Sources of blood glycerol during fasting

To determine the source(s) of blood and very low density lipoprotein (VLDL) -triglyceride glycerol during fasting, four men ingested (H2O)-H-2 from 14 to 20 h into a 60-h fast to achieve similar to0.5% body water enrichment. A t 60 h of fasting, glycerol flux was measured using [2-C-14] glycerol. Bloo d was taken for measurement of H-2 enrichment at carbon 6 of glucose and at carbon 3 of free glycerol and VLDL-triglyceride glycerol. H-2 enrichment o f the 2 hydrogens bound to carbon 3 of VLDL-triglyceride glycerol was 105 /- 2% of the H-2 enrichment of the 2 hydrogens bound to carbon 6 of glucose , indicating isotopic equilibrium between hepatic glyceraldehyde 3-P and gl ycerol 3-P. The H-2 enrichment of the 2 hydrogens bound to carbon 3 of free glycerol was 17 +/- 3% of VLDL-triglyceride glycerol, indicating that a si gnificant percentage of free glycerol in blood originated from the hydrolys is of circulating VLDL-triglyceride or a pool of glycerol with similar H-2 enrichment. Glycerol flux was 6.3 +/- 1.1 mu mol.kg(-1).min(-1). Glycerol a ppearing from nonadipose tissue sources was then similar to1.1 mu mol.kg(-1 ).min(-1). Seven other subjects were fasted for 12, 42, and 60 h. A small p ercentage of glycerol in the circulation after 12 h of fasting was enriched with H-2. The enrichment of the 2 hydrogens bound to carbon 3 of free glyc erol in the longer periods of fasting was similar to 16% of the enrichment of the 2 hydrogens bound to carbon 6 of glucose. Therefore, as much as 15-2 0% of systemic glycerol turnover during fasting is not from lipolysis of ad ipose tissue triglyceride.