Gupta, Sameer

To determine the source(s) of blood and very low density lipoprotein (VLDL)-triglyceride glycerol during fasting, four men ingested2H2O from 14 to 20 h into a 60-h fast to achieve ∼0.5% body water enrichment. At 60 h of fasting, glycerol flux was measured using [2-14C]glycerol. Blood was taken for measurement of2H enrichment at carbon 6 of glucose and at carbon 3 of free glycerol and VLDL-triglyceride glycerol.2H enrichment of the 2 hydrogens bound to carbon 3 of VLDL-triglyceride glycerol was 105 ± 2% of the2H enrichment of the 2 hydrogens bound to carbon 6 of glucose, indicating isotopic equilibrium between hepatic glyceraldehyde 3- P and glycerol 3- P. The2H enrichment of the 2 hydrogens bound to carbon 3 of free glycerol was 17 ± 3% of VLDL-triglyceride glycerol, indicating that a significant percentage of free glycerol in blood originated from the hydrolysis of circulating VLDL-triglyceride or a pool of glycerol with similar2H enrichment. Glycerol flux was 6.3 ± 1.1 μmol · kg−1· min−1. Glycerol appearing from nonadipose tissue sources was then ∼1.1 μmol · kg−1· min−1. Seven other subjects were fasted for 12, 42, and 60 h. A small percentage of glycerol in the circulation after 12 h of fasting was enriched with2H. The enrichment of the 2 hydrogens bound to carbon 3 of free glycerol in the longer periods of fasting was ∼16% of the enrichment of the 2 hydrogens bound to carbon 6 of glucose. Therefore, as much as 15–20% of systemic glycerol turnover during fasting is not from lipolysis of adipose tissue triglyceride.