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Biomedical subjects

F J Service

Publications and source records attributed to F J Service.

At least 109 records · Page 6Linked to original sources
PubMed1979

The surgical aspects of insulinomas.

The clinical diagnosis of insulinoma rests on the demonstration of Whipple's triad (symptoms of hypoglycimia, low circulating glucose and prompt relief of symptoms after glucose administration). Biochemically, the association of an increased value of immunoreactive insulin with a low glucose value is diagnostic of insulin-mediated hypoglycemia. Angiographic localization of these tumors is accomplished in more than 90% of cases. The pathologic changes are usually due to a single adenoma, for which surgical enucleation is the procedure of choice. Malignancy and persistent hypoglycemia occur in slightly less than 10% of cases and can be fairly successfully managed by diazoxide and streptozotocin.

Adenoma, Islet Cell↗
PubMed1979

Effect of intermittent endogenous hyperglucagonemia on glucose homeostasis in normal and diabetic man.

UNLABELLED: Infusion of glucagon causes only a transient increase in glucose production in normal and diabetic man. To assess the effect of intermittent endogenous hyperglucagonemia that might more closely reflect physiologic conditions, arginine (10 g over 30 min) was infused four times to 8 normal subjects and 13 insulin-dependent diabetic subjects (4 of whom were infused concomitantly with somatostatin to examine effects of arginine during prevention of hyperglucagonemia). Each arginine infusion was separated by 60 min. Diabetic subjects were infused throughout the experiments with insulin at rates (0.07-0.48 mU/kg per min) that had normalized base-line plasma glucose and rates of glucose appearance (Ra) and disappearance (Rd). Basal plasma glucagon and arginine-induced hyperglucagonemia were similar in both groups; basal serum insulin in the diabetics (16+/-1 muU/ml, P < 0.05) exceeded those of the normal subjects (10+/-1 muU/ml, P < 0.05) but did not increase with arginine. Serum insulin in normal subjects increased 15-20 muU/ml with each arginine infusion. In both groups each arginine infusion increased plasma glucose and Ra. Increments of Ra in the diabetics exceeded those of normal subjects, (P < 0.02); Rd was similar in both groups. In normal subjects, plasma glucose returned to basal levels after each arginine infusion, whereas in the diabetics hyperglycemia persisted reaching 151+/-15 mg/dl after the last arginine infusion. When glucagon responses were prevented by somatostatin, arginine infusions did not alter plasma glucose or Ra. CONCLUSIONS: Infusion of arginine acutely increases plasma glucose and glucose production in man solely by stimulating glucagon secretion; physiologic increments in plasma glucagon (100-150 pg/ml) can result in sustained hyperglycemia when pancreatic beta cell function is limited.

Adolescent↗
PubMed1979

Pancreatic alpha-cell function in diabetic hemochromatotic subjects.

To clarify further the etiology of the carbohydrate intolerance in idiopathic hemochromatosis, we investigated the glucose, insulin, C-peptide, and glucagon responses to arginine (0.5 g/kg) infused during 30 min in lean normal subjects; in insulin-requiring subjects with hemochromatosis, genetic diabetes, and total pancreatectomy; and in nondiabetic cirrhotic subjects without portosystemic shunting. Serum insulin, C-peptide, and glucagon responses (30K antibody) were determined by RIA, and glucose level was determined by a glucose oxidase technique. Hemochromatotic and genetic diabetic subjects had similar basal glucose (157 +/- 25 vs. 168 +/- 40 mg/dl) and C-peptide (0.73 +/- 0.42 vs. 0.65 +/- 0.22 ng/ml) values, with subnormal C-peptide peak responses to stimulation (1.05 +/- 0.38 and 1.40 +/- 0.83 vs. 3.95 +/- 0.4 ng/ml in normals; P less than 0.05). No glucagon or C-peptide response to arginine was seen in any pancreatectomized subject. Similar but excessive glucagon levels were present in hemochromatosis, diabetes, and cirrhosis under basal conditions (166 +/- 24, 232 +/- 111, and 263 +/- 116 vs. 76 +/- 15 pg/ml; P less than 0.05) and after arginine stimulation (782 +/- 80, 834 +/- 123, and 902 +/- 275 vs. 489 +/- 81 pg/ml; P less than 0.05) when compared with normals. The excessive glucagon levels found in hemochromatosis, diabetes mellitus, and cirrhosis contrast to the absent response in pancreatectomized subjects and indicate that generalized islet cell destruction is not the major factor in diabetic hemochromatotic subjects.

Adult↗
PubMed1979

Calcium homeostasis in diabetes mellitus.

