Objective: Increased low-density lipoprotein (LDL) glycation in diabetics could facilitate LDL oxidation, which is proatherogenic. I studied plasma oxidized LDL (OxLDL) levels in diabetics and non-diabetics, their relation to glycemic control, and their circadian variations. Methods: OxLDL in diabetics (n=32) and in non-diabetics without coronary artery diseases (n=20) were compared. OxLDL in diabetics (n=24) was measured on Days 2, 3, 4, 8 and the last day of hospitalization. Circadian variation in OxLDL in diabetics (n=18) was also examined. Glycemic control was implemented during hospitalization. Patients: The diabetics were divided into two groups; moderately-controlled (MC) group (HbA1c < 9.0% at admission, n = 15) and poorly-controlled (PC) group (HbA1c ≧ 9.0% at admission, n = 9). Results: In the MC group, OxLDL decreased by 20.8% after glycemic control (p = 0.0139), but not in the PC group. OxLDL is correlated with LDL on Days 3, 4, 8 (r = 0.837, 0.864, 0.801, respectively), TG on Day 8(r = 0.932), and Lp(a) at discharge (r = 0.871). In the PC group, OxLDL was 15.8% higher on the average in the daytime than at night (p = 0.0024). Conclusion: Plasma OxLDL is decreased by glycemic control, particularly in moderately glycemic controlled patients. OxLDL has a circadian variation, particularly in poorly glycemic controlled patients. Long-term glycemic control could reduce the progression of atherosclerosis, by reducing OxLDL levels.
Published in | Science Journal of Clinical Medicine (Volume 3, Issue 5) |
DOI | 10.11648/j.sjcm.20140305.13 |
Page(s) | 91-97 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2014. Published by Science Publishing Group |
Diabetes Mellitus, Oxidized LDL, Circadian Variation
[1] | “Epidemiology of Diabetes Interventions and Complications (EDIC) Design, implementation, and preliminary results of a long-term follow-up of the Diabetes Control and Complications Trial cohort,” Diabetes Care 22:99-111, 1999 |
[2] | K.T. Khaw, N. Wareham, R. Luben, S. Bingham, S. Oakes, et al., “Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of european prospective investigation of cancer and nutrition (EPIC-Norfolk),” BMJ 322:15-18, 2001 |
[3] | A.I. Adler, H.A. Neil, S.E. Manley, R.R. Holman, and R.C. Turner, “Hyperglycemia and hyperinsulinemia at diagnosis of diabetes and their association with subsequent cardiovascular disease in the United Kingdom prospective diabetes study (UKPDS 47),” Am Heart J 138:S353-S359, 1999 |
[4] | E. Schleicher, T. Deufel, and O.H. Wieland,“Non-enzymatic glycosylation of human serum lipoproteins. Elevated epsilon-lysine glycosylated low density lipoprotein in diabetic patients,” FEBS Lett 129:1-4, 1981 |
[5] | E.C. Tsai, I.B. Hirsch, J.D. Brunzell, and A. Chait, “Reduced plasma peroxyl radical trapping capacity and increased susceptibility of LDL to oxidation in poorly controlled IDDM,” Diabetes 43:1010-1014, 1996 |
[6] | K. Kobayashi, J. Watanabe, F. Umeda, and H. Nawata, “Glycation accelerates the oxidation of low density lipoprotein by copper ions,” Endocr J 42:461-465, 1995 |
[7] | A. Bowie, D. Owens, P. Collins, A. Johnson, and G.H. Tomkin, “Glycosylated low density lipoprotein is more sensitive to oxidation: implications for the diabetic patient?,” Atherosclerosis 102:63-67, 1993 |
