Author： Alberici Luciane C. Oliveira Helena C. F. Bighetti Eliete J. B. de Faria Eliana C. Degaspari Giovana R. Souza Claudio T. Vercesi Anibal E.
Publisher： Springer Publishing Company
ISSN： 0145-479X
Source： Journal of Bioenergetics and Biomembranes, Vol.35, Iss.5, 2003-10, pp. : 451-457
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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.
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