» Articles » PMID: 14740893

Hypertriglyceridemia Increases Mitochondrial Resting Respiration and Susceptibility to Permeability Transition

Overview
Publisher Springer
Date 2004 Jan 27
PMID 14740893
Citations 4
Authors
Affiliations
Soon will be listed here.
Abstract

High plasma level of triglycerides (TGs) is a common feature in atherosclerosis, obesity, diabetes, alcoholism, stress, and infection. Since mitochondria have been implicated in cell death under a variety of metabolic disorders, we examined liver mitochondrial functions in hypertriglyceridemic transgenic mice. Hypertriglyceridemia increased resting respiration and predisposed to mitochondrial permeability transition (MPT). Ciprofibrate therapy reduced plasma TG levels, normalized respiration, and prevented MPT. The higher resting respiration in transgenic mitochondria remained in the presence of the adenine nucleotide carrier inhibitor, carboxyatractyloside, bovine serum albumin, and the uncoupling proteins (UCPs) inhibitor, GDP. UCP2 content was similar in both control and transgenic mitochondria. We propose that faster resting respiration represents a regulated adaptation to oxidize excess free fatty acid in the transgenic mice.

Citing Articles

Liver proteomic response to hypertriglyceridemia in human-apolipoprotein C-III transgenic mice at cellular and mitochondrial compartment levels.

Ehx G, Gerin S, Mathy G, Franck F, Oliveira H, Vercesi A Lipids Health Dis. 2014; 13:116.

PMID: 25047818 PMC: 4112841. DOI: 10.1186/1476-511X-13-116.


Activation of the mitochondrial ATP-sensitive K+ channel reduces apoptosis of spleen mononuclear cells induced by hyperlipidemia.

Alberici L, Paim B, Zecchin K, Mirandola S, Pestana C, Castilho R Lipids Health Dis. 2013; 12:87.

PMID: 23764148 PMC: 3693968. DOI: 10.1186/1476-511X-12-87.


Mitochondrial energy metabolism and redox responses to hypertriglyceridemia.

Alberici L, Vercesi A, Oliveira H J Bioenerg Biomembr. 2011; 43(1):19-23.

PMID: 21258853 DOI: 10.1007/s10863-011-9326-y.


Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism.

Golomb B, Evans M Am J Cardiovasc Drugs. 2009; 8(6):373-418.

PMID: 19159124 PMC: 2849981. DOI: 10.2165/0129784-200808060-00004.

References
1.
Faergeman O . Hypertriglyceridemia and the fibrate trials. Curr Opin Lipidol. 2000; 11(6):609-14. DOI: 10.1097/00041433-200012000-00007. View

2.
LARDY H, PRESSMAN B . Effect of surface active agents on the latent ATPase of mitochondria. Biochim Biophys Acta. 1956; 21(3):458-66. DOI: 10.1016/0006-3002(56)90182-2. View

3.
Ito Y, Azrolan N, OConnell A, Walsh A, Breslow J . Hypertriglyceridemia as a result of human apo CIII gene expression in transgenic mice. Science. 1990; 249(4970):790-3. DOI: 10.1126/science.2167514. View

4.
Kaplan R, Pedersen P . Characterization of phosphate efflux pathways in rat liver mitochondria. Biochem J. 1983; 212(2):279-88. PMC: 1152045. DOI: 10.1042/bj2120279. View

5.
Lanni A, Mancini F, Sabatino L, Silvestri E, Franco R, De Rosa G . De novo expression of uncoupling protein 3 is associated to enhanced mitochondrial thioesterase-1 expression and fatty acid metabolism in liver of fenofibrate-treated rats. FEBS Lett. 2002; 525(1-3):7-12. DOI: 10.1016/s0014-5793(02)02828-4. View