[8] | G. Sobal, J. Menzel, and H. Sinzinger, “Why is glycated LDL more sensitive to oxidation than native LDL? A comparative study,” Prostaglandins Leukot Essent Fatty Acids. 63:177-86, 2000 |
[9] | S. Parthasarathy, N. Santanam, S. Ramachandran, and O. Meilhac, “Oxidants and antioxidants in atherogenesis: an appraisal,” J. Lipid Res. 40: 2143 – 2157, 1999 |
[10] | S. Parthasarathy, and S.M. Rankin, “Role of oxidized low density lipoprotein in atherogenesis,” Prog Lipid Res. 31:127-143, 1992 |
[11] | Y. Higashi, T. Peng, J. Du, S. Sukhanov, Y. Li, et al., “A redox-sensitive pathway mediates oxidized LDL-induced downregulation of insulin-like growth factor-1 receptor” J. Lipid Res. 46:1266-1277, 2005 |
[12] | S. Sukhanov, and P. Delafontaine, “Protein chip-based microarray profiling of oxidized low density lipoprotein-treated cells,” Proteomics 5:1274-1280, 2005 |
[13] | S. Sukhanov, Y.H. Song, and P. Delafontaine, “Global analysis of differentially expressed genes in oxidized LDL-treated human aortic smooth muscle cells,” Biochem. Biophys. Res. Commun. 306:443-449, 2003 |
[14] | Y. Li, Y. Higashi, H. Itabe, Y.H. Song, J. Du, et al., “Insulin-Like Growth Factor-1 Receptor Activation Inhibits Oxidized LDL-Induced Cytochrome C Release and Apoptosis via the Phosphatidylinositol 3 Kinase/Akt Signaling Pathway” Arterioscler Thromb Vasc Biol 23: 2178-2184, 2003 |
[15] | World Medical Association Declaration of Helsinki, “Recommendations guiding physicians in biomedical research involving human subjects,” Cardiovasc Res 35:2-3, 1997 |
[16] | S. Toshima, A. Hasegawa, M. Kurabayashi, H. Itabe, T. Takano, et al., “Circulating oxidized low density lipoprotein levels. A biochemical risk marker for coronary heart disease,” Arterioscler Thromb Vasc Biol 20:2243-2247, 2000 |
[17] | H. Kohno, N. Sueshige, K. Oguri, H. Izumidate, T. Masunari, et al., “Simple and practical sandwich-type enzyme immunoassay for human oxidatively modified low density lipoprotein using antioxidized phosphatidylcholine monoclonal antibody and antihuman apolipoprotein-B antibody,” Clin Biochem 33:243-253, 2000 |
[18] | T. Shoji, Y. Nishizawa, M. Fukumoto, K. Shimamura, J. Kimura, et al., “Inverse relationship between circulating oxidized low density lipoprotein (oxLDL) and anti-oxLDL antibody levels in healthy subjects,” Atherosclerosis 148:171-177, 2000 |
[19] | T.J. Lyons, R.L. Klein, J.W. Baynes, H.C. Stevenson, and M.F. Lopes-Virella, “Stimulation of cholesteryl ester synthesis in human monocyte-derived macrophages by low-density lipoproteins from type 1 (insulin-dependent) diabetic patients: the influence of non-enzymatic glycosylation of low-density lipoproteins,” Diabetologia 30:916-923, 1987 |
[20] | K. Katoh, “Possible relevance of lipid peroxidation and thromboxane production to the initiation and/or evolution of microangiopathy in non-hyperlipidemic type 2 diabetes mellitus,” Diabetes Res Clin Pract 18:89-98, 1992 |
[21] | W.A. Oranje, G.J. Rondas-Colbers, G.N. Swennen, H. Jansen, and B. Wolffenbuttel, “Lack of effect on LDL oxidation and antioxidant status after improvement of metabolic control in type 2 diabetes,” Diabetes Care 22:2083-2084, 1999 |
[22] | J.L. Sanchez-Quesada, R. Homs-Serradesanferm, J. Serrat-Serrat, J.R. Serra-Grima, F. Gonzalez-Sastre, et al., “Increase of LDL susceptibility to oxidation occurring after intense, long duration aerobic exercise,” Atherosclerosis 118:297-305, 1995 |
