Lactose tolerance in a Slavic population

In order to gather data on the frequency of primary lactase deficiency in various population groups, lactose tolerance tests were performed on 38 healthy adults of Slavic origin who had recently left Eastern Europe and are presently living in Western Canada. Twenty-one of the subjects were born in Poland and 17 in Czechoslovakia. There were 16 males and 22 females, aged 17–65 years, with a mean of 29.8 years. The tests revealed that 9 (23.9%) of the 38 subjects were lactose intolerant on the basis of both criteria, showing a maximum rise in blood glucose of less than 20 mg/100 ml above the fasting blood glucose level after ingesting 50 g of lactose, and experiencing gastrointestinal symptoms during the test. The mean maximum rise in blood glucose was 39.1 mg/100 ml in the 29 lactose tolerant subjects and 7.3 mg/100 ml in the 9 lactose intolerant subjects. Gastrointestinal symptoms during the test were observed in all 9 subjects with a low rise in blood glucose, and no symptoms were produced in any of the 29 subjects with a significant rise in blood glucose (> 20 mg/100 ml). Most of the subjects consumed 1 cup of milk per day. In addition, they were irregularly consuming lactose-containing products such as ice cream, chocolate drinks, etc. The results suggest a relatively low frequency of lactose intolerance among Eastern Europeans of Slavic origin, and in this respect, they resemble Northern Europeans.Supported by grants from the National Research Council of Canada (A6249), and from the Committee on Research of The University of British Columbia (26–9682).The author wishes to thank Dr. J. A. Birkbeck for his assistance.     

Lactase deficiency in Jewish communities in Israel

Lactase deficiency and lactose tolerance were studied in several Jewish communities in Israel. Lactase deficiency was found in 60% of biopsied subjects. Forty-one biopsies were peroral and 22, surgical; histologically, the jejunal mucosa of all specimens was normal. Lactose tolerance tests were performed on 217 subjects, 118 patients and 99normals. A low glucose rise was found in 44.4% of Yemenites, 62.5% of North Africans (Sephardi), 72.2% of others (Sephardi), 79.2% of Ashkenazi, 84.2% of Iraqis and 85.0% of others (Oriental); the overall incidence was 71.1%. Statistical analysis confirmed that the population studied was heterogenous. Most subjects with a low glucose rise had symptoms during the test. Milk intake, low in almost all subjects, did not correlate with lactose tolerance. Most lactose intolerant subjects were not aware of milk intolerance; the condition is not usually symptomatic in Israel. Lactase deficiency in various population groups has been reviewed and evidence in favor of a genetic etiology emphasized.The authors wish to thank the staff of the Tel-Aviv Government Municipal Hospitals, in particular, the Department of Pediatrics-B for their help in carrying out this investigation and for permission to study their patients; Dr. A. Adam, Department of Human Genetics, Tel-Aviv University Medical School, for helpful advice and criticism. Blood sugar estimations were performed at the Central Biochemical Laboratory of the Workers Sick Fund, Tel-Aviv.     

Lactose intolerance in Canadian West Coast Indians

Lactose tolerance tests were performed on 30 healthy Canadian West Coast Indians and 16 non-Indians of Northern European extraction. Among the Indians, there were 7 males and 23 females, aged 14–24 years, with only 1 above 20 years of age (mean 15.8 years). The non-Indians consisted of 3 males and 13 females, aged 15–26 years, with only 2 above 18 years of age (mean 17.4 years). The tests revealed that of the 30 Indians, 19 (63.3%) were lactose intolerant on the basis of maximal blood glucose rise of less than 20 mg/100 ml above the fasting level after the lactose load. Gastrointestinal symptoms during or after the test were observed in 68.4% of the subjects with a flat blood glucose curve and in 18.2% of those with normal curves. In contrast, of the 16 non-Indians, only 1 (6.3%) was lactose intolerant, and none experienced abdominal discomfort during or after the test. Milk consumption among most of the Indian subjects seems to be low by North American standards, as judged by their past milk-drinking habits. The results suggest a high incidence of lactose intolerance among West Coast Indians during adolescence.Supported by National Health Grant 609-7-236 and NRC Grant A6249, Canada.The authors wish to thank Father T. Lobsinger and the students at the Cariboo Student Residence, Williams Lake, British Columbia for their cooperation; and Dr. J. A. Birkbeck and Miss Ilse Borgen for their assistance.     

