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Biomedical subjects

F J Service

Publications and source records attributed to F J Service.

At least 37 records · Page 2Linked to original sources
PubMed1986

Neurotensin in diabetes and obesity.

Basal and postprandial concentrations of immunoreactive neurotensin were measured in insulin dependent diabetic patients and lean and obese noninsulin dependent diabetic patients when partially withdrawn from subcutaneous (s.c.) insulin treatment and again when near normoglycemia had been achieved from insulin infusion by an artificial endocrine pancreas (AEP). Neither basal nor postprandial neurotensin differed among the 3 groups of diabetic patients during s.c. insulin treatment nor from weight matched nondiabetic subjects. In addition, AEP resulted in no significant change in postprandial neurotensin responses. No differences in neurotensin levels were observed between lean and obese nondiabetic subjects. In contrast to observations in experimental diabetes, these observations do not support the presence of an abnormality of neurotensin in human diabetes.

Blood Glucose↗
PubMed1986

What is "tight control" of diabetes? Goals, limitations, and evaluation of therapy.

Complete normalization of the blood glucose concentration is the ideal goal in patients with diabetes. Because of deficiencies in therapeutic modalities for diabetes, achievement of approximation of normoglycemia is usually a satisfactory result. Generally, blood glucose ranges of 70 to 120 mg/dl preprandially and less than 160 to 180 mg/dl 90 minutes postprandially in nonpregnant patients with diabetes are considered appropriate. Diurnal variations in glycemia can be caused by the size and composition of meals, the time of day a meal is eaten, stress, and exercise. Self-monitoring of blood glucose by the patient and measurement of glycosylated hemoglobin have been useful in achieving control of diabetes.

Blood Glucose↗
PubMed1986

Benign pancreatic insulinoma: preoperative and intraoperative sonographic localization.

Twenty-nine patients with surgically proved benign pancreatic insulinoma were studied by preoperative or intraoperative sonography. Twenty-five patients had solitary pancreatic tumors; four had multiple tumors. Six of the patients with solitary insulinomas and one of the patients with multiple insulinomas had undergone previous unsuccessful exploration. Preoperative sonography was performed in 24 patients with solitary insulinomas, and 15 (63%) were localized. Intraoperative sonography was performed in 22 patients with solitary insulinomas, and 19 (86%) were visualized without having been previously located by palpation. Four of these visible solitary tumors (18%) were not detected by palpation at surgery. All the solitary insulinomas were detected with the combination of palpation and intraoperative sonography. In each of the six patients with solitary insulinoma who had undergone previous surgery, the tumor was visible with intraoperative sonography, which also demonstrated nonpalpable insulinomas in two of the four patients with multiple tumors. Preoperative real-time sonography is a sensitive, noninvasive, inexpensive method for localization of insulinoma. Intraoperative high-frequency sonography is a highly sensitive method for the detection of insulinoma. Intraoperative sonography is also valuable to determine the relationship of the insulinoma to pancreatic and bile ducts and thereby facilitate safe enucleation.

Adenoma, Islet Cell↗
PubMed1985

Diabetic neuropathy.

The incidence and prevalence of diabetic neuropathies in Insulin Dependent (IDDM) and Non-Insulin Dependent (NIDDM) Diabetes Mellitus is not known because in previous studies the heterogeneity of diabetes and of the neuropathies was not taken into account, criteria for diagnosis and surveillance for neuropathy were variable, and studies were not prospective or population based. We have begun such prospective epidemiologic studies using a uniform algorithm for the classification of the diabetic disorders and uniform and validated approaches for the assessment of symptoms, neurologic deficits and various quantitative end-points of neural dysfunction. As regards cause, a key question which we are trying to answer is whether hyperglycemia and associated metabolic alterations affect neural tissue directly or whether there is an intervening tissue alteration between metabolic derangement and tissue change. Improved control of hyperglycemia does not appear to be associated with rapid neurologic improvement, possibly arguing for an intervening tissue alteration. The recently observed decrease in nerve oxygen tension and blood flow in streptozotocin diabetes suggests that an alteration of the nerve microenvironment may relate importantly to the cause of diabetic neuropathy.

Diabetes Mellitus, Type 1↗
PubMed1985

Near normoglycaemia improved nerve conduction and vibration sensation in diabetic neuropathy.

Twelve C-peptide deficient Type 1 (insulin-dependent) diabetic patients with abnormal peripheral nerve function were randomly assigned to continuation of conventional insulin therapy (CIT) or to continuous subcutaneous insulin infusion (CSII). There were no statistically significant differences at entry to the study between the two treatment groups in nerve function assessed by neurologic disability score, computer assisted sensation examination and measurements of amplitudes, distal latencies, F-wave latencies and somatosensory evoked potential latencies over the spine and conduction velocities of motor and sensory fibers of ulnar, median, peroneal, tibial, plantar and sural nerves. In addition, mean plasma glucose from 24 h profiles (12.5 vs 10.6 mmol/l, respectively) and HbA1 (11.0 vs 11.6%, respectively) did not differ significantly between the two treatment groups at entry. Despite improved glycaemia from CSII in 5 patients (one dropped out of the study after 2 months) contrasted to CIT in 6 patients (5.3 vs 9.9 mmol/l, respectively, p = 0.002) and HbA1 (8.5 vs 10.7%, respectively, p = 0.002), there were no significant differences in measurements of peripheral nerve function after 4 months. After 8 months of improved glycaemia (4.4 vs 10.2 mmol/l, p = 0.004) and improved HbA1 (8.3 vs 10.5%, p = 0.002), nerve conduction (p = 0.03) and vibratory sensation threshold (p = 0.002) were significantly better in patients treated with CSII than those who received CIT. The improvements in nerve function, although small, provide further evidence that some clinical endpoints of neuropathy are favorably influenced by improved control of glycaemia.

