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Hepatic autoregulation: response of glucose production and gluconeogenesis to increased glycogenolysis

¹Medical Endocrinological Department, Odense University Hospital, Odense, Denmark; ²Medical Department, Hanusch Hospital, Vienna, Austria; ³Division of Endocrinology and Metabolism, General Hospital of Vienna, Vienna, Austria; ⁴Department of Medical Physiology, Panum Institute, University of Copenhagen, Copenhagen, Denmark; and Departments of ⁵Epidemiology and Biostatistics and ⁶Medicine, Case Western Reserve University, Cleveland, Ohio

Submitted 10 August 2006 ; accepted in final form 25 December 2006

The effect of increased glycogenolysis, simulated by galactose's conversion to glucose, on the contribution of gluconeogenesis (GNG) to hepatic glucose production (GP) was determined. The conversion of galactose to glucose is by the same pathway as glycogen's conversion to glucose, i.e., glucose 1-phosphate glucose 6-phosphate glucose. Healthy men (n = 7) were fasted for 44 h. At 40 h, hepatic glycogen stores were depleted. GNG then contributed 90% to a GP of 8 µmol·kg^–1·min^–1. Galactose, 9 g/h, was infused over the next 4 h. The contribution of GNG to GP declined from 90% to 65%, i.e., by 2 µmol·kg^–1·min^–1. The rate of galactose conversion to blood glucose, measured by labeling the infused galactose with [1-²H]galactose (n = 4), was also 2 µmol·kg^–1·min^–1. The 41st h GP rose by 1.5 µmol·kg^–1·min^–1 and then returned to 9 µmol·kg^–1·min^–1, while plasma glucose concentration increased from 4.5 to 5.3 mM, accompanied by a rise in plasma insulin concentration. Over 50% of the galactose infused was accounted for in blood glucose and hepatic glycogen formation. Thus an increase in the rate of GP via the glycogenolytic pathway resulted in a concomitant decrease in the rate of GP via GNG. While the compensatory response to the galactose administration was not complete, since GP increased, hepatic autoregulation is operative in healthy humans during prolonged fasting.

liver; galactose; deuterium oxide

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