A standardized milk tolerance test

Inability to hydrolyze lactose does not always cause symptoms. The lactose tolerance test commonly used in diagnosis pinpoints the biochemical anomaly but does not establish whether it causes a functional disability. I therefore compared a milk tolerance test (500 ml milk) with the standard lactose tolerance test in 40 healthy adult volunteers for rise in blood sugar. A maximum glucose rise of 9 mg/100 ml or less indicated lactose malabsorption. Only one subject was misclassified by the milk tolerance test when compared with the lactose tolerance test (specificity 91.7%; sensitivity 100%). The test not only reproduces the worst symptoms that the subject is likely to suffer due to usual milk intake, but also accurately identifies the lactose malabsorber, thus yielding more information than the standard lactose tolerance test.     

Use of the lactose-ethanol tolerance test in diabetes.

The standard lactose tolerance test involves measuring a patient's blood glucose after the ingestion of lactose. If the patient has lactase deficiency and is unable to hydrolyze lactose and absorb its monosaccharides, glucose and galactose, the blood glucose does not usually increase greater than 20 mg/100 ml. Since factors other than the absorption of glucose can cause an increase in the blood glucose of greater than 20 mg/100 ml in a diabetic, this test could be unreliable when it is performed on a diabetic. The present study was performed to determine whether the lactose-ethanol tolerance test could be used to diagnose lactoase deficiency in diabetics. This test involves measuring the blood galactase level, instead of the blood glucose, and the administration of ethyl alcohol to a subject prior to the test to delay the clearance of galactose from the circulation. The results indicate that the standard lactose tolerance test in which the blood glucose is measured is unreliable when performed on insulin-dependent diabetics, but that it can be reliable when performed on non-insulin-dependent diabetics. The lactose-ethanol tolerance test gave results in each type of diabetic which were qualitatively similar to those of nondiabetics. It was concluded that the latter test is a useful screening test for lactase deficiency in diabetics.     

Changes in plasma free fatty acid concentration following oral lactose tolerance tests as a test for lactose absorption in infants and children

Changes in blood glucose and plasma free fatty acid (FFA) following oral lactose tolerance tests (LTT) were measured in three groups of children. In three out of seventeen infants with secondary lactose intolerance, only a small increase (less than 25 mg/100 ml) in glucose was found, but a normal decline (more than 50% of fasting value) in FFA concentration occurred. Resumption of milk feeding proved that they were not intolerant to lactose. Six infants (37%) without lactose intolerance who were on a normal lactose-containing diet showed only small increases in glucose; five of them showed a normal decline in plasma FFA. Nine out of thirteen children with no symptoms following oral LTT failed to show an increase in blood glucose, while in only one there was a decline of less than 50% in FFA concentration. Our results suggest that measurement of plasma FFA following oral LTT may be a more reliable test for cleavage and absorption of lactose than LTT alone, but for the final evaluation of this test a study of larger groups is obviously needed.     

Carbohydrate Intolerance in Carcinoma of the Lung

Summary: Oral two hour glucose tolerance tests were performed in 53 patients with carcinoma of the lung and in 45 control subjects of comparable age.
In male subjects, mean blood sugars were significantly higher at 90 and 120 minutes after glucose in the patients with cancer, and blood sugar levels greater than 120 mg/100 ml were seen in 69% of men with cancer, as compared with 38% of control subjects. Glucose tolerance improved with the removal of the tumours in a small group of patients.
As a group, men with carcinoma of the lung had higher plasma insulin and plasma growth hormone concentrations than controls, but these changes were not correlated with carbohydrate in-tolerance in individuals. The Impaired tolerance is not due to "starvation diabetes".     

Manifestation and occurrence of selective adult-type lactose malabsorption in Finnish teenagers

In 1969–1970, a simple random sample of 129 Finnish school-aged children was examined to study selective adult-type lactose malabsorption (SLM) in this age category. SLM was found in 8 children. All subjects were reexamined 5 years later. SLM was reconfirmed in these 8 persons and found in 3 additional subjects who had normal lactose absorption in the first examination. The prevalence of SLM was 9.3%, being 8.5% in the age category 12–15 years and 9.9% in that 16–20 years. Low rise of blood glucose in the lactose tolerance test of the first examination, very low milk consumption, milk intolerance, and history of gastrointestinal symptoms were found to be of low predictive value as indicators of SLM. It was also concluded that information about dietetic sources of lactose is important to persons with SLM, but categorical exclusion of lactose from the diet is not necessary, at least in the Finnish population.The study was supported by the Finnish Cultural Foundation and the Foundation for Pediatric Research in Finland.     

