The effect of PPAR-α agonism on apolipoprotein metabolism in humans

Shah, Amber M.; Rader, Daniel J.; Millar, John S.

doi:10.1016/j.atherosclerosis.2009.11.010

Cited by 110 publications

(94 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, fibrates increase LPL activity and decrease the hepatic secretion and VLDL concentration of apoC3 (66). Kinetic studies (67) have indicated that fibrates lower VLDL apoB-100 levels through enhanced clearance and decreased production. Fibrates increase apoA-I and apoA-II transcription, enhance reverse cholesterol transport, and indirectly, through altered VLDL metabolism, increase HDL levels (66).…”

Section: Genetic and Environmental Factors In Tg Elevationmentioning

confidence: 99%

Pharmacological Targeting of the Atherogenic Dyslipidemia Complex: The Next Frontier in CVD Prevention Beyond Lowering LDL Cholesterol

et al. 2016

View full text Add to dashboard Cite

Notwithstanding the effectiveness of lowering LDL cholesterol, residual CVD risk remains in high-risk populations, including patients with diabetes, likely contributed to by non-LDL lipid abnormalities. In this Perspectives in Diabetes article, we emphasize that changing demographics and lifestyles over the past few decades have resulted in an epidemic of the "atherogenic dyslipidemia complex," the main features of which include hypertriglyceridemia, low HDL cholesterol levels, qualitative changes in LDL particles, accumulation of remnant lipoproteins, and postprandial hyperlipidemia. We briefly review the underlying pathophysiology of this form of dyslipidemia, in particular its association with insulin resistance, obesity, and type 2 diabetes, and the marked atherogenicity of this condition. We explain the failure of existing classes of therapeutic agents such as fibrates, niacin, and cholesteryl ester transfer protein inhibitors that are known to modify components of the atherogenic dyslipidemia complex. Finally, we discuss targeted repurposing of existing therapies and review promising new therapeutic strategies to modify the atherogenic dyslipidemia complex. We postulate that targeting the central abnormality of the atherogenic dyslipidemia complex, the elevation of triglyceriderich lipoprotein particles, represents a new frontier in CVD prevention and is likely to prove the most effective strategy in correcting most aspects of the atherogenic dyslipidemia complex, thereby preventing CVD events.

show abstract

Section: Genetic and Environmental Factors In Tg Elevationmentioning

confidence: 99%

Pharmacological Targeting of the Atherogenic Dyslipidemia Complex: The Next Frontier in CVD Prevention Beyond Lowering LDL Cholesterol

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Statins increase the HDL-C level by increasing the production of HDL in the liver because of increased hepatic expressions of apoA-I and ABCA1. 16 Fibrates Fibrates, agonists of peroxisome proliferatoractivated receptor α (PPARα), 71 raise the level of HDL-C by 2-20% depending on the TG level. 72 Fibrates increase the HDL-C level by increasing the hepatic synthesis of the major HDL apoproteins, 73 apoA-I and apoA-II, by activating PPARα.…”

Section: Pharmacologic Therapies That Raise the Hdl-c Levelmentioning

confidence: 99%

Therapeutic Approaches to the Regulation of Metabolism of High-Density Lipoprotein

Zhang

Kawachi

Miura

et al. 2013

Circ J

View full text Add to dashboard Cite

“…Fibrates -Fibric acid derivatives are a class of medications which bind to peroxisome proliferator alpha (PPARα) receptors and are capable of increasing serum HDL while simultaneously lowering TG and are an effective adjunct in treating patients with HTGP who cannot be managed with diet alone 162 . They are typically used in treating primary HTG and include drugs such as gemfibrozil, bezafibrate and fenofibrate 163 .…”

Section: Medicationsmentioning

confidence: 99%