[23] | T.J. Vasankari, U.M. Kujala, T.M. Vasankari, and M. Ahotupa, “Reduced oxidized LDL levels after a 10-month exercise program,” Med Sci Sports Exerc 30:1496-1501, 1998 |
[24] | G. Sobal, J.E. Menzel, and H. Sinzinger, “Do E-series prostaglandins and their metabolites influence oxidation of native and glycated low-density lipoproteins?,” Prostaglandins Other Lipid Mediat 55:67-76, 1998 |
[25] | V. Gouaze, N. Dousset, J.C. Dousset, and P. Valdiguie, “Effect of nicotine and cotinine on the susceptibility to in vitro oxidation of LDL in healthy non smokers and smokers,” Clin Chim Acta 277:25-37, 1998 |
[26] | L. Cominacini, U. Garbin, A.M. Pastorino, A. Davoli, M. Campagnola, et al., “Predisposition to LDL oxidation in patients with and without angiographically established coronary artery disease,” Atherosclerosis 99:63-70, 1993 |
[27] | E. Maggi, E. Marchesi, V. Ravetta, A. Martignoni, G. Finardi, et al., “Presence of autoantibodies against oxidatively modified low-density lipoprotein in essential hypertension: a biochemical signature of an enhanced in vivo low-density lipoprotein oxidation,” J Hypertens 13:129-138, 1995 |
[28] | A. Hjalmarson, E.A. Gilpin, P. Nicod, H. Dittrich, H. Henning, et al. “Differing circadian patterns of symptom onset in subgroups of patients with acute myocardial infarction,” Circulation 80:267-275, 1989 |
[29] | J.R. Marler, T.R. Price, G.L. Clark, J.E. Muller, T. Robertson, et al., “Morning increase in onset of ischemic stroke,” Stroke 20:473-476, 1989 |
[30] | H. Yoshida, T. Ishikawa, and H. Nakamura, “Vitamin E/lipid peroxide ratio and susceptibility of LDL to oxidative modification in non-insulin-dependent diabetes mellitus,” Arterioscler Thromb Vasc Biol 17:1438-1446, 1997 |
[31] | S. Ehara, M. Ueda, T. Naruko, K. Haze, A. Itoh, et al., “Elevated levels of oxidized low density lipoprotein show a positive relationship with the severity of acute coronary syndromes,” Circulation 103:1955-1960, 2001 |
[32] | K. Kugiyama, S. Sugiyama, H. Soejima, H. Kawano, T. Sakamoto, et al., “Increase in plasma levels of oxidized low-density lipoproteins in patients with coronary spastic angina,” Atherosclerosis 154:463-467, 2001 |
APA Style
Koichi Ono. (2014). Effect of Glycemic Control on Plasma Oxidized Low Density Lipoprotein Levels in Diabetics. Science Journal of Clinical Medicine, 3(5), 91-97. https://doi.org/10.11648/j.sjcm.20140305.13
ACS Style
Koichi Ono. Effect of Glycemic Control on Plasma Oxidized Low Density Lipoprotein Levels in Diabetics. Sci. J. Clin. Med. 2014, 3(5), 91-97. doi: 10.11648/j.sjcm.20140305.13
AMA Style
Koichi Ono. Effect of Glycemic Control on Plasma Oxidized Low Density Lipoprotein Levels in Diabetics. Sci J Clin Med. 2014;3(5):91-97. doi: 10.11648/j.sjcm.20140305.13
@article{10.11648/j.sjcm.20140305.13, author = {Koichi Ono}, title = {Effect of Glycemic Control on Plasma Oxidized Low Density Lipoprotein Levels in Diabetics}, journal = {Science Journal of Clinical Medicine}, volume = {3}, number = {5}, pages = {91-97}, doi = {10.11648/j.sjcm.20140305.13}, url = {https://doi.org/10.11648/j.sjcm.20140305.13}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.sjcm.20140305.13}, abstract = {Objective: Increased low-density lipoprotein (LDL) glycation in diabetics could facilitate