Restored synergistic entero-hormonal response after addition of dietary fibre to patients with impaired glucose tolerance and reactive hypoglycaemia

Although some dietary fibres (DF) improve glucose tolerance by slowing carbohydrate absorption, other mechanisms are certainly involved. Some of the entero-hormonal responses after DF were investigated in six patients with impaired glucose tolerance and reactive hypoglycaemia. All patients received two different breakfasts, each containing 25 g of starch supplied either as white bread (WB) or a fibre-enriched bread preparation (FB): 4 g hemicellulose and 4 g guar. Metabolic and hormonal responses were evaluated over 5 hours. Compared to WB, the FB had a blunting effect on the resulting blood glucose peak (116 +/- 9 mg/100 ml with FB vs. 148 +/- 15 with WB P less than 0.025) or trough (88 +/- 3 mg/100 ml with FB vs. 79 +/- 5 with WB), and upon the insulin response at 60 min (20 +/- 4 micro U/ml with FB vs. 70 +/- 20 with WB). Gut glucagon immunoreactivity was diminished with FB at 90 min (185 +/- 39 vs. 242 +/- 42 P less than 0.05) and 150 min (180 +/- 39 vs. 242 +/- 40). Pancreatic glucagon was initially similar after FB and WB, but a significant rise was observed with FB at 180 min (116 +/- 17 pg/ml vs. 67 +/- 18 P less than 0.05). The improvement of the blood glucose pattern with DF, especially the suppression of reactive hypoglycaemia, seems to depend partly on reduced and delayed response of the entero-hormonal axis. This in turn results in a better synergistic secretion of insulin and glucagon in the late post-prandial period.     

Glucose tolerance, blood lipid, insulin and glucagon concentration after single or continuous administration of aspartame in diabetics

A nutritive sweetener, aspartame (L-aspartyl-L-phenylalanine methylester) was administered orally to normal controls and diabetic patients in order to evaluate effects on blood glucose, lipids and pancreatic hormone secretion. An oral glucose tolerance test was also performed in the same subjects as a control study of aspartame administration. In 7 normal controls and 22 untreated diabetics, a single dose of 500 mg aspartame, equivalent to 100 g glucose in sweetness, induced no increase in blood glucose concentration. Rather, a small but significant decrease in blood glucose was noticed 2 or 3 h after administration. The decrease in blood glucose was found to be smallest in the control and became greater as the diabetes increased in severity. No significant change in blood insulin or glucagon concentration during a 3-h period was observed in either the controls or the diabetics. The second study was designed to determine the effects of 2 weeks' continuous administration of 125 mg aspartame, equal in sweetness to the mean daily consumption of sugar (20-30 g) in Japan, to 9 hospitalized diabetics with steady-state glycemic control. The glucose tolerance showed no significant change after 2 weeks' administration. Fasting, 1 h and 2 h postprandial blood glucose, blood cholesterol, triglyceride and HDL-cholesterol were also unaffected. From these and other published results, aspartame would seem to be a useful alternative nutrient sweetener for patients with diabetes mellitus.     

Simultaneous evaluation of insulin secretion and action using a model

For the simultaneous evaluation of insulin secretion and insulin sensitivity, a glucose regulation model has been developed. In order to estimate the parameters of the model, an intravenous glucose infusion test (GIT, 100 mg/kg.min x 2 min and 10 mg/kg.min x 118 min) was carried out on 15 healthy subjects (N), 12 subjects with impaired glucose tolerance (IGT), 20 non-insulin-dependent diabetics (NIDDM) and 13 patients with chronic pancreatitis (CP). The coefficient (microU/mg) for insulin secretion depending on blood glucose concentration in IGT, NIDDM and CP were lower (35.9 +/- 2.7, 24.5 +/- 3.3, 43.1 +/- 3.1) than in N (77.5 +/- 7.9). The coefficients (microU.min/mg) for insulin secretion depending on rate of change in blood glucose concentration in IGT and NIDDM were significantly lower (6.5 +/- 2.1, 3.8 +/- 1.2) than in N (52.8 +/- 8.8). The insulin sensitivity index (ISI; 10(-2) mg/(microU/ml).kg.min) in NIDDM was lower (4.98 +/- 0.75) than in N (11.37 +/- 1.08). Administration of exogenous insulin did not significantly affect the value of ISI in N and NIDDM. ISI showed a tendency to increase (15.09 +/- 1.92) in CP. It was demonstrated that the proposed model which estimates both insulin secretory ability and insulin sensitivity simultaneously is quite useful for analyzing the mechanism of impaired glucose tolerance.     

