Influence of Maturity-onset Diabetes on Splanchnic Glucose Balance After Oral Glucose Ingestion

Author:

Felig Philip1,Wahren John1,Hendler Rosa1

Affiliation:

1. Department of Internal Medicine, Yale University School of Medicine New Haven, Connecticut, and the Department of Clinical Physiology, Karolinska Institute and Huddinge Hospital Stockholm, Sweden

Abstract

To determine the extent to which altered splanchnic glucose balance contributes to postprandial hyperglycemie in diabetes, splanchnic glucose exchange was determined in seven maturity-onset diabetics and 10 healthy control subjects in the basal state and for three hours following oral ingestion of 100 gm. of glucose. In the basal fasting state, arterial glucose levels in the diabetics (153±24 mg./100 ml.) were 75 to 80 mg./100 ml. higher than in controls while splanchnic glucose output was similar in the two groups (132 to 145 mg. per minute). Following glucose ingestion, arterial glucose concentration in the diabetics rose to peak levels (295 ±35 mg./100 ml.) that were 55 per cent higher than in controls and remained 100 to 125 mg./100 ml. above basal levels and 150 to 200 mg./100 ml. above control levels three hours after glucose. Splanchnic glucose output rose rapidly in the diabetics to values four times the basal rate at 15 to 30 minutes after glucose feeding and remained 60 per cent or more above basal levels throughout the three-hour period. In contrast, in the controls following a similar early rise, splanchnic glucose output returned to basal levels by 90 minutes. As a consequence, total splanchnic glucose output over three hours in the diabetics (53±4 gm.) was 33 per cent greater than in controls. In addition, the increment in splanchnic glucose output above basal levels in the diabetics (30±5 gm.) was 100 per cent greater than in controls and could account for 75 per cent of the augmented glucose accumulation in body fluids observed at three hours. It is concluded that in maturity-onset diabetics (1) net splanchnic glucose output is increased after glucose ingestion, suggesting that a greater proportion of an oral glucose load enters the systemic circulation than in healthy controls; (2) failure of splanchnic glucose retention is the major factor responsible for postprandial hyperglycémie in maturity-onset diabetes.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

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