LDL oxidation, which is proatherogenic. I studied plasma oxidized LDL (OxLDL) levels in diabetics and non-diabetics, their relation to glycemic control, and their circadian variations. Methods: OxLDL in diabetics (n=32) and in non-diabetics without coronary artery diseases (n=20) were compared. OxLDL in diabetics (n=24) was measured on Days 2, 3, 4, 8 and the last day of hospitalization. Circadian variation in OxLDL in diabetics (n=18) was also examined. Glycemic control was implemented during hospitalization. Patients: The diabetics were divided into two groups; moderately-controlled (MC) group (HbA1c < 9.0% at admission, n = 15) and poorly-controlled (PC) group (HbA1c ≧ 9.0% at admission, n = 9). Results: In the MC group, OxLDL decreased by 20.8% after glycemic control (p = 0.0139), but not in the PC group. OxLDL is correlated with LDL on Days 3, 4, 8 (r = 0.837, 0.864, 0.801, respectively), TG on Day 8(r = 0.932), and Lp(a) at discharge (r = 0.871). In the PC group, OxLDL was 15.8% higher on the average in the daytime than at night (p = 0.0024). Conclusion: Plasma OxLDL is decreased by glycemic control, particularly in moderately glycemic controlled patients. OxLDL has a circadian variation, particularly in poorly glycemic controlled patients. Long-term glycemic control could reduce the progression of atherosclerosis, by reducing OxLDL levels.}, year = {2014} }
TY - JOUR T1 - Effect of Glycemic Control on Plasma Oxidized Low Density Lipoprotein Levels in Diabetics AU - Koichi Ono Y1 - 2014/10/10 PY - 2014 N1 - https://doi.org/10.11648/j.sjcm.20140305.13 DO - 10.11648/j.sjcm.20140305.13 T2 - Science Journal of Clinical Medicine JF - Science Journal of Clinical Medicine JO - Science Journal of Clinical Medicine SP - 91 EP - 97 PB - Science Publishing Group SN - 2327-2732 UR - https://doi.org/10.11648/j.sjcm.20140305.13 AB - Objective: Increased low-density lipoprotein (LDL) glycation in diabetics could facilitate LDL oxidation, which is proatherogenic. I studied plasma oxidized LDL (OxLDL) levels in diabetics and non-diabetics, their relation to glycemic control, and their circadian variations. Methods: OxLDL in diabetics (n=32) and in non-diabetics without coronary artery diseases (n=20) were compared. OxLDL in diabetics (n=24) was measured on Days 2, 3, 4, 8 and the last day of hospitalization. Circadian variation in OxLDL in diabetics (n=18) was also examined. Glycemic control was implemented during hospitalization. Patients: The diabetics were divided into two groups; moderately-controlled (MC) group (HbA1c < 9.0% at admission, n = 15) and poorly-controlled (PC) group (HbA1c ≧ 9.0% at admission, n = 9). Results: In the MC group, OxLDL decreased by 20.8% after glycemic control (p = 0.0139), but not in the PC group. OxLDL is correlated with LDL on Days 3, 4, 8 (r = 0.837, 0.864, 0.801, respectively), TG on Day 8(r = 0.932), and Lp(a) at discharge (r = 0.871). In the PC group, OxLDL was 15.8% higher on the average in the daytime than at night (p = 0.0024). Conclusion: Plasma OxLDL is decreased by glycemic control, particularly in moderately glycemic controlled patients. OxLDL has a circadian variation, particularly in poorly glycemic controlled patients. Long-term glycemic control could reduce the progression of atherosclerosis, by reducing OxLDL levels. VL - 3 IS - 5 ER -