Increase in insulin response after treatment of overt maturity-onset diabetes is independent of the mode of treatment

Summary The changes in insulin response to a 100 g glucose tolerance test after treatment by diet, sulphonylurea and insulin were compared in non-ketotic diabetic patients who had fasting blood glucose concentrations higher than 160 mg/100 ml. Patients were selected so that their pre-treatment and post-treatment blood glucose levels were comparable between different treatment groups. Their insulin responses were poor initially but increased significantly when the diabetic state was improved by each treatment. The degree of improvement of insulin response was similar between different treatment groups, when their fasting blood glucose decreased below 140 mg/100 ml and the glucose tolerance curves were improved to a similar extent. Preand post-treatment IRI values (sum of insulin values during glucose tolerance test, mean±SD) were 102±50 and 200±37 U/ml in diet-treated group (n = 28), 90±40 and 195±53 U/ml in sulphonylurea-treated-group (n=48), and 83±28 and 193±38 U/ml in insulin-treated group (n = 13), respectively. The data suggest that the poor insulin response in overt diabetes results not only from an inherent insensitivity of B-cells to glucose but also from the metabolic derangement of diabetes. Poor insulin response and overtly diabetic metabolism seems to form a vicious cycle.     

Metabolic and hormonal investigations in long-term streptozotocin diabetic rats on different dietary regimens

Summary Groups of diabetic rats (65 mg/kg streptozotocin SC) were fed ad lib on three different dietary regimens for 43 weeks: a standard control diet (68% of calories as carbohydrate, 20% as protein, and 12% as fat), a low carbohydrate high protein diet (6% carbohydrate, 63% protein, 31% fat) or a low carbohydrate-high fat diet (5% carbohydrate, 75% fat, 20% protein). The high fat diet resulted in a fall of blood glucose from 700 to 350 mg/100 ml. Rats fed the high protein diet showed a similar initial decrease in blood glucose concentration, and a further improvement was evident from the 28th week on. After 43 weeks blood glucose levels were below 180 mg/100 ml and glycosuria below 100 mg/24 h in all rats fed the high protein diet. When rats exhibiting blood glucose levels below 180 mg/dl were transferred temporarily to standard diet blood glucose levels increased and marked glycosuria was observed. Rats on the standard diet maintained blood glucose concentrations greater than 500 mg/100 ml and glycosuria of about 16 g/24 h throughout the experiment. The pancreatic insulin content at death of rats fed the standard diet or the high fat diet was 1% of normal rats, whereas the values for the rats on the high protein diet were increased to 9%. Animals fed the low carbohydrate diets showed greater weight gain. In the high fat diet group there was a marked rise after 43 weeks in plasma triglycerides, free fatty acids, 3-hydroxybutyrate and acetoacetate in the plasma. Urea excretion was raised in the animals on the high protein diet. Thus, treatment with low carbohydrate diets for 10 months regardless of fat and protein content markedly improved the diabetic state of rats.     

Hemoglobin A1c levels in a diabetes detection program.

Hemoglobin A1c concentration (HbA1c) was compared to the plasma glucose responses at 1 and 2 h of an oral glucose tolerance test (OGTT) in 63 subjects preselected because of postprandial hyperglycemia. HbA1c concentrations were correlated with 1- and 2-hour plasma glucose responses during the OGTT (r = 0.776 and 0.8602, respectively). The OGTT responses were diabetic-like in 21, indeterminate in 15, and normal in 27 subjects. HbA1c values were within normal limits in all subjects who had a normal or indeterminate OGTT response and in 10 out of 21 with a diabetic OGTT. The 2-h OGTT response among the 10 diabetic responders with normal HbA1c was 200 +/- 31 mg/100 ml (mean +/- SD), while that of the 11 diabetic responders with elevated HbA1c was 352 +/- 122 mg/100 ml. All subjects with an elevated HbA1c had a 2-h plasma glucose above 228 mg/100 ml, whereas only 7% of subjects with a normal HbA1c had a 2-h glucose above this value. It is concluded that only about half of the patients currently diagnosed as having mild or chemical diabetes by OGTT have elevated HbA1c and that an elevated HbA1c is usually associated with 2-h OGTT levels above 228 mg/100 mg.     

