effects of heparin and aminoguanidine on glomerular basement membrane thickening in diabetic rats. APMIS 1996; 104: 259-64.
[66]
Suji G, Sivakami S. DNA damage by free radical production by aminoguanidine. Ann N Y Acad Sci 2006; 1067: 191-9.
[67]
Rinto, Suhartono MT. 3-Hidroxy-3-methylglutaryl-coenzym a reductase and inhibitor: The medies potential of the enzyme inhibitor. Res J Pharm Biol Chem Sci 2016; 7: 1569-77.
[68]
Alvi SS, Iqbal D, Ahmad S, Khan MS. Molecular rationale delineating the role of lycopene as a potent HMG-CoA reductase inhibitor: in vitro and in silico study. Nat Prod Res 2016; 30(18): 2111-4.
[69]
Zhou Q, Liao JK. Pleiotropic effects of statins: Basic research and clinical perspectives. Circ J 2010; 74(5): 818-26.
[70]
Paniagua JA, Lopez-Miranda J, Escribano A, et al. Cerivastatin improves insulin sensitivity and insulin secretion in early-state obese type 2 diabetes. Diabetes 2002; 51(8): 2596-603.
[71]
Alvi SS, Ansari IA, Khan I, Iqbal J, Khan MS. Potential role of lycopene in targeting proprotein convertase subtilisin/kexin type-9 to combat hypercholesterolemia. Free Radic Biol Med 2017; 108: 394-403.
[72]
Alvi SS, Ansari IA, Ahmad MK, Iqbal J, Khan MS. Lycopene amends LPS induced oxidative stress and hypertriglyceridemia via modulating PCSK-9 expression and Apo-CIII mediated lipoprotein lipase activity. Biomed Pharmacother 2017; 96: 1082-93.
[73]
Athyros VG, Mitsiou EK, Tziomalos K, Karagiannis A, Mikhailidis DP. Impact of managing atherogenic dyslipidemia on cardiovascular outcome across different stages of diabetic nephropathy. Expert Opin Pharmacother 2010; 11(5): 723-30.
[74]
Fujii M, Inoguchi T, Maeda Y, et al. Pitavastatin ameliorates albuminuria and renal mesangial expansion by downregulating NOX4 in db/db mice. Kidney Int 2007; 72(4): 473-80.
[75]
Kolavennu V, Zeng L, Peng H, Wang Y, Danesh FR. Targeting of RhoA/ROCK signaling ameliorates progression of diabetic nephropathy independent of glucose control. Diabetes 2008; 57(3): 714-23.
[76]
Rosario RF, Prabhakar S. Lipids and diabetic nephropathy. Curr Diab Rep 2006; 6(6): 455-62.
[77]
Thomas MC, Rosengård-Bärlund M, Mills V, et al. Serum lipids and the progression of nephropathy in type 1 diabetes. Diabetes Care 2006; 29: 317-22.
[78]
Thomas MT, Li J, Kislinger T, Qu W, et al. Blockade of receptor for advanced glycation end-products restores effective wound healing in diabetic mice. Am J Pathol 2001; 159(2): 513-25.
[79]
Deane R, Du Yan S, Submamaryan RK, et al. RAGE mediates amyloid-beta peptide transport across the blood-brain barrier and accumulation in brain. Nat Med 2003; 9(7): 907-13.
[80]
Xu L, Zang P, Feng B, Qian Q. Atorvastatin inhibits the expression of RAGE induced by advanced glycation end products on aortas in healthy Sprague–Dawley rats. Diabetol Metab Syndr 2014; 6: 1-10.
[81]
Fried LF. Effects of HMG-CoA reductase inhibitors (statins) on progression of kidney disease. Kidney Int 2008; 74(5): 571-6.
[82]
Ishibashi Y, Yamagishi S, Matsuia T, et al. Pravastatin inhibits advanced glycation end products (AGEs)-induced proximal tubular cell apoptosis and injury by reducing receptor for AGEs (RAGE) level. Metabolism 2012; 61(8): 1067-72.
