Ingested fructose is rapidly utilized by the liver and is either stored as glycogen, converted to glucose, or oxidized to CO2 for energy. The glycemic response to fructose is known to be modest. However, the relative importance of these pathways in humans is unclear. In the present study, a tritiated glucose tracer dilution technique was used to determine the effect of fructose ingestion on the glucose appearance rate (Ra) in the peripheral circulation over an 8-hour period beginning at 8:00 AM. Six normal healthy males ingested 50 g fructose with 500 mL water. On a separate occasion, the same subjects received 500 mL water without fructose as a control. Serum insulin, triglycerides, plasma glucagon, glucose, lactate, alanine, urea nitrogen, and total amino acids also were determined. The plasma glucose concentration was not significantly different following ingestion of fructose or water, other than a transient increase beginning at 8:30 AM of 0.8 mmol/L in response to ingested fructose. Glucose appearing in the peripheral circulation as a result of ingestion of 50 g fructose was calculated to be 9.8 ± 2.4 g. Following the ingestion of fructose, there was a small increase in glucagon but a 2-fold increase in insulin concentration. There was a large transient increase in lactate and alanine concentrations. The total amino acid concentration remained unchanged, as did the urea production rate. In summary, in men fasted overnight, ingestion of 50 g fructose resulted in a modest increase in the circulating glucose concentration. However, it is likely that a larger proportion of the ingested fructose was converted to glucose in the liver and stored as glycogen and that fructose substituted, at least in part, for lactate and alanine as a gluconeogenic substrate. The increase in glucose production occurred even in the presence of an increase in the insulin concentration and an unchanged glucagon concentration. The metabolic fate of the remaining fructose is yet to be determined.
Bibliographical noteFunding Information:
From the Section of Endocrinology, Metabolism and Nutrition, Minneapolis Veterans Affairs Medical Center; and the Departments of Medicine and Food Science and Nutrition, University of Minnesota, Minneapolis, MN. Submitted December 22, 1999; accepted May 16, 2000. Supported by merit review funds from the Department of Veterans Affairs. Address reprint requests to F.Q. Nuttall, MD, PhD, Chief, Section of Endocrinology, Metabolism and Nutrition, VA Medical Center (111G), One Veterans Drive, Minneapolis, MN 55417. Copyright r 2000 by W.B. Saunders Company 0026-0495/00/4912-0009$10.00/0 doi:10.1053/meta.2000.18553