Key result
High-fat diet feeding in mice does not impair adipocyte mitochondrial respiratory capacity but causes an enduring increase in mitochondrial reactive oxygen species within white adipose tissue.
Why the study?
The effect of long-term high-fat diet on mitochondrial reactive oxygen species in white adipose tissue, when accounting for adipocyte hypertrophy rather than tissue weight, was not elucidated.
Does a high-fat diet alter mitochondrial respiration and mtROS emission in white adipose tissue of C57BL/6N mice?
Does a high-fat diet alter mitochondrial respiration and mtROS emission in white adipose tissue of C57BL/6N mice?
Long-term high-fat feeding in mice increases mitochondrial reactive oxygen species in white adipose tissue without impairing mitochondrial respiratory capacity per adipocyte.
High-fat diet effects on adipose mtROS in mice should not yet inform clinical practice; leaves open mechanistic role in human metabolic disease.
White adipose tissue (WAT) dysfunction in obesity is implicated in the onset of whole body insulin resistance. Alterations in mitochondrial bioenergetics, namely impaired mitochondrial respiration and increased mitochondrial reactive oxygen species (mtROS) production, have been suggested to contribute to this metabolic dysregulation. However, techniques investigating mitochondrial function are classically normalized to tissue weight, which may be confounding when considering obesity-related adipocyte hypertrophy. Furthermore, the effect of long-term high-fat diet (HFD) on mtROS in WAT has yet to be elucidated. Therefore, we sought to determine the HFD-mediated temporal changes in mitochondrial respiration and mtROS emission in WAT. C57BL/6N mice received low-fat diet or HFD for 1 or 8 wk and changes in inguinal WAT (iWAT) and epididymal WAT (eWAT) were assessed. While tissue weight-normalized mitochondrial respiration was reduced in iWAT following 8-wk HFD-feeding, this effect was mitigated when adipocyte cell size and/or number were considered. These data suggest HFD does not impair mitochondrial respiratory capacity per adipocyte within WAT. In support of this assertion, within eWAT compensatory increases in lipid-supported and maximal succinate-supported respiration occurred at 8 wk despite cell hypertrophy and increases in WAT inflammation. Although these data suggest impairments in mitochondrial respiration do not contribute to HFD-mediated WAT phenotype, lipid-supported mtROS emission increased following 1-wk HFD in eWAT, while both lipid and carbohydrate-supported mtROS were increased at 8 wk in both depots. Combined, these data establish that while HFD does not impair adipocyte mitochondrial respiratory capacity, increased mtROS is an enduring physiological occurrence within WAT in HFD-induced obesity.
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Politis‐Barber et al. (2020) studied Obesity / Insulin resistance. High-fat diet vs. Low-fat diet was evaluated on Mitochondrial respiration and mtROS emission in white adipose tissue. High-fat diet feeding in mice does not impair adipocyte mitochondrial respiratory capacity but causes an enduring increase in mitochondrial reactive oxygen species within white adipose tissue.
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