Journal
ATHEROSCLEROSIS
Volume 239, Issue 2, Pages 483-495Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2015.01.039
Keywords
Type 2 diabetes; Dyslipidemia; Triglycerides; Fatty liver; beta-oxidation; De novo lipogenesis (DNL); CVD
Funding
- EU-project RESOLVE [305707]
- Leducq Foundation [11 CVD 03]
- Helsinki University Central Hospital Research Foundation [TYH2012134]
- Swedish Research Council
- Sigrid Juselius Foundation
- Novo Nordisk Foundation
- Swedish Diabetes Foundation
- Diabetes Wellness
- Sahlgrenska University Hospital ALF Research Grants
- Swedish Heart-Lung Foundation
- Novo Nordisk Fonden [NNF14OC0010799] Funding Source: researchfish
Ask authors/readers for more resources
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality for patients with type 2 diabetes, despite recent significant advances in management strategies to lessen CVD risk factors. A major cause is the atherogenic dyslipidemia, which consists of elevated plasma concentrations of both fasting and postprandial triglyceride-rich lipoproteins (TRLs), small dense low-density lipoprotein (LDL) and low high-density lipoprotein (HDL) cholesterol. The different components of diabetic dyslipidemia are not isolated abnormalities but closely linked to each other metabolically. The underlying disturbances are hepatic overproduction and delayed clearance of TRLs. Recent results have unequivocally shown that triglyceride-rich lipoproteins and their remnants are atherogenic. To develop novel strategies for the prevention and treatment of dyslipidaemia, it is essential to understand the pathophysiology of dyslipoproteinaemia in humans. Here, we review recent advances in our understanding of the pathophysiology of diabetic dyslipidemia. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available