guanosine-diphosphate and ciprofibrate

guanosine-diphosphate has been researched along with ciprofibrate* in 1 studies

Other Studies

1 other study(ies) available for guanosine-diphosphate and ciprofibrate

Article	Year
Hypertriglyceridemia increases mitochondrial resting respiration and susceptibility to permeability transition. Journal of bioenergetics and biomembranes, 2003, Volume: 35, Issue:5 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. Topics: Animals; Atractyloside; Cell Respiration; Clofibric Acid; Fibric Acids; Guanosine Diphosphate; Hypertriglyceridemia; Hypolipidemic Agents; Ion Channels; Liver; Membrane Potentials; Membrane Transport Proteins; Mice; Mice, Transgenic; Mitochondria; Mitochondrial Proteins; Serum Albumin, Bovine; Triglycerides; Uncoupling Protein 2	2003

Article

Year

Hypertriglyceridemia increases mitochondrial resting respiration and susceptibility to permeability transition.

Journal of bioenergetics and biomembranes, 2003, Volume: 35, Issue:5

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.

Topics: Animals; Atractyloside; Cell Respiration; Clofibric Acid; Fibric Acids; Guanosine Diphosphate; Hypertriglyceridemia; Hypolipidemic Agents; Ion Channels; Liver; Membrane Potentials; Membrane Transport Proteins; Mice; Mice, Transgenic; Mitochondria; Mitochondrial Proteins; Serum Albumin, Bovine; Triglycerides; Uncoupling Protein 2

2003