Why Focus on Complications?

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Presentation transcript:

Why Focus on Complications? Emilia Pauline Liao, MD Endocrinology and Metabolism Clinics Volume 42, Issue 4, Pages xvii-xxii (December 2013) DOI: 10.1016/j.ecl.2013.06.006 Copyright © 2013 Elsevier Inc. Terms and Conditions

Fig. 1 How hyperglycemia causes cellular damage: unifying mechanism. AGE, advanced glycation end products; ET, endothelin; PAI, plasminogen activator inhibitor; PKC, protein kinase C; TGF, transforming growth factor; VEGF, vascular endothelial growth factor. (Adapted from Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes 2005;54:1615–25.) Endocrinology and Metabolism Clinics 2013 42, xvii-xxiiDOI: (10.1016/j.ecl.2013.06.006) Copyright © 2013 Elsevier Inc. Terms and Conditions

Fig. 2 Relationship between dyslipidemia and diabetes. Excess circulating free fatty acids (FFAs) from diet and visceral fat lead to beta cell dysfunction, increased gluconeogenesis, and high triglycerides (TGs), causing insulin resistance and hyperglycemia. HDL, high-density lipoprotein; sdLDL, small dense LDL; TC, total cholesterol. (Adapted from Bardini G, Rotella CM, Giannini S. Dyslipidemia and diabetes: reciprocal impact of impaired lipid metabolism and beta cell dysfunction on micro and macrovascular complications. Rev Diabet Stud 2012;9:87.) Endocrinology and Metabolism Clinics 2013 42, xvii-xxiiDOI: (10.1016/j.ecl.2013.06.006) Copyright © 2013 Elsevier Inc. Terms and Conditions

Emilia Pauline Liao, MD, Editor Endocrinology and Metabolism Clinics 2013 42, xvii-xxiiDOI: (10.1016/j.ecl.2013.06.006) Copyright © 2013 Elsevier Inc. Terms and Conditions

Leonid Poretsky, MD, Editor Endocrinology and Metabolism Clinics 2013 42, xvii-xxiiDOI: (10.1016/j.ecl.2013.06.006) Copyright © 2013 Elsevier Inc. Terms and Conditions