Measures of metabolism and energy expenditure did not appear to be associated with brown adipose tissue activation in patients with emphysematous chronic obstructive pulmonary disease (COPD).
Activation of brown adipose tissue (BAT) does not appear to be related to hypermetabolism in patients with emphysematous chronic obstructive pulmonary disease (COPD), according to a new report.
Patients with COPD experience disturbances in whole body and cellular energy metabolism, often leading to weight loss and muscle wasting, especially in cases of emphysematous COPD, wrote corresponding author Annemie M. W. J. Schols, PhD, of Maastricht University Medical Center, in the Netherlands, and colleagues.
A number of causes have been proposed to explain hypermetabolism in cachexia, including systemic inflammation and the workload associated with breathing due to lung hyperinflation. Yet, Schols and colleagues said their own research did not show a role for the latter.
Another proposed mechanism of hypermetabolism is the activation of BAT or the browning of white adipose tissue (WAT).
“BAT tissue is characterized by abundance of mitochondria and by heat production via the process of proton leakage over the mitochondrial membrane mediated by uncoupling protein 1,” the authors wrote in the Journal of Cachexia, Sarcopenia and Muscle.
Previous research in teenagers has shown that patients with BAT had higher levels of cold-induced energy expenditure compared to healthy lean subjects without BAT.
“This increase in energy expenditure upon cold in the absence of shivering (i.e. non-shivering thermogenesis) implies that BAT thermogenesis may be a significant component of facultative thermogenesis and thereby plays a role in regulation of body weight as suggested by an inverse association between cold-induced BAT activity and body mass index in adults,” they reported.
Yet, to date, little research has been conducted looking at the role of BAT in cachexia among patients with COPD. In hopes of confirming whether BAT activation is a trigger for hypermetabolism and cachexia, the investigators recruited 20 patients with COPD, half of whom were male and half of whom were female. The patients had a median body mass index (BMI) of 22.4 kg/m2, with a range of 15.1-32.5kg/m2.
Schols and colleagues measured basal metabolic rate (BMR) and total daily energy expenditure (TDEE) on all 20 participants. In a subset of 10 patients, BAT and WAT were analyzed, alongside the same analysis on 6 age-, gender-, and BMI-matched healthy controls. BAT glucose uptake, lung function and systemic inflammation were also assessed.
The analysis showed that there did not appear to be a correlation between BMR or TDEE and BAT activity in patients with emphysematous COPD.
“In contrast to our hypothesis, emphysematous patients did not exhibit enhanced BAT activity or altered gene expression of BAT markers in WAT compared with age-matched, gender-matched and BMI-matched healthy non-smoking controls,” the authors wrote.
The authors also included 2 case reports with cachectic cancer patients, a 61-year-old man and a 70-year-old woman, but the investigators similarly could not find a correlation with BAT in those patients.
Schols and colleagues conceded that their findings were limited by the study’s small sample size.
“Nevertheless, the consistency of our findings in the hypermetabolic COPD patients and confirmed in the two cancer cases do not support a role for BAT activation as trigger of disease-induced hypermetabolism and cachexia,” they concluded.
Sanders KJC, Wierts R, van Marken Lichtenbelt WD, et al. Brown adipose tissue activation is not related to hypermetabolism in emphysematous chronic obstructive pulmonary disease patients. J Cachexia Sarcopenia Muscle. Published online February 15, 2022. doi:10.1002/jcsm.12881