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

2. 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  , xvii-xxiiDOI: ( /j.ecl )
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3. 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  , xvii-xxiiDOI: ( /j.ecl )
Copyright © 2013 Elsevier Inc. Terms and Conditions

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

5. Leonid Poretsky, MD, Editor
Endocrinology and Metabolism Clinics  , xvii-xxiiDOI: ( /j.ecl )
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