We randomized 749 insulin-treated patients on the rolls of the Mount Sinai Medical Center Diabetes Clinic in a controlled trial of diabetic patient education; 345 agreed to participate, of whom 165 were assigned to the education group and 180 to the control group. Cognitive scores increased from 5.3 +/- 1.6 to 5.8 +/- 1.6 in the education group, but there was no change in the control group, whose score was 5.3 +/- 1.7 before and after the intervention (P = .0073). HbA1c fell from 6.8 +/- 2.1 to 6.1 +/- 2.0% in the education group and from 6.6 +/- 2.0 to 6.3 +/- 2.0% in the control group, an insignificant difference (P = .1995). The fasting blood glucose decreased from 223 +/- 94 to 179 +/- 73 mg/dl in the education group and from 199 +/- 81 to 185 +/- 76 mg/dl in the controls (P = .1983). Triglycerides, high- and low-density lipoprotein cholesterol, and insulin dosage also failed to show significant variation among groups. The foot-lesion score showed similar progression in the education and control groups. Neither diastolic nor systolic blood pressure showed significantly greater change in the education or the control group, with falls noted, particularly in diastolic pressures, in both patient groups. Differences between the groups were not significant for sick days, hospitalizations, emergency room visits, or outpatient visits. The sample sizes of the study and control populations were sufficiently large to detect a difference in means between the education and control groups in the HbA1c, the primary outcome variable, of greater than 1.0%, with alpha = .05 and a power of .95. Thus, our study suggests that patient education may not be an efficacious therapeutic intervention in most adults with insulin-treated diabetes mellitus.

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The present study examines the question of whether lowering the basal plasma glucagon concentration alters the response of the liver to an intravenous glucose load under conditions where insulin is present at near-basal concentrations. Acute hyperglycaemia of 220-240 mg/dl was induced by peripheral venous glucose infusion in two groups of normal men who had undergone hepatic vein catheterization. Somatostatin (0.9 mg/h) was infused in both groups together with an infusion of insulin (0.15 mU/kg/min) to maintain arterial insulin levels at 7-12 ~tU/ml. Glucagon (1.5ng/kg/min) was infused in one group resulting in a rise in plasma glucagon levels from 148 _+ 37 to 228 + 25 pg/ml, thus mimicking basal portal glucagon concentrations, whereas in the second group glucagon was not replaced, resulting in a fall in circulating glucagon levels from 132 + 21 to 74 _+ 15 pg/ml. In the glucagon-deprived group, net splanchnic glucose production (NSGP) fell from 143 + 31 to-72.5 + 39 rag/ rain (p < 0.01), indicating that net splanchnic glucose uptake had occurred. By contrast, NSGP did not change significantly (137 +_ 20 vs 151 + 60 rag/rain) in the group in which both insulin and glucagon were replaced during hyperglycaemia. These data thus suggest that during hyperglycaemia, when the insulin concentration is fixed at basal levels, glucagon may play an important role in determining whether or not the liver diminishes its output of glucose and stores glucose in response to a glucose load.

Hepatic uptake and gut and splanchnic output of amino acids were determined after administration of protein and glucose loads in conscious dogs with indwelling catheters in the femoral artery and portal and hepatic veins. Oral or parenteral glucose given with a beef meal blunted the rise in arterial amino acids relative to that seen with ingestion of beef alone. Gut amino acid output was considerably delayed with oral hypertonic glucose, but was unchanged with parenteral glucose and with oral isotonic glucose. Ingestion of beef with oral hypertonic mannitol, a nonabsorbable sugar alcohol, delayed the rise in gut amino acid output in a manner similar to that seen with beef plus oral hypertonic glucose. We have evaluated the relationship between circulating amino acids, circulating hormone concentrations, and amino acid metabolism. Significant correlations with hepatic amino acid uptake were found for insulin, for arterial and portal amino acid levels, and for gut amino acid output. Partial correlation analysis suggests that gut amino acid output is the major determinant of hepatic amino acid uptake.