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World J Diabetes. Apr 15, 2014; 5(2): 165-175
Published online Apr 15, 2014. doi: 10.4239/wjd.v5.i2.165
Published online Apr 15, 2014. doi: 10.4239/wjd.v5.i2.165
Origin and therapy for hypertriglyceridaemia in type 2 diabetes
Jing Pang, Dick C Chan, Gerald F Watts, School of Medicine and Pharmacology, University of Western Australia, Perth, WA 6847, Australia
Gerald F Watts, Lipid Disorders Clinic, Royal Perth Hospital, Perth, WA 6847, Australia
Author contributions: All the authors contributed to this paper.
Correspondence to: Gerald F Watts, DSc, MD, PhD, FRACP, FRCP, School of Medicine and Pharmacology, University of Western Australia, GPO Box X2213, Perth, WA 6847, Australia. gerald.watts@uwa.edu.au
Telephone: +6-8-92240245 Fax: +6-8-92240245
Received: November 5, 2013
Revised: March 8, 2014
Accepted: March 17, 2014
Published online: April 15, 2014
Revised: March 8, 2014
Accepted: March 17, 2014
Published online: April 15, 2014
Core Tip
Core tip: Diabetic dyslipidemia relates collectively to hyperglycaemia, insulin resistance, hyperinsulinaemia, abdominal visceral adipose disposition, increased liver fat content, and dysregulated fatty acid metabolism. Insulin resistance in diabetes induces hypertriglyceridaemia by increasing the enterocytic production of chylomicrons and an impaired clearance capacity is also involved. Usual care for diabetic dyslipidemia is statin treatment, but a significant proportion of patients have residual dyslipidemia, related to hypertriglyceridaemia and atherogenic dyslipidemia. Current evidence supports the use of fenofibrate in type 2 diabetics with high triglyceride levels.