Examining the effects of housing temperature on mitochondrial adaptations to exercise and the browning of white adipose tissue

Abstract

The thermoneutral zone for small rodents is ~29–31°C and with decreases in ambient temperature below this there are consequent increases in metabolism to promote thermogenesis. Despite this, many studies report housing mice at room temperature for the convenience of the researchers studying them. As such, the conflicting reports between human and rodent models of exercise‐induced mitochondrial biogenesis in adipose tissue and the browning of white adipose tissue may be explained by the often‐overlooked variable, housing temperature. Male 8‐week‐old C57BL/6 mice were housed in cages with (VWR) or without (SED) running wheels (n = 12/group/condition) for 5–6 weeks at room temperature (RT; 22°C) or at thermoneutrality (TN; ~29°C). Mice housed at TN ran a greater distance. VWR protected against weight gain independent of housing temperature however food intake was greater in both VWR and SED mice housed at RT compared to TN. Inguinal white adipose tissue (iWAT) and epididymal white adipose tissue (eWAT) mass were reduced following VWR independent of housing temperature and there were main effects of both exercise and temperature to reduce brown adipose tissue (BAT) mass. There was no effect of housing temperature on circulating glucose or glycerol concentrations however NEFA, insulin, and the HOMA‐IR were increased at TN. In eWAT there was a main effect of exercise to increase cytochrome c oxidoreductase core I subunit (CORE1), cytochrome c oxidase, and peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α) protein content with a main effect of housing temperature for PGC‐1α as well. There was a strong trend for an exercise‐induced increase in pyruvate dehydrogenase (PDH). In iWAT, there was a main effect of exercise and temperature on mitochondrial proteins with VWR leading to the expected increases in PDH, CORE1, COX IV, and PGC‐1α, but reduced markers of mitochondrial content at TN. Most notably protein content of the thermogenic uncoupling protein‐1 (UCP‐1) was undetectable in iWAT at TN. Qualitative histological analysis revealed patches of multilocular adipocytes in iWAT with VWR at RT but not at TN. Together our findings provide novel evidence that while housing mice at TN reduces markers of mitochondrial content in adipose tissue under sedentary conditions, the ability of exercise to increase mitochondrial protein content remains largely intact.Support or Funding InformationOntario Graduate Scholarship Canada Research Chairs ProgramThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.