Tissue-Specific Regulation of Postprandial Non-Esterified Fatty Acid Metabolism in individuals with prediabetes

This is the authors' abstract. We don't add key points for this paper.

After a meal, it is generally assumed that tissue non-esterified fatty acids (NEFA) uptake falls in proportion of the reduction of systemic NEFA appearance from insulin-mediated suppression of adipose tissue lipolysis. Here, we combined dynamic [11C]palmitate PET/CT, stable isotope tracers, and MRI to measure palmitate uptake, oxidation, and esterification in the heart, liver, skeletal muscle, and subcutaneous and visceral adipose tissue, in the fasted state and 60min after a mixed meal in individuals with prediabetes. Net palmitate uptake decreased in all tissues, but most tissues extracted a larger fraction of circulating palmitate after the meal. The intracellular fate of palmitate differed between organs. The heart shifted toward oxidation, the liver toward esterification, maintaining VLDL-palmitate release, and this shift was smaller in individuals with more liver fat. Both adipose depots increased fractional esterification, and visceral fat almost stopped releasing palmitate. Thus, plasma NEFA overestimates the postprandial reduction in lean tissue NEFA exposure.