Reinvestigation of lactose intolerant children: lack of correlation between continuing lactose intolerance and small intestinal morphology, disaccharidase activity, and lactose tolerance tests.

Thirty children on a lactose-free diet aged from 2-38 months who had previously been diagnosed as having secondary lactose intolerance were reinvestigated on 32 occasions by an oral lactose tolerance test, small intestinal biopsy, and measurement of disaccharidase activity in order to detect the presence of continuing lactose intolerance before reintroduction of milk. No correlation was found between continuing lactose intolerance, as diagnosed by the development of watery stools containing excess reducing substances after an oral load of lactose, and maximum blood glucose rise during a lactose tolerance test, lactase levels, and small intestinal morphology.     

Serum immunoreactive insulin after the oral administration of single dose of tolbutamide. I. Peripheral vein immunoreactive insulin in normal subjects and mild diabetics (author's transl)]

It has been confirmed in numerous studies that the hypoglycemic effect of sulfonyl-ureas is mainly owing to its insulinogenic action. Intravenous administrations of the drugs have been adopted in many of these studies. But the oral administrations of the drugs in a few studies lead to conflicting results concerning its insulinogenic action. In this study, the concentrations of blood glucose, serum immunoreactive insulin (IRI), serum free fatty acid (FFA) and serum tolbutamide were measured following the oral administration of single dose of tolbutamide in six normal and eleven maturity onset mild diabetic subjects. The same parameters were measured after the oral administration of tolbutamide plus sodium bicarbonate in six normal subjects. The changes of these parameters were compared with the changes following the intravenous administration of sodium tolbutamide in six normal subjects. The oral administration of three grams of tolbutamide alone caused a gradual but significant decrease of blood glucose level. Serum FFA response showed an initial decrease, followed by a rebound elevation. In spite of 21 per cent reduction of blood glucose level, serum IRI level did not show any significant change throughout the observation for five hours. Serum tolbutamide concentration rose gradually and reached to 24.4+/-3.9 mg per 100 ml (Mean+/-SEM) at the end of the observation. Almost identical results were obtained in diabetic subjects. Three grams of tolbutamide plus the same dose of sodium bicarbonate were administered orally to the normal subjects. A profound decrease of blood glucose level with a nadir (35 per cent reduction) at 45 minutes and a significant increase of serum IRI level with a peak (273 per cent increase) at 20 minutes were obtained, and associated with a comparatively rapid elevation of serum tolbutamide concentration reached to 31.9+/-3.3 mg per 100 ml after three hours. From these results, it is suggested that slow rise of serum tolbutamide concentration after the oral administration of tolbutamide alone might lead to moderate secretion of insulin and sooner rise might evoke larger secretion into the pancreatic vein, and that an existence of moderate hyperinsulinism in the pancreatic venous blood after the oral administration of tolbutamide alone might cause a decrease of gluconeogenesis in the liver. And the failure of serum IRI response in the peripheral blood in spite of hyperinsulinism in the pancreatic vein might be due to hepatic trapping of the secreted insulin.     

Incidence and Clinical Significance of Lactose Malabsorption in Adult Coeliac Disease

Fifty-one adult patients with coeliac disease, verified by a proximal small-intestinal biopsy, were investigated. Before treatment with a gluten-free and low-lactose diet 52% showed a slight rise in blood glucose during the lactose tolerance test. Seventy-nine per cent of these patients had watery stools, and 88% had three or more bowel movements a day—statistically significantly different from the coeliac patients with a normal lactose tolerance test. After treatment 12% had a flat lactose tolerance curve. Half of them (6%) had specific lactase deficiency. This is approximately the incidence of lactose malabsorption in the general Danish population. The small-intestinal disaccharidases and alkaline phosphatase levels were severely depressed before treatment. After treatment the activities increased, but not to normal. We conclude that lactose malabsorption is a clinically important condition in many patients with untreated coeliac disease, giving rise to more frequent and more watery stools. In well-treated coeliac disease lactose malabsorption is not commoner than in the general population. The lactose activity in a proximal intestinal biopsy specimen was found to be an unreliable indicator of lactose malabsorption in coeliac disease.     

