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Recent studies from this laboratory (1) have shown that insulin has an immediate and profound effect upon net hepatic glucose balance. When insulin was administered at a rate (2) estimated to minimize the counter-regulatory responses to hypoglycemia, the decline in blood glucose which ensued was largely the consequence of a diminished hepatic release of glucose (1). Since, under physiologic circumstances, endogenous insulin secretion is stimulated by the rising blood glucose concentration (3, 4) which follows a carbohydrate meal, the effect of insulin in regulating hepatic glucose metabolism is best assessed in the presence of a glucose load. Whether or not hyperglycemia, with its attendant release of endogenous insulin, results in a decrease or cessation of hepatic glucose output has been a controversial subject (5-13). However, in all but one of the previous studies (5), the conclusions were based upon inferential data, since net hepatic glucose balance was not measured. The present studies were undertaken to determine the effect of hyperglycemia and the concomitant release of endogenous insulin upon hepatic glucose metabolism. Hyperglycemia was produced by the intravenous infusion of glucose. The rate of glucose administration was varied in order to define better some of the factors that con-

the journal of clinical investigation/the journal of clinical investigation

THE PHYSIOLOGICAL SIGNIFICANCE OF THE SECRETION OF ENDOGENOUS INSULIN INTO THE PORTAL CIRCULATION. IV. HEPATIC UPTAKE OF GLUCOSE DURING GLUCOSE INFUSION IN NON-DIABETIC DOGS*