Hipertrigliceridemia aumenta a respiração de repouso mitocondrial e susceptibilidade a transição de permeabilidade

AUTOR(ES)
DATA DE PUBLICAÇÃO

2003

RESUMO

High plasma leveI of triglycerides 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 triglyceride levels, normalized respiration and prevented MPT. The higher resting respiration in transgenic mitochondria remained in the presence of the adenine nucleotide carrier inhibitor, carboxyatractyloside, BSA and the 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 ftee fatty acid in the transgenic mice

ASSUNTO(S)

mitocondria triglicerides camundongo

Documentos Relacionados