Postprandial Oxidative Metabolism of Human Brown Fat Indicates Thermogenesis

Human studies suggest that a meal elevates glucose uptake in brown adipose tissue (BAT). However, in postprandial state the thermogenic activity and the metabolism of non-esterified fatty acids (NEFAs) in BAT remain unclear. Using indirect calorimetry combined with positron emission tomography and computed tomography (PET/CT), we showed that whole-body and BAT thermogenesis (oxygen consumption) increases after the ingestion of a mixed carbohydrate-rich meal, to the same extent as in cold stress. Postprandial NEFA uptake into BAT is minimal, possibly due to elevated plasma insulin inhibiting lipolysis. However, the variation in postprandial NEFA uptake is linked to BAT thermogenesis. We identified several genes participating in lipid metabolism to be expressed at higher levels in BAT compared with white fat in postprandial state, and to be positively correlated with BAT UCP1 expression. These findings suggest that substrates preferred by BAT in postprandial state are glucose or LPL-released NEFAs due to insulin stimulation. [Display omitted] •A carbohydrate-dominant meal triggers human brown fat thermogenesis•After a meal, the genes involved in fatty acid metabolism are highly expressed in BAT•BAT uptake of circulatory fatty acids after meal consumption is minimal•Postprandial thermogenesis in BAT is linked to circulatory fatty acid uptake Using PET/CT imaging, U Din et al. show that eating a carbohydrate-rich meal triggers human brown adipose tissue (hBAT) thermogenesis to the same extent as cold stress, though the substrates used are different. Glucose and LPL-derived fatty acids are preferentially taken up by hBAT in the postprandial state.