[83]
Danesh FR, Sadeghi MM, Amro N, et al. 3-Hydroxy-3-methylglutaryl CoA reductase inhibitors prevent high glucose-induced proliferation of mesangial cells via modulation of Rho GTPase p21 signaling pathway: Implications for diabetic nephropathy. Proc Natl Acad Sci USA 2002; 99(12): 8301-5.
[84]
Mallappallil M, Friedman EA, Delano BG, McFarlane SI, Salifu MO. Chronic kidney disease in the elderly: Evaluation and management. Clin Pract (Lond) 2014; 11(5): 525-35.
[85]
Navaneethan SD, Yehnert H, Moustarah F, Schreiber MJ, Schauer PR, Beddhu S. Weight loss interventions in chronic kidney disease: a systematic review and meta-analysis. Clin J Am Soc Nephrol 2009; 4(10): 1565-74.
[86]
Sanguankeo A, Upala S, Cheungpasitporn W, Ungprasert P, Knight EL. Effects of statins on renal outcome in chronic kidney disease patients: A systematic review and meta-analysis. PLoS One 2015; 10(7): 1-13.
[87]
Geng Q, Ren J, Song J, Li S, Chen H. Meta-analysis of the effect of statins on renal function. Am J Cardiol 2014; 114(4): 562-70.
[88]
Palmer SC, Navaneethan SD, Craig JC, et al. HMG CoA reductase inhibitors (statins) for people with chronic kidney disease not requiring dialysis. Cochrane Db Syst Rev 2014; 31(5): CD007784.
[89]
Nozue T, Yamagishi S, Takeuchi M, et al. Effect of statins on the serum soluble form of receptor for advanced glycation end-products and its association with coronary atherosclerosis in patients with angina pectoris. IJC Metab Endocr 2014; 4: 47-52.
[90]
Davis TME, Yeap BB, Davis WA, Bruce DG. Lipid-lowering therapy and peripheral sensory neuropathy in type 2 diabetes: the Fremantle Diabetes Study. Diabetologia 2007; 51(4): 562-6.
[91]
Ali TK, El-Remessy AB. Diabetic retinopathy: current management and experimental therapeutic targets. Pharmacotherapy 2009; 29(2): 182-92.
[92]
Van Leiden HA, Dekker JM, Moll AC, et al. Blood pressure, lipids, and obesity are associated with retinopathy: the Hoorn study. Diabetes Care 2002; 25(8): 1320-5.
[93]
El-Azab MF, Mysona BA, El-Remessy AB. Statins for prevention of diabetic-related blindness: a new treatment option? Expert Rev Ophthalmol 2011; 6(3): 269-72.
[94]
Caldwell RB, Bartoli M, Behzadian MA, et al. Vascular endothelial growth factor and diabetic retinopathy: pathophysiological mechanisms and treatment perspectives. Diabetes Metab Res Rev 2003; 19(6): 442-55.
[95]
Bartoli M, Al-Shabrawey M, Labazi M, et al. HMG-CoA Reductase Inhibitors (Statin) prevents retinal neovascularization in a model of oxygen-induced retinopathy. Invest Ophthalmol Vis Sci 2009; 50: 4934-40.
[96]
Jakobisiak M, Golab J. Potential antitumor effects of statins. Int J Oncol 2003; 23(4): 1055-69.
[97]
Cuccurullo C, Iezzi A, Fazia ML, et al. Suppression of RAGE as a basis of Simvastatin dependent plaque stabilization in type 2 diabetes. Arterioscler Thromb Vasc Biol 2006; 26(12): 2716-23.
[98]
Hofmann MA, Drury S, Fu C, et al. RAGE mediates a novel proinflammatory axis: the cell surface receptor for S100/calgranulin polypeptides. Cell 1999; 97(7): 889-901.
[99]
Ando H, Takamura T, Ota T, Nagai Y, Kobayashi K. Cerivastatin improves survival of mice with lipopolysaccharide-induced sepsis. J Pharmacol Exp Ther 2000; 294(3): 1043-6.
[100]
Calkin AC, Giunti S, Sheehy KJ, et al. The HMG-CoA reductase inhibitor rosuvastatin and the angiotensin receptor antagonist candesartan attenuate atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes via effects on advanced glycation, oxidative stress and inflammation. Diabetologia 2008; 51(9): 1731-40.
