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Biomedical subjects

F J Service

Publications and source records attributed to F J Service.

At least 91 records · Page 5Linked to original sources
PubMed1981

Effect of artificial pancreas treatment on peripheral nerve function in diabetes.

To determine whether the complete correction of hyperglycemia of diabetes can rapidly improve abnormal peripheral nerve function, eight hyperglycemic insulin-requiring diabetics underwent 3 days of glucose control with an artificial endocrine pancreas, the BIOSTATOR Glucose Controller. Comparison of neurologic assessment before and after BIOSTATOR treatment showed improvement only in ulnar sensory conduction velocity (+ 3.2 +/- 1.4 meters per second, p less than 0.032) and no significant changes in 24 other nerve conduction measurements, computer-assisted examination, and scored neurologic assessment. Any significant beneficial effect on nerve function resulting from correction of hyperglycemia probably requires more than 3 days to be manifested.

Adolescent↗
PubMed1981

Pathogenesis of hypoglycemia in insulinoma patients: suppression of hepatic glucose production by insulin.

To determine the mechanism by which hyperinsulinemia causes hypoglycemia in insulinoma patients, rates of glucose production and utilization, and circulating levels of insulin, glucagon, alanine, lactate, and glycerol were measured in 6 insulinoma patients during development of fasting hypoglycemia and in 8 normal volunteers studied over an identical interval. Initially, insulinoma patients had a greater plasma insulin (42 +/- 9 versus 15 +/- 1 microunits/ml) and glucagon levels (214 +/- 31 versus 158 +/- 21 pg/ml) than normal subjects, P less than 0.05, but their plasma glucose levels (81 +/- 4 mg/dl) and rates of glucose production and utilization (1.71 +/- 0.08 and 1.74 +/- 0.08 mg/kg . min, respectively) were not significantly different from those of normal subjects (93 +/- 2 mg/dl, 1.93 +/- 0.11, and 1.92 +/- 0.13 mg/kg . min, respectively). During a subsequent 8-h fast, glucose production and glucose utilization decreased in both groups, but more markedly in insulinoma patients. Since glucose utilization exceeded glucose production to a greater extent in insulinoma patients than in normal subjects, plasma glucose decreased to 44 +/- 3 mg/dl in insulinoma patients, but only to 84 +/- 1 mg/dl in normal subjects (P less than 0.001). Glucose utilization in insulinoma patients never exceeded that of normal subjects. These results demonstrate that fasting hypoglycemia in the insulinoma patients is usually due to suppression of glucose production rather than to acceleration of glucose utilization, as is widely thought. A direct effect of insulin on the liver is probably responsible, since circulating levels of gluconeogenic precursors are normal and since plasma glucagon increases during development of hypoglycemia in insulinoma patients.

Adenoma, Islet Cell↗
PubMed1981

Effect of peripheral versus portal venous administration of insulin on postprandial hyperglycemia and glucose turnover in alloxan-diabetic dogs.

The effects of peripheral venous and portal venous delivery of insulin by a closed-loop insulin infusion device (Biostator GCIIS) on postprandial hyperglycemia and rates of glucose appearance, disappearance, and clearance were compared in alloxan-diabetic dogs. The amounts of insulin required and the peripheral venous plasma insulin concentrations achieved were not different for the two routes of insulin administration. No statistically significant differences in postprandial hyperglycemia or patterns of glucose disposal were observed between the two routes of insulin delivery. These studies indicate that in terms of hepatic versus extrahepatic disposal of glucose, there appears to be no practical advantage of portal venous over peripheral venous administration of insulin when a closed-loop insulin infusion device is used.

Alloxan↗
PubMed1981

Effect on hemoglobin A1 of rapid normalization of glycemia with an artificial endocrine pancreas.

Six insulin-requiring chronically hyperglycemic diabetic patients underwent glucose control for 72 hours with an artificial endocrine pancreas, the Biostator Glucose Controller. Euglycemia was within 4 hours and was maintained (110 leads to 2 mg/dl) thereafter. The concentration of hemoglobin A (HbA) was elevated, at 12.5 leads to 0.6%, at the initiation of Biostator treatment. Decreases in HbA, of 0.5 leads to 0.1% (P less than 0.01) were observed within 4 hours of Biostator therapy. Over the first 16 hours, the slope was less steep, -0.018 leads to 0.004% per hour (P less than 0.01). After 72 hours, decreases in HbA of 1.8 leads to 0.4% (P less than 0.01) were observed. The current concept of HbA as an indication of integrated glycemia over weeks and months requires modification to account for a small, rapidly reversible component. Interpretation of the value of HbA when measured by a kit method must take into consideration that small changes in HbA may occur over a few hours as a result of a large and persistent change in glycemia.

Adolescent↗
PubMed1980

Control of blood sugar in insulin-dependent diabetes: comparison of an artificial endocrine pancreas, continuous subcutaneous insulin infusion, and intensified conventional insulin therapy.