Incidence and clinical significance of lactose malabsorption in adult coeliac disease

Fifty-one adult patients with coeliac disease, verified by a proximal small-intestinal biopsy, were investigated. Before treatment with a gluten-free and low-lactose diet 52% showed a slight rise in blood glucose during the lactose tolerance test. Seventy-nine per cent of these patients had watery stools, and 88% had three or more bowel movements a day--statistically significantly different from the coeliac patients with a normal lactose tolerance test. After treatment 12% had a flat lactose tolerance curve. Half of them (6%) had specific lactase deficiency. This is approximately the incidence of lactose malabsorption in the general Danish population. The small-intestinal disaccharidases and alkaline phosphatase levels were severely depressed before treatment. After treatment the activities increased, but not to normal. We conclude that lactose malabsorption is a clinically important condition in many patients with untreated coeliac disease, giving rise to more frequent and more watery stools. In well-treated coeliac disease lactose malabsorption is not commoner than in the general population. The lactose activity in a proximal intestinal biopsy specimen was found to be an unreliable indicator of lactose malabsorption in coeliac disease.     

Blood glucose response after oral intake of lactulose in healthy volunteers: A randomized,controlled, cross-over study

AIM To investigate possible changes of blood glucose levels after oral intake of lactulose in healthy subjects.METHODS The study was performed as prospective, randomized, two-part study with 4-way cross-over design with n = 12 in each study arm. Capillary blood glucose levels were determined over a time period of 180 min after intake of a single dose of 10 g or 20 g lactulose provided as crystal or liquid formulation. During the manufacturing process of lactulose, impurities with sugars(e.g., lactose, fructose, galactose) occur. Water and 20 g glucose were used as control and reference. Because lactulose is used as a functional food ingredient, it may also be consumed by people with impaired glucose tolerance, including diabetics. Therefore, it is of interest to determine whether the described carbohydrate impurities may increase blood glucose levels after ingestion. RESULTS The blood glucose concentration-time curves after intake of 10 g lactulose, 20 g lactulose, and water were almost identical. None of the three applications showed any changes in blood glucose levels. After intake of 20 g glucose, blood glucose concentration increased by approximately 3 mmol/L(mean Cmax = 8.3 mmol/L), reaching maximum levels after approximately 30 min and returning to baseline within approximately 90 min, which was significantly different to the corresponding 20 g lactulose formulations(P 0.0001). Comparing the two lactulose formulations, crystals and liquid, in the dosage of 10 g and 20 g, there was no difference in the blood glucose profile and calculated pharmacokinetic parameters despite the different amounts of carbohydrate impurities(1.5% for crystals and 26.45% for liquid). Anyhow, the absolute amount of single sugars was low with 0.3 g in crystals and 5.29 g in liquid formulation in the 20 g dosages. Lactulose was well tolerated by most volunteers, and only some reported mild to moderate mainly gastrointestinal side effects. CONCLUSION The unchanged blood glucose levels after lactulose intake in healthy subjects suggest its safe use in subjects with impaired glucose tolerance.     

Failure of indomethacin to affect arginine-induced C-peptide and glucagon release in insulin-treated diabetics

Summary Fourteen insulin-treated diabetics were submitted to an arginine infusion test performed with either 11.7 or 5.85mg kg^-1 min^-1 arginine monohydrochloride infused during 40 min with or without previous oral administration of a low (75+50 mg) or a high (75 mg + 3 mg/kg) dose of indomethacin. Blood glucose, plasma non-esterified fatty acids, insulin, C-peptide and glucagon were determined at regular intervals before, during and after the arginine infusion. These parameters were totally unaffected by the two doses of indomethacin both in the basal state and during the arginine infusions at the two loads tested. Eight subjects had a basal C-peptide level above 0.07 pmol/ml and a mean (± SEM) maximal rise of 0.21±0.04 pmol/ml during the arginine infusion, whereas the remaining six patients had virtually zero values throughout the tests. The arginine-induced plasma glucagon rise was similar for the two rates of arginine infusion; the sum of the increments in plasma glucagon averaged 877±120 and 647±92 pg/ml (p>0.1) for the high and low rates of arginine infusion, respectively. The magnitude of the blood glucose rise appeared independent of the amount of arginine infused. Confirming previous reports, we found that the blood glucose rise after arginine was three to four times higher in subjects without C-peptide than in subjects with C-peptide. The mean glucagon response did not differ significantly between subjects with or without C-peptide. Thus, residual B cell function determines the magnitude of the blood glucose rise but not the glucagon response after intravenous arginine.