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1 Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 55905; 2 Departments of Medicine, Biochemistry and Nutrition, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106; and 3 Division of Clinical Physiology, Karolinska Hospital, S-171 76 Stockholm, Sweden
To determine the
source(s) of blood and very low density lipoprotein (VLDL)-triglyceride
glycerol during fasting, four men ingested 2H2O
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 of
2H 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 the 2H enrichment of the 2 hydrogens
bound to carbon 6 of glucose, indicating isotopic equilibrium between
hepatic glyceraldehyde 3-P and glycerol 3-P. The
2H 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 similar 2H enrichment. Glycerol flux was 6.3 ± 1.1 µmol · kg
1 · min1.
Glycerol appearing from nonadipose tissue sources was then ~1.1 µmol · kg1 · min1. 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 with 2H. 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.
triglyceride; very low density lipoprotein; lipolysis; deuterated water
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