Experimentally diabetic rats have low serum 1,25-dihydroxyvitamin D, intestinal malabsorption of calcium, secondary hyperparathyroidism, and bone loss. To examine the hypothesis that abnormalities similar to those in the diabetic rat might explain human diabetic osteopenia, we studied calcium metabolism in 40 healthy control and 82 diabetic patients aged 18--75 yr [47 untreated: fasting plasma glucose (mean +/- SE), 267 +/- 8 mg/dl; 19 treated but hyperglycemic: glucose 305 +/- 24 mg/dl; 16 treated and in better control: glucose, 146 +/- 8 mg/dl]. Serum total calcium, ionic calcium, immunoreactive parathyroid hormone (Arnaud method, GP-1M and CH-12M antisera), 25-hydroxyvitamin D (Haddad method), and 1,25-dihydroxyvitamin D (Lambert method) concentrations were normal in all 3 groups of diabetics and were not significantly different from values in the control group. We determined absorption of calcium from the intestine by a double isotope method (100 mg Ca carrier; normal range, 40--80%) in 11 control and 13 untreated, uncontrolled diabetics (mean plasma glucose, 285 +/- 17 mg/dl). Absorption of calcium in controls was 60 +/- 3% and in diabetics was 56 +/- 3% (not significantly different). We have found no derangement of calcium metabolism in adults with insulin-requiring juvenile- and adult-onset diabetes regardless of treatment status. The experimental diabetic rat model does not appear to be useful for determining the pathogenesis of adult human diabetic osteopenia.

Adolescent↗
PubMed1979

Renal transplantation in patients with diabetes mellitus--revisited.

Sixty-one patients with end-stage renal failure due to diabetic nephropathy received 68 renal allografts from June 1970 to February 1978. Patient and graft survival results equaled those for nondiabetic patients, as reported by the Human Renal Transplant Registry (HRTR). Renal allografts from siblings or pretreated cadaver donors had a significantly longer survival time than did allografts from nonpretreated cadaver donors. It is concluded that renal transplantation with living related and pretreated cadaver donor kidneys continues to be the treatment of choice and is superior to other forms of treatment in the insulin-dependent diabetic patient with end-stage renal disease.

Adult↗
PubMed1978

Combined deficiency of glucose-6-phosphatase and fructose-1, 6-diphosphatase. Studies of glucagon secretion and fuel utilization.

An adult woman with hypoglycemia, hyperlactatemia, hyperuricemia, hypertriglyceridemia, hyperketonemia and inability to make new glucose from galactose, fructose, glycerol and alanine was found to have no hepatic glucose-6-phosphatase and deficient fructose-1,6-diphosphatase. Nonautonomous hyperglucagonemia was demonstrated and shown to contribute to the hyperlactatemia and hyperketonemia. A paradoxic hyperlactatemic response to glucose and galactose was observed. Studies of substrate utilization showed prompt adaptation to changes in dietary supply of energy which probably accounted for her never having experienced symptoms of hypoglycemia.

Adult↗
PubMed1978

Direct effect of insulin on secretion of insulin, glucagon, gastric inhibitory polypeptide, and gastrin during maintenance of normoglycemia.

The direct effect of insulin on the secretion of insulin (as measured by C-peptide), glucagon, gastric inhibitory polypeptide, and gastrin was studied in normal subjects by infusing insulin while the plasma level of glucose was maintained in the normal fasting range (euglycemic clamp). Insulin-induced hypoglycemia resulted in increases in circulating glucagon and gastric inhibitory polypeptide, a decrease in C-peptide, and no change in gastrin levels. In contrast, during the euglycemic clamp, insulin was found to behave a direct suppressive effect on the secretion of glucagon, C-peptide, and gastrin, but no effect on levels of gastric inhibitory polypeptide.

Blood Glucose↗
PubMed1978

Hypoglycemia.

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Blood Glucose↗
PubMed1978

Normalization of plasma glucose of unstable diabetes: studies under ambulatory, fed conditions with pumped intravenous insulin.

A program using continuously pumped IVI was devised to restore glycemia of unstable diabetes under ambulatory, fed conditions to that of nondiabetic subjects. Five patients with unstable diabetes were studied. The daily regimen consisted of four meals of equal carbohydrate, fat, and protein content taken at 8 A.M., 2 P.M., 8 P.M., and 2 A.M. and 1 hr of standardized exercise in the second postprandial hour (except after the 2 A.M. meal). Confirmation of physiologic replacement of insulin by the IVI program was possible because four patients had low insulin-binding antibodies and minimal distortion of serum IRI. Best glucose control was achieved by increasing the basal flow rate (mean, 0.15 mU/kg/min) 10-fold from 15 to 60 min after daytime meals and from 15 to 105 min after the 2 A.M. meal and doubling the basal rate overnight. Contrasted to the results with SCI, the IVI program significantly improved the mean blood glucose and mean amplitude of glycemic excursions. The IVI program restored the time to glucose peak and postprandial baseline glucose recovery to normal; the amplitude of glucose increase to peak remained somewhat greater than normal.

