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Impact of dietary induced fatty liver on mitochondrial oxidative phosphorylation
Author(s) -
Newell Christopher,
Hughey Curtis,
Nyamandi Vongai,
Johnsen Virginia,
Shearer Jane
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1209.21
Subject(s) - respiration , oxidative phosphorylation , mitochondrion , adenosine triphosphate , medicine , endocrinology , cellular respiration , adenosine diphosphate , biology , respiratory system , bioenergetics , atp synthase , chemistry , biochemistry , platelet , enzyme , anatomy , platelet aggregation
High fat (HF) diet has been linked to mitochondrial dysfunction. Alteration of HF diet duration has shown that although mitochondrial impairments are present initially (2–4 weeks), these impairments are abolished or exceed control level function after prolonged HF feeding (>; 8 weeks). Male C‐57 mice (n=14) were randomly assigned to one of two dietary groups; chow (CH, 10% kcal fat) and high fat (HF, 60% kcal fat). HF mice were obese with elevated liver triglycerides. Isolated mitochondria from mouse liver tissue were measured using high‐resolution respirometry. Animals within the HF group possessed higher state 3 & 4 respiration (p<0.05), as well as higher respiratory control ratios (p<0.05). Mitochondria are termed to be in state 3 respiration when actively respiring, meaning the rate where they are capable of converting adenosine diphosphate (ADP) to adenosine triphosphate (ATP) through oxygen consumption. State 4 refers to the rate of oxygen depletion after all ADP has been phosphorylated, also termed leak respiration. This indicates that mitochondria in HF animals are able to adapt to metabolic stressors such as a high fat diet by elevating state 3 respiratory rates above normal levels. Moreover, mitochondria can increase their active respiratory rate within fatty liver tissues as a direct result of excess lipid availability and accumulation.