We compared the ability of closed-loop intravenous insulin infusion (i.e., an artificial "pancreas"), open-loop continuous subcutaneous insulin infusion, and intensified conventional insulin therapy (preprandial injections of regular insulin, with injection of long-acting zinc-suspension insulin before breakfast) to bring the hyperglycemia of insulin-dependent diabetic subjects to a level comparable to that of normal, nondiabetic subjects. The mean circadian levels of plasma glucose, mean amplitude of glycemic excursions, and M values (defined in Methods) did not significantly differ among the three regimens. Although these levels in the diabetic subjects approximated those in the normal subjects, the levels of plasma insulin, mean amplitude of glycemic excursions, and M values were significantly higher than those in normal subjects (P < 0.01). Therefore, at least on a short-term basis, all three regimens can produce comparable, nearly normal levels of blood sugar in such patients; moreover, closed-loop devices can be used to determine insulin requirements for conventional therapy.

Adult↗
PubMed1980

Are elevated pancreatic polypeptide levels in patients with insulinoma secondary to hypoglycaemia?

In 13 patients with insulinoma, human pancreatic polypeptide (hPP) was measured under basal conditions, after a mixed meal, and during a fast of up to 72 h. Significant negative correlatons between hPP and plasma-glucose levels were found both under basal conditions and during fasting. Patients with insulinoma and basal plasma-glucose values above 60 mg/dl had hPP values similar to those in control subjects, whereas insulinoma patients with plasma-glucose values under 60 mg/dl had significantly higher hPP values (323 versus 115 pg/ml). The mean hPP response to a mixed meal was similar in patients with insulinoma and in control subjects. hPP values during symptomatic hypoglycaemia were higher in insulinoma patients than controls fasted for comparable times (751 versus 171 pg/ml). Under conditions of euglycaemia, hPP is not a reliable marker for insulinoma.

Adenoma, Islet Cell↗
PubMed1980

Reactive hypoglycemia.

The clinical characteristics and scores on the Minnesota Multiphasic Personality Inventory (MMPI) of 192 patients undergoing a five-hour oral glucose tolerance test (OGTT) for evaluation of reactive hypoglycemia were assessed. There were twice as many women as men. One hundred twenty-nine patients had spells of light-headedness, shakiness, diaphoresis, weakness, and fatigue. Hypoglycemic symptoms occurring during the test were not related to level of plasma glucose nadir or to rate of descent of glucose level. Hypoglycemia was not found when glucose levels were measured during occurrence of spontaneous symptoms in 86 patients. MMPI scores were significantly different from those of general medical patients. Both men and women evinced a conversion V profile. The five-hour OGTT seems unreliable for the diagnosis of reactive hypoglycemia, and most patients with symptoms suggestive of hypoglycemia may have emotional disturbances.

Adolescent↗
PubMed1980

Human diabetic endoneurial sorbitol, fructose, and myo-inositol related to sural nerve morphometry.

Fascicles of the sural nerve from each of 20 diabetic patients, mostly with maturity-onset diabetes, were studied by biochemical and pathological techniques, and results were compared to values found in nerve specimens from 15 healthy persons. The sorbitol and fructose content was much more variable in diabetic than in healthy nerves. More than one-third of the diabetic nerves had sorbitol and fructose values above the highest levels for controls. myo-Inositol and scyllo-inositol content was not reduced in diabetic nerves. The sorbitol, fructose, and inositol concentrations could not be related to clinical, neurophysiological, or pathological severity of neuropathy. A comparison of scored symptoms and signs and clinical neurophysiological studies against morphometric and teased fiber studies of sural nerve demonstrated that the former three provide sensitive and reliable measures of severity of neuropathy that can be used for controlled clinical trials of diabetic neuropathy. The presence and type of teased fiber abnormalities could be related to the duration of diabetes and to symptoms of neuropathy. In untreated diabetics without symptoms of neuropathy, a higher than normal frequency of teased fibers showing segmental demyelination and remyelination was found. Untreated diabetics with symptomatic neuropathy showed two kinds of abnormalities: fibers with segmental demyelination and remyelination and fibers undergoing axonal degeneration. In treated diabetics, who often had longstanding neuropathy, the most common abnormalities were fibers undergoing axonal degeneration.

Diabetes Mellitus, Type 1↗
PubMed1980

Diagnosis of pancreatic islet hyperplasia causing hypoglycemia in a patient with portacaval anastomosis.