Adolescent↗
PubMed1985

Clinical and neuropathological criteria for the diagnosis and staging of diabetic polyneuropathy.

Scored symptoms, neurological deficits, detection threshold of cutaneous sensation and parameters of nerve conduction were compared with quantitated neuropathological abnormalities in the sural nerve in 47 healthy subjects and 36 diabetic patients, 32 with and 4 without neuropathy. The fifth percentile line of a new Index of Pathology, which combines loss of myelinated fibres and abnormality of the remaining fibres, was found to provide a sensitive and reliable minimum neuropathological criterion for the diagnosis of polyneuropathy. Abnormality, as assessed by two clinical evaluations, similarly separated healthy subjects and diabetic patients into those with and without neuropathy. For the detection of diabetic polyneuropathy, vibration sense was more sensitive than touch-pressure or thermal cooling. Abnormalities of nerve conduction were found to be both sensitive and reliable in the detection of polyneuropathy. Velocity was most frequently abnormal, but only slightly more often than F wave latency and amplitude. We conclude that abnormality, as judged independently from two different types of evaluation, provides a sensitive and reliable minimal criterion for the diagnosis of neuropathy. Although symptoms, neurological deficits and abnormalities of nerve conduction are statistically associated, they should be evaluated separately to provide adequate characterization.

Adolescent↗
PubMed1985

Observations on control of glycemia with conventional insulin therapy or continuous subcutaneous insulin infusion.

Determination of glycemic differences between groups treated with continuous subcutaneous insulin infusion (CSII) or conventional insulin therapy (CIT) was central to the major objective of the study. Assessment of glycemia was based on 24-h inhospital profiles of plasma glucose; pre- and postprandial and bedtime (seven time points) diurnal profiles performed monthly on outpatient samples; and glycosylated hemoglobin (HbA1) measured bimonthly at each center. The correlation between plasma glucose determinations in the central laboratory and in local laboratories was 0.988. Significance of differences between treatments was by analysis of variance and least-squares regression. At baseline, mean inhospital plasma glucose and HbA1 concentrations and insulin dosages were identical in the groups randomized to CSII or CIT. A prompt decrement of indices of glycemic control during CSII was observed such that mean decrements sustained over the 8-mo treatment period in home and in hospital plasma glucose profiles and HbA1 relative to values obtained during CIT (P less than 0.0001). The likelihood of CSII-treated patients achieving glycemic indices within the normal range was increased. The standardization of the mean and the M-value calculated from inhospital glucose profiles during CSII and CIT at 4 and 8 mo indicated that there was less plasma glucose fluctuation during CSII. The method of pooling standardized local HbA1 measurements from the six centers appeared to be an adequate substitute for centrally performed HbA1 determinations. Advantages of inhospital plasma glucose measurements in terms of accuracy and ability to obtain nocturnal samples contrasted with the likelihood of increased realism and superior correlation with HbA1 in home-obtained samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1985

Conference on insulin pump therapy in diabetes. Multicenter study of effect on microvascular disease. The pump life. Patient responses and clinical and technological problems.

As part of a randomized, prospective trial in subjects with insulin-dependent diabetes assigned to either continuous subcutaneous insulin infusion (CSII) or to their unchanged conventional insulin treatment (CIT) for 8 mo, patients completed questionnaires dealing with general responses and clinical and technological problems. Although there was no significant difference between treatment groups with respect to the number of patients experiencing severe hypoglycemia (i.e., requiring intravenous glucose or intramuscular glucagon injection), there were nine episodes in six patients during CSII compared with one episode during CIT. Diabetic ketoacidosis occurred significantly more often in the CSII group (nine episodes in eight patients) than in the CIT group (no episodes). A number of CSII-related failures occurred, including omission of premeal bolus, needle dislodgement, pump accidentally turned off, and leakage at the infusion site. At 8 mo, 85% of CSII-treated patients wished to continue indefinitely on the pump, and almost all would continue with self-monitoring of blood glucose even if they stopped CSII.

Canada↗
PubMed1984

Abnormal meal carbohydrate disposition in insulin-dependent diabetes. Relative contributions of endogenous glucose production and initial splanchnic uptake and effect of intensive insulin therapy.

Postprandial hyperglycemia in insulin-deficient, insulin-dependent diabetic subjects may result from impaired suppression of endogenous glucose production and/or abnormal disposition of meal-derived glucose. To investigate the relative contributions of these processes and to determine whether 2 wk of near normoglycemia achieved by using intensive insulin therapy could restore the pattern of glucose disposal to normal, meal-related and endogenous rates of glucose appearance were measured isotopically after ingestion of a mixed meal that contained deuterated glucose in seven lean insulin-dependent and five lean nondiabetic subjects. Diabetic subjects were studied once when insulin deficient and again during intensive insulin therapy after 2 wk of near normoglycemia. Total glucose production was determined by using tritiated glucose and the contribution of meal-related glucose was determined by using the plasma enrichment of deuterated glucose. The elevated basal and peak postprandial plasma glucose concentrations (252