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Effects of Enterectomy on Postoperative Visceral Organ Glucose Exchange

Departments of Surgery and Biochemistry, The University of Florida College of Medicine, Gainesville, Florida, Department of Surgery, The University of Texas Medical School, Houston, Texas

Patrick T. Roughneen, M.B., CH.B.

Departments of Surgery and Biochemistry, The University of Florida College of Medicine, Gainesville, Florida, Department of Surgery, The University of Texas Medical School, Houston, Texas

Diane L. Goldwater, M.D., PH.D.

Departments of Surgery and Biochemistry, The University of Florida College of Medicine, Gainesville, Florida, Department of Surgery, The University of Texas Medical School, Houston, Texas

R. Lawrence Reed, M.D.

Departments of Surgery and Biochemistry, The University of Florida College of Medicine, Gainesville, Florida, Department of Surgery, The University of Texas Medical School, Houston, Texas

Brian J. Rowlands, M.D., FRCS, FACS

Departments of Surgery and Biochemistry, The University of Florida College of Medicine, Gainesville, Florida, Department of Surgery, The University of Texas Medical School, Houston, Texas

The effects of a 60% small-bowel resection on postoperative visceral organ glucose exchange was studied in order to gain further understanding of the role of the intestinal tract as a supplier of gluconeogenic substrate to the liver following operative stress. We determined the flux of glucose across the gastrointestinal tract, liver, and kidneys in 20 postoperative dogs. With enterectomy portal bloodflow and total hepatic bloodflow were diminished by 33% and 25%, respectively. Arterial glucose was slightly lower in the enterectomized group 6 hr following the operation. Intestinal glucose uptake was diminished by more than 50% in the enterectomized dogs (p < 0.01). Net hepatic glucose release fell from 22 µmole/kg/ min to 8 µmole/kg/min (p < 0.01). In control animals the kidney was an organ of slight glucose uptake while in the enterectomized group, the kidney released glucose at the rate of 4.1 µmole/kg/min (p < 0.05). The data suggest that the gut is an important supplier of gluconeogenic precursors to the liver which are used to support gluconeogenesis in the postoperative period. The ability of the kidney to accelerate glucose production in this setting suggests that metabolic adaptation and cooperation between organs occurs during organ absence or dysfunction which helps preserve glucose homeostasis. (Journal of Parenteral and Enteral Nutrition 13:128-131, 1989)

Journal of Parenteral and Enteral Nutrition, Vol. 13, No. 2, 128-131 (1989)
DOI: 10.1177/0148607189013002128


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