Adult↗
PubMed1977

Hypoglycemia.

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Adult↗
PubMed1977

C-peptide suppression test for insulinoma.

During hypoglycemia induced by an infusion of porcine insulin, impaired suppression of endogenous insulin secretion as measured by C-peptide was demonstrated in 11 of 12 patients with insulinoma. During hypoglycemia (plasma glucose less than or equal to 40 mg/dl) the mean C-peptide immunoreactivity (CPR) of normal subjects was less than or equal to 1.2 ng/ml, whereas 11 of 12 insulinoma patients had a mean CPR of larger than or equal to 1.9 ng/ml. One patient showed normal CPR suppression by these criteria but may have shown impaired CPR suppression for glucose less than or equal to 30 mg/dl. Impaired CPR suppression during insulin-induced hypoglycemia may prove to be a useful test for insulinoma.

Adenoma, Islet Cell↗
PubMed1976

Plasma insulin and glucose levels after renal transplantation.

Plasma insulin and glucose levels were measured before and for twenty-four hours after operation in 13 patients who had undergone renal transplantation, 4 who had undergone bilateral nephrectomy, and 5 who had undergone donor nephrectomy. Postoperative hyperglycemia was noted in all patients, but the hyperglycemia was much greater after renal transplantation. Peripheral insulin antagonism rather than decreased insulin secretion appeared to account for the hyperglycemia. The peripheral insulin antagonism was largely due to surgical stress, but intravenous immunosuppressive medications contributed to the exaggerated hyperglycemia, hyperinsulinemia, and insulin antagonism observed in the transplant patient.

Adult↗
PubMed1976

Insulinoma: clinical and diagnostic features of 60 consecutive cases.

Insulinoma is a rare tumor, occurring more often in women and in the older age range. Eighty percent of patients have a single benign tumor, usually less than or equal to 2 cm in diameter, located with about equal frequency in body, head, or tail of the pancreas and amenable to surgical cure. About 10% have multiple tumors; in this group there is a high incidence of multiple endocrine neoplasia type I syndrome. The remaining 10% of patients have metastatic malignant insulinoma. Symptoms are intermittent, recur at irregular intervals in the food-deprived state over a median of 1 1/2 years, and arise from varying degrees of neuroglycopenia. Symptoms often lead to misdiagnosis as a neurologic or psychiatric disorder. Transient neurologic deficits and EEG abnormalities can be observed during hypoglycemia. Diagnosis requires repeated demonstration of hypoglycemia (glucose less than or equal to 40 mg/dl) during spontaneous or provoked symptoms, relief with ingestion of carbohydrates, simultaneous hyperinsulinemia (serum insulin greater than 6 muU/ml), and absence of insulin antibodies. A useful diagnostic adjunct is the intravenous tolbutamide test, for which new diagnostic criteria are presented.

Adenoma, Islet Cell↗
PubMed1976

Hypoglycemias.

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Adenoma, Islet Cell↗
PubMed1975

Hyperosmolar nonketotic syndrome and steroid diabetes. Occurrence after renal transplantation.

So-called steroid (glucocorticoids) diabetes developed in 11 (5.5%) of 202 patients receiving 216 renal allografts between December 1963 and June 1974. In three of the 11 patients, hyperosmolar nonketotic syndrome was present at diagnosis; all of the three recovered. Eight of the 11 patients survived with functioning allografts, and only one of the eight requires insulin. Hyperglycemia has been detected in most transplant patients tested in the immediate postoperative period. Factors (including stress from surgery and treatment with drugs such as furosemide) predispose to this condition.

Adolescent↗
PubMed1975

C-peptide analysis in diagnosis of factitial hypoglycemia in an insulin-dependent diabetic.

Factitial hypoglycemia from the surreptitious self-administration of insulin by an insulin-dependent diabetic, shown to have C-peptide secretory ability by glucose and tolbutamide stimulation tests, was strongly suspected by finding low plasma C-peptide immuno-reactivity and high plasma insulin levels during "spontaneous" hypoglycemia whereas during hyperglycemia the D-peptide immunoreacitivity was higher and the plasma insulin was lower.

Adult↗