A patient with biopsy-proved biliary cirrhosis and previous gastrojejunostomy and portacaval anastomosis experienced episodes of severe hypoglycemia. She was found to have hyperinsulinemia and hyperglucagonemia. An oral glucose tolerance test showed postgastrectomy hypoglycemia. Results of the intravenous tolbutamide test were diagnostic for insulinoma, but results of the intravenous glucagon test and prolonged fast (96 hours) were not. Failure, on two occasions, to suppress C-peptide normally during insulin-induced hypoglycemia led to a diagnosis of pancreatogenous hyperinsulinemia. The pancreas showed a 10-fold increase in islet volume, with intensely positive staining with anti-insulin and anti-glucagon antiserums in addition to anti-somatostatin and anti-pancreatic polypeptide antiserums. Incidental findings at pancreatic exploration were a mesothelioma, which did not stain with anti-insulin antiserum, and, at autopsy one year later, a hepatoma.

Blood Chemical Analysis↗
PubMed1980

Glucose clamping using the Biostator GCIIS.

The Biostator GCIIS was used to clamp circulating glucose at hypoglycemic (42 +/- 1 mg/dl), euglycemic (86 +/- 2 mg/dl), and hyperglycemic (142 +/- 1 mg/dl) levels in normal subjects during a concomitant infusion of insulin (0.1 U/kg/h). Because of limitations in maximal glucose infusion (1 g/min) from the Biostator, a supplementary infusion of glucose was required to accomplish euglycemic and hyperglycemic clamps. The coefficients of variation of blood glucose were 7.06 +/- 1.3%, 5.9 +/- 0.5%, and 6.1 +/- 0.9 for 120 minutes of hypoglycemic, euglycemic, and hyperglycemic clamps, respectively. Despite the occasional interruption of blood flow in the double-lumen catheter and the occasional poor correlation between Biostator and reference glucose method, satisfactory glucose clamps could be maintained for 2 hours.

Adult↗
PubMed1980

Interaction of fat-stimulated gastric inhibitory polypeptide on pancreatic alpha and beta cell function.

Gastric inhibitory polypeptide (GIP) is considered to be the principal mediator of the enteroinsular axis. A glucose-insulin clamp technique was used to study the effects of differing blood glucose levels on the insulinotropic and glucagonotropic actions of fat-stimulated GIP in seven healthy subjects, as well as the effect of physiologic hyperinsulinemia on GIP secretion. Blood glucose levels were clamped for 4 h at 43+/-2 mg/dl (hypoglycemic clamp), 88+/-1 mg/dl (euglycemic clamp), and 141+/-2 mg/dl (hyperglycemic clamp) in the presence of a constant insulin infusion (100 m U/kg per h). Under hypoglycemic clamp conditions there was no increase in C-peptide nor glucagon after Lipomul ingestion, despite an increase of GIP of 51.7+/-8.7 ng/ml per 120 min. Under euglycemic clamp conditions, small and inconsistent increases in C-peptide and glucagon were observed after fat ingestion and a concomitant increase of GIP of 35.2+/-9.4 ng/ml per 120 min. Under hyperglycemic clamp conditions after fat ingestion and a GIP increase of 24.0+/-5.7 ng/ml per 120 min, C-peptide increased from 6.4+/-5 ng/ml to 11.0+/-1.1 ng/ml (P < 0.01) but glucagon did not change. These findings confirm that in healthy man GIP exerts its insulinotropic properties only under hyperglycemic conditions and indicate that GIP is not glucagonotropic. Under euglycemic clamp conditions (plasma glucose, 89+/-1 mg/dl) and physiologic hyperinsulinemia (serum immunoreactive insulin, 137+/-3 muU/ml) GIP responses to fat ingestion (39.7+/-9.8 ng/ml per 120 min) were not different from the GIP responses to fat ingestion in the absence of hyperinsulinemia (39.7+/-11.1 ng/ml per 120 min). Therefore, insulin under normoglycemic conditions does not exert an inhibitory effect on fat-stimulated GIP secretion. The higher GIP response to oral fat in the hypoglycemic clamp, and the lower GIP response in the hyperglycemic clamp compared to the response in the euglycemic clamp suggests an effect of glycemia itself on GIP secretion in the presence of hyperinsulinemia.

Adult↗
PubMed1980

Interrelationships among insulin, glucagon, and gastric inhibitory polypeptide in insulinoma.

The interrelationships of serum insulin, glucagon, and gastric inhibitory polypeptide were examined in 13 patients with insulinoma during fed and fasted states. Compared with normal subjects, patients with insulinoma had significantly lower glucose and higher insulin levels during both the fed and the fasted states. Although glucagon concentration was higher at the completion of the fast in patients with insulinoma compared with normals, no significant differences were apparent during the fed state. No difference was noted in gastric inhibitory polypeptide either during the fed state or at the termination of the fast. Under the conditions of the study, no direct suppressive effect of insulin on glucagon or gastric inhibitory polypeptide secretion was apparent. In addition, as opposed to that in normals, the insulinotropic effect of glucagon did not appear to be blunted by hypoglycemia in most of the patients. After glucagon injection, all symptomatically hypoglycemic patients experienced an amelioration of symptoms and restoration of the plasma glucose into the normal range.

Adenoma, Islet Cell↗
PubMed1980

Insulinoma.

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Adenoma, Islet Cell↗