Cold exposure stimulated cross-tissue metabolic rewiring, quantifying 11,394 proteins across six tissues to reveal enhanced glucose utilization and oxygen consumption in brown adipose tissue.
Cold exposure drives cross-tissue metabolic rewiring, highlighting systemic adaptations that support enhanced glucose utilization in brown adipose tissue and suggesting overlap with obesity mechanisms.
To gain insight into the root causes of metabolic dysfunction, it is essential to understand how tissues communicate and coordinate their metabolic functions. Here, we sought to address this in the context of cold exposure, a well-studied metabolic perturbation. We performed proteomics across six metabolic tissues and plasma, quantifying 11,394 proteins. Beginning our investigation in brown adipose tissue (BAT), we identified a mechanism to explain enhanced glucose utilization in cold-adapted BAT. This was characterized by select remodeling of upper glycolysis and pentose cycling to increase oxygen consumption, likely by increasing uncoupling protein 1 activity through the production of reactive oxygen species. Cold-induced remodeling of the plasma proteome appeared to underpin the ability of BAT to modify its fuel preference, stimulating lipolysis in white adipose tissue and glucose production in the liver. These findings emphasize the importance of considering metabolic adaptations in the context of the whole body and suggest overlap between the mechanisms of cold adaptation and obesity.
Cutler et al. (Wed,) conducted a other in Metabolic adaptation to cold exposure. Cold exposure was evaluated on Proteomic changes across metabolic tissues and plasma. Cold exposure stimulated cross-tissue metabolic rewiring, quantifying 11,394 proteins across six tissues to reveal enhanced glucose utilization and oxygen consumption in brown adipose tissue.