Absorption and disposition of a glucose load in the conscious dog.

The quantitative disposition of an intragastrically administered glucose load was studied in eight conscious 18-h fasted dogs using isotopic and arteriovenous (A-V) techniques. During the control period, the gut utilized 25% of the basal net hepatic glucose output (2.8 +/- 0.2 mg.kg-1.min-1). After glucose ingestion, 80% of the load was absorbed as glucose, 11% was converted across the gut to lactate and alanine, and 4% was oxidized to CO2. Two percent of the load remained in the gut 4 h after glucose administration and 3% was unaccounted for. During the absorptive period, net hepatic glucose balance (NHGB) varied considerably (mean range = output of 1.8 to uptake of 9.1 mg.kg-1.min-1), while endogenous hepatic glucose production (Ra hp) showed a consistent 80% suppression. The total net hepatic glucose uptake during the absorptive period (150 +/- 10 min) accounted for the disposal of 24 +/- 10% of the ingested load, and the amount of glucose escaping the splanchnic bed was 40 +/- 3%. Overall NHGB correlated positively with basal arterial glucose and insulin levels and negatively with basal arterial glycerol and FFA and with peak absorptive arterial glucose and insulin levels. These data suggest that the hepatic response to an ingested glucose load depends in part on the degree of metabolic fast of the animal at the time of glucose ingestion; the latter may be a major determinant of the roles played by the tissues in glucose disposal.

[1]  R. Steele,et al.  Effect of insulin on utilization and production of circulating glucose. , 1957, The American journal of physiology.

[2]  R. Steele,et al.  ON THE HORMONAL REGULATION OF CARBOHYDRATE METABOLISM; STUDIES WITH C14 GLUCOSE. , 1963, Recent progress in hormone research.

[3]  C. M. Leevy,et al.  Estimation of hepatic blood flow with indocyanine green. , 1962, The Journal of clinical investigation.

[4]  G. Hetényi,et al.  Glucoregulatory responses in normal and diabetic dogs recorded by a new tracer method. , 1971, Metabolism: clinical and experimental.

[5]  L. Hagenfeldt.  A simplified procedure for the measurement of 14CO2 in blood. , 1967, Clinica chimica acta; international journal of clinical chemistry.

[6]  W. Shoemaker,et al.  Glucose and fructose absorption in the unanesthetized dog. , 1963, Gastroenterology.

[7]  T. McDonald,et al.  Initial splanchnic extraction of ingested glucose in normal man. , 1978, Metabolism: clinical and experimental.

[8]  R. DeFronzo,et al.  Influence of hyperinsulinemia, hyperglycemia, and the route of glucose administration on splanchnic glucose exchange. , 1978, Proceedings of the National Academy of Sciences of the United States of America.

[9]  A. Dunn,et al.  Glucose-2-t as a tracer for glucose metabolism. , 1967, Biochemistry.

[10]  J. McGarry,et al.  In vitro reversal of the fasting state of liver metabolism in the rat. Reevaluation of the roles of insulin and glucose. , 1981, The Journal of clinical investigation.

[11]  R. Crane.  Intestinal absorption of sugars. , 1960, Physiological reviews.

[12]  R. Steele,et al.  Glucose Uptake and Production During the Oral Glucose Tolerance Test , 1968, Diabetes.

[13]  B. Issekutz,et al.  Estimation of hepatic glucose output in non-steady state. The simultaneous use of 2-3H-glucose and 14C-glucose in the dog. , 1974, Canadian journal of physiology and pharmacology.

[14]  P. Felig,et al.  Influence of Oral Glucose Ingestion on Splanchnic Glucose and Gluconeogenic Substrate Metabolism in Man , 1975, Diabetes.

[15]  J. Liljenquist,et al.  Lack of a role for glucagon in the disposal of an oral glucose load in normal man. , 1979, The Journal of clinical endocrinology and metabolism.