Brief Cutting Edge Report
Brown adipose tissue does not seem to mediate metabolic adaptation to overfeeding in men
See Commentary, pg. 499.
Funding agencies: This work was partially supported by R01 DK060412 (to ER) and P30 DK072476 (to ER, NORC Center Grant). CMP was supported by KL2 TR001419 from the NIH's National Center for Advancing Translational Sciences.
Disclosure: ER reports past consulting activities with Energesis Pharmaceuticals. The other authors declared no conflict of interest.
Author contributions: ER and MN designed and conducted the study. MO, CMP, and MN designed the software to measure BAT activity. CMP and DNJ analyzed the data. All authors contributed to and edited the final manuscript.
Clinical trial registration: ClinicalTrials.gov identifier NCT01672632.
Brown adipose tissue (BAT) generates heat in response to cold, and low BAT activity has been linked to obesity. However, recent studies were inconclusive as to whether BAT is involved in diet-induced thermogenesis and mitigates weight gain from prolonged overeating. Therefore, this study investigated whether BAT activity is related to metabolic adaptation arising from 8 weeks of overfeeding in humans.
Fourteen men (aged 24 ± 3 years, BMI 24.5 ± 1.6 kg/m2) were overfed by 40% for 8 weeks. Before and after, energy expenditure and metabolic adaptation were measured by whole-room respiratory calorimetry. A marker of BAT activity was measured using infrared imaging of the supraclavicular BAT depot.
At the end of 8 weeks of overfeeding, metabolic adaptation—defined as the percent increase in sleeping energy expenditure beyond that expected from weight gain—rose from −0.9 ± 3.9% to 4.7 ± 5.6% (P = 0.001). However, BAT thermal activity was unchanged (P = 0.81). Moreover, BAT thermal activity did not correlate with the degree of metabolic adaptation (P = 0.32) or with the change in body weight (P = 0.51).
BAT thermal activity does not change in response to overfeeding, nor does it correlate with adaptive thermogenesis. Our data suggest that BAT does not mediate metabolic adaptation to overeating in humans.