[101]
Santilli F, Bucciarelli L, Noto D, et al. Decreased plasma soluble RAGE in patients with hypercholesterolemia: Effects of statins. Free Radic Biol Med 2007; 43(9): 1255-62.
[102]
Yamagishi S, Nakamura K, Matsui T, Sato T, Takeuchi M. Potential utility of statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in diabetic retinopathy. Med Hypotheses 2006; 66(5): 1019-21.
[103]
Yamagishi S, Matsui T, Nakamura K. Atorvastatin and diabetic vascular complications. Curr Pharm Des 2006; 12: 1549-54.
[104]
Jinnouchi Y, Yamagishi S, Takeuchi M, et al. Atorvastatin decreases serum levels of advanced glycation end products (AGEs) in patients with type 2 diabetes. Clin Exp Med 2006; 6: 191-3.
[105]
Bayturan O, Kapadia S, Nicholls SJ. , Tuzcu, et al Clinical predictors of plaque progression despite very low levels of low-density lipoprotein cholesterol. J Am Coll Cardiol 2010; 55(24): 2736-42.
[106]
Shrivastava U, Misra A, Mohan V, Unnikrishnan R, Bachani D. Obesity, diabetes and cardiovascular diseases in india: public health challenges. Curr Diabetes Rev 2017; 13: 65-80.
[107]
Roberto S, Crisafulli A. consequences of type 1 and 2 diabetes mellitus on the cardiovascular regulation during exercise: a brief review. Curr Diabetes Rev 2017; 13: 560-5.
[108]
Felício JS, Koury CC, Carvalho CT, et al. Present insights on cardiomyopathy in diabetic patients. Curr Diabetes Rev 2016; 12: 384-95.
[109]
Wanderley RDR, Jorge AR, Braulio VB, Arbex AK, Marcadenti A. Visceral adiposity measurements, metabolic and inflammatory profile in obese patients with and without type 2 diabetes mellitus: a crosssectional analysis. Curr Diabetes Rev 2017; 13: 11-8.
[110]
Bonora E, Kiechl S, Mayr A, et al. High-normal HbA1c is a strong predictor of type 2 diabetes in the general population. Diabetes Care 2011; 34(4): 1038-40.
[111]
Eeg-Olofsson K, Cederholm J, Nilsson PM, et al. New aspects of HbA1c as a risk factor for cardiovascular diseases in type 2 diabetes: an observational study from the Swedish National Diabetes Register (NDR). J Intern Med 2010; 268(5): 471-82.
[112]
Elley CR, Kenealy T, Robinson E, Drury PL. Glycated haemoglobin and cardiovascular outcomes in people with Type 2 diabetes: a large prospective cohort study. Diabet Med 2008; 25(11): 1295-301.
[113]
Takayama T, Hiro T, Yamagishi M, et al. Effect of rosuvastatin on coronary atheroma in stable coronary artery disease: multicenter coronary atherosclerosis study measuring effects of rosuvastatin using intravascular ultrasound in Japanese subjects (COSMOS). Circ J 2009; 73(11): 2110-7.
[114]
Takayama T, Hiro T, Yamagishi M, et al. Rationale and design for a study using intravascular ultrasound to evaluate effects of rosuvastatin on coronary artery atheroma in Japanese subjects: COSMOS study (Coronary Atherosclerosis Study Measuring Effects of Rosuvastatin Using Intravascular Ultrasound in Japanese Subjects). Circ J 2007; 71(2): 271-5.
[115]
Van de Ree MA, Huisman MV, Princen HMG, Meinders AE, Kluft C. The DALI-Study Group Strong decrease of high sensitivity C-reactive protein with high-dose atorvastatin in patients with type 2 diabetes mellitus. Atherosclerosis 2003; 166: 129-35.
[116]
Neil HAW, Ceglarek U, Thiery J, Paul S, Farmera A, Holman RR. Impact of atorvastatin and omega-3 ethyl esters 90 on plasma plant sterol concentrations and cholesterol synthesis in type 2 diabetes: A randomised placebo controlled factorial trial. Atherosclerosis 2010; 213: 512-7.
