The presence of brown adipose tissue (BAT) in human adults opens attractive perspectives to treat metabolic disorders. This is because BAT dissipates energy as heat via the uncoupling protein-1 (UCP1). So instead of storing energy (calories from our diet), it's burned off as heat. In fact, this is the basis behind being "warm-blooded" and non-shivering thermogenesis (heat production without the use of shivering).
BAT are located in specific deposits or can emerge among white
fat through the so-called browning process. I discussed this briefly last year, in THIS POST. Although numerous inducers
have been shown to drive this process, no study has investigated whether
it could be controlled by specific metabolites. This newly published study on mice, it showed that
lactate (lactic acid), an important metabolic intermediate, induces browning of white adipose cells by expression of a functional UCP1 protein. This happens through redox (reduction-oxidation) signalling, which tells the cell how "reduced" or "oxidized" it currently is.
Lactate-induced browning also occurs in cultured human cells and in vivo.
Further, the ketone body β-hydroxybutyrate, another metabolite that
impacts redox state, is also a strong browning inducer. Since this
redox-dependent increase in UCP1 expression promotes an oxidative
phenotype (by uncoupling the mitochondria),
browning appears as an adaptive mechanism to alleviate redox pressure. These findings open new perspectives for the control of adipose tissue
browning and its physiological relevance.
Click HERE to subscribe to Know Guff.
Source: Browning of White Adipose Cells by Intermediate Metabolites:An Adaptive Mechanism to Alleviate Redox Pressure.