Cardiovascular disease in recent onset diabetes mellitus.
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[1] S. Yamagishi,et al. Combination Therapy with Nateglinide and Telmisartan Ameliorates Insulin Resistance in Zucker Fatty Rats by Suppressing Advanced Glycation End Product Receptor Axis , 2010, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.
[2] A. Ceriello,et al. The importance of glycated haemoglobin (HbA(1c)) and postprandial glucose (PPG) control on cardiovascular outcomes in patients with type 2 diabetes. , 2010, Diabetes research and clinical practice.
[3] S. Yamagishi,et al. An α-glucosidase inhibitor, acarbose treatment decreases serum levels of glyceraldehyde-derived advanced glycation end products (AGEs) in patients with type 2 diabetes , 2010, Clinical and Experimental Medicine.
[4] S. Yamagishi. Advanced Glycation End Products and Receptor–Oxidative Stress System in Diabetic Vascular Complications , 2009, Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy.
[5] A. Ceriello. Hypothesis: the "metabolic memory", the new challenge of diabetes. , 2009, Diabetes research and clinical practice.
[6] R. Vasan,et al. Triglycerides as vascular risk factors: new epidemiologic insights , 2009, Current opinion in cardiology.
[7] A. Ceriello. The metabolic memory , 2009 .
[8] S. Yamagishi,et al. Clinical Utility of Acarbose, an α-Glucosidase Inhibitor in Cardiometabolic Disorders , 2009 .
[9] R. Holman,et al. 10-year follow-up of intensive glucose control in type 2 diabetes. , 2008, The New England journal of medicine.
[10] S. Yamagishi,et al. Agents that block advanced glycation end product (AGE)-RAGE (receptor for AGEs)-oxidative stress system: a novel therapeutic strategy for diabetic vascular complications , 2008, Expert opinion on investigational drugs.
[11] A. Saiki,et al. Effect of acarbose, an alpha-glucosidase inhibitor, on serum lipoprotein lipase mass levels and common carotid artery intima-media thickness in type 2 diabetes mellitus treated by sulfonylurea. , 2008, Journal of atherosclerosis and thrombosis.
[12] T. Yoshikawa,et al. The alpha-glucosidase inhibitor acarbose reduces the net electronegative charge of low-density lipoprotein in patients with newly diagnosed type 2 diabetes. , 2008, Clinica chimica acta; international journal of clinical chemistry.
[13] U. Smith,et al. Inflamed Adipose Tissue: A Culprit Underlying the Metabolic Syndrome and Atherosclerosis , 2007, Arteriosclerosis, thrombosis, and vascular biology.
[14] A. Hamsten,et al. Post-prandial endothelial dysfunction in hypertriglyceridemic subjects: molecular mechanisms and gene expression studies. , 2007, Atherosclerosis.
[15] S. Yamagishi,et al. Potential utility of telmisartan, an angiotensin II type 1 receptor blocker with peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-modulating activity for the treatment of cardiometabolic disorders. , 2007, Current molecular medicine.
[16] B. Nordestgaard,et al. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. , 2007, JAMA.
[17] N. Katsilambros,et al. High postprandial triglyceridemia in patients with type 2 diabetes and microalbuminuria Published, JLR Papers in Press, October 3, 2006. , 2007, Journal of Lipid Research.
[18] H. Daida,et al. Acarbose, an alpha-glucosidase inhibitor, improves endothelial dysfunction in Goto-Kakizaki rats exhibiting repetitive blood glucose fluctuation. , 2006, Biochemical and biophysical research communications.
[19] Jean-Paul Cristol,et al. Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes. , 2006, JAMA.
[20] N. Takasu,et al. Effects of a single administration of acarbose on postprandial glucose excursion and endothelial dysfunction in type 2 diabetic patients: a randomized crossover study. , 2006, The Journal of clinical endocrinology and metabolism.
[21] A. Ceriello,et al. Intermittent high glucose enhances ICAM-1, VCAM-1 and E-selectin expression in human umbilical vein endothelial cells in culture: the distinct role of protein kinase C and mitochondrial superoxide production. , 2005, Atherosclerosis.
[22] T. Imaizumi,et al. Diabetic vascular complications: pathophysiology, biochemical basis and potential therapeutic strategy. , 2005, Current pharmaceutical design.
[23] R. Marfella,et al. Regression of Carotid Atherosclerosis by Control of Postprandial Hyperglycemia in Type 2 Diabetes Mellitus , 2004, Circulation.
[24] A. Cavarape,et al. The post‐prandial state in Type 2 diabetes and endothelial dysfunction: effects of insulin aspart , 2004, Diabetic medicine : a journal of the British Diabetic Association.
[25] Antonio Ceriello,et al. Intermittent high glucose enhances apoptosis related to oxidative stress in human umbilical vein endothelial cells: the role of protein kinase C and NAD(P)H-oxidase activation. , 2003, Diabetes.
[26] W. Hsueh,et al. Role of endothelial dysfunction in insulin resistance. , 2003, The American journal of cardiology.
[27] Markolf Hanefeld,et al. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial. , 2003, JAMA.
[28] Claude Colette,et al. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: variations with increasing levels of HbA(1c). , 2003, Diabetes care.
[29] A. Ceriello,et al. Evidence for an Independent and Cumulative Effect of Postprandial Hypertriglyceridemia and Hyperglycemia on Endothelial Dysfunction and Oxidative Stress Generation: Effects of Short- and Long-Term Simvastatin Treatment , 2002, Circulation.
[30] A. Ceriello,et al. Role of hyperglycemia in nitrotyrosine postprandial generation. , 2002, Diabetes care.
[31] M. Laakso,et al. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial , 2002, The Lancet.
[32] B. Szwergold,et al. alpha-Dicarbonyls increase in the postprandial period and reflect the degree of hyperglycemia. , 2001, Diabetes care.
[33] H. Iso,et al. Serum triglycerides and risk of coronary heart disease among Japanese men and women. , 2001, American journal of epidemiology.
[34] S. Jackson,et al. The relationships between post-prandial lipaemia, endothelial function and oxidative stress in healthy individuals and patients with type 2 diabetes. , 2001, Atherosclerosis.
[35] Y. Iwamoto,et al. Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes. , 2000, Diabetes care.
[36] S. Kiechl,et al. Impaired glucose tolerance, Type II diabetes mellitus and carotid atherosclerosis: prospective results from the Bruneck Study , 2000, Diabetologia.
[37] E. Feskens,et al. Glucose tolerance and mortality: comparison of WHO and American Diabetic Association diagnostic criteria , 1999, The Lancet.
[38] A Sekikawa,et al. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glucose. The Funagata Diabetes Study. , 1999, Diabetes care.
[39] M. Hanefeld,et al. Postprandial plasma glucose is an independent risk factor for increased carotid intima-media thickness in non-diabetic individuals. , 1999, Atherosclerosis.
[40] M. Laakso,et al. Hyperglycemia and cardiovascular disease in type 2 diabetes. , 1999, Diabetes.
[41] R. Holman,et al. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. , 1998 .
[42] Uk-Prospective-Diabetes-Study-Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33) , 1998, The Lancet.
[43] M. Hanefeld,et al. Risk factors for myocardial infarction and death in newly detected NIDDM: the Diabetes Intervention Study, 11-year follow-up , 1996, Diabetologia.
[44] M. Pirisi,et al. Hyperglycemia-Induced Thrombin Formation in Diabetes: The Possible Role of Oxidative Stress , 1995, Diabetes.
[45] M. Laakso,et al. NIDDM and Its Metabolic Control Predict Coronary Heart Disease in Elderly Subjects , 1994, Diabetes.
[46] M. Laakso,et al. Non‐Insulin‐Dependent Diabetes and Its Metabolic Control Are Important Predictors of Stroke in Elderly Subjects , 1994, Stroke.
[47] L. Niskanen,et al. Ten-year cardiovascular mortality in relation to risk factors and abnormalities in lipoprotein composition in Type 2 (non-insulin-dependent) diabetic and non-diabetic subjects , 1993, Diabetologia.
[48] M. Shipley,et al. CORONARY-HEART-DISEASE RISK AND IMPAIRED GLUCOSE TOLERANCE The Whitehall Study , 1980, The Lancet.
[49] K. Pyörälä. Relationship of Glucose Tolerance and Plasma Insulin to the Incidence of Coronary Heart Disease: Results from Two Population Studies in Finland , 1979, Diabetes Care.
[50] I. Pless,et al. West Indian one-year-olds. A comparative analysis of health and service utilisation. , 1967, Lancet.
[51] S. Yamagishi,et al. Clinical utility of acarbose, an alpha-glucosidase inhibitor in cardiometabolic disorders. , 2009, Current drug metabolism.
[52] S. Yamagishi,et al. Role of oxidative stress in the development of vascular injury and its therapeutic intervention by nifedipine. , 2008, Current medicinal chemistry.
[53] Teven,et al. MORTALITY FROM CORONARY HEART DISEASE IN SUBJECTS WITH TYPE 2 DIABETES AND IN NONDIABETIC SUBJECTS WITH AND WITHOUT PRIOR MYOCARDIAL INFARCTION , 2000 .
[54] K. Pyörälà,et al. Relationship of glucose tolerance and plasma insulin to the incidence of coronary heart disease: results from two population studies in Finland. , 1979, Diabetes care.