[117]
Konduracka E, Galicka-Latala D, Cieslik G, et al. Effect of atorvastatin on endothelial function and inflammation in long-duration type 1 diabetic patients without coronary heart disease and arterial hypertension. Diabetes Obes Metab 2008; 10: 719-25.
[118]
Chu CS, Lee KT, Lee MY, et al. Effects of rosiglitazone alone and in combination with atorvastatin on non-traditional markers of cardiovascular disease in patients with type 2 diabetes mellitus. Am J Cardiol 2006; 97: 646-50.
[119]
Adeshara K, Tupe R. Antiglycation and cell protective actions of metformin and glipizide in erythrocytes and monocytes. Mol Biol Rep 2016; 43(3): 195-205.
[120]
Sun YP, Gu JF, Tan XB, et al. Curcumin inhibits advanced glycation end product induced oxidative stress and inflammatory responses in endothelial cell damage via trapping methylglyoxal. Mol Med Rep 2016; 13(2): 1475-86.
[121]
Meeprom A, Sompong W, Chan CB, Adisakwattana S. Isoferulic acid, a new anti-glycation agent, inhibits fructose and glucose-mediated protein glycation in vitro. Molecules 2013; 18(6): 6439-54.
[122]
Anwar S, Younus H. Antiglycating potential of ellagic acid against glucose and methylglyoxal-induced glycation of superoxide dismutase. J Proteins and Proteom 2017; 8(1): 1-12.
[123]
Muthenna P, Akileshwari C, Reddy GB. Ellagic acid, a new antiglycating agent: its inhibition of Nε-(carboxymethyl) lysine. Biochem J 2012; 442(1): 221-30.
[124]
Kim HY, Lee JM, Yokozawa T, Sakata K, Lee S. Protective activity of flavonoid and flavonoid glycosides against glucose-mediated protein damage. Food Chem 2011; 126(3): 892-5.
[125]
Dhar A, Desai KM, Wu L. Alagebrium attenuates acute methylglyoxal-induced glucose intolerance IN sprague-dawley rats. Br J Pharmacol 2010; 159(1): 166-75.
[126]
Kim T, Spiegel DA. The unique reactivity of n-phenacyl-derived thiazolium salts toward α-dicarbonyl compounds. Rejuv Res 2013; 16(1): 43-50.
[127]
Ashraf JM, Shahab U, Tabrez S, Leea EJ, Choia I, Ahmad S. Quercetin as a finer substitute to aminoguanidine in the inhibition of glycation products. Int J Biol Macromol 2015; 77: 188-92.
[128]
Alvi SS, Ansari IA, Khan MS. Pleiotropic role of lycopene in protecting various risk factors mediated atherosclerosis. Ann Phytomedicine 2015; 4(1): 54-60.
[129]
Qiu YY, Tang LQ, Wei W. Berberine exerts renoprotective effects by regulating the AGEs-RAGE signaling pathway in mesangial cells during diabetic nephropathy. Mol Cell Endocrinol 2017; 443: 89-105.
[130]
Tama HL, Shiua SWM, Wonga Y, Chowa WS, Betteridge DJ, Tana KCB. Effects of atorvastatin on serum soluble receptors for advanced glycation end-products in type 2 diabetes. Atherosclerosis 2010; 209(1): 173-7.
[131]
Mahajan N, Bahl A, Dhawan V. C-reactive protein (CRP) up-regulates expression of receptor for advanced glycation end products (RAGE) and its inflammatory ligand EN-RAGE in THP-1 cells: Inhibitory effects of atorvastatin. Int J Cardiol 2010; 142(3): 273-8.
[132]
Nakamura T, Sato E, Fujiwara N, et al. Atorvastatin reduces proteinuria in non-diabetic chronic kidney disease patients partly via lowering serum levels of advanced glycation end products (AGEs). Oxid Med Cell Longev 2010; 3: 304-7.
[133]
Hwang AR, Han JH, Lim JH, Kang YJ, Woo CH. Fluvastatin inhibits AGE-induced cell proliferation and migration via an ERK5- dependent Nrf2 pathway in vascular smooth muscle cells. PLoS One 2017; 12(5): 1-14.

Rights & Permissions Print Cite
Article Metrics
80
7
1
2
© 2024 Bentham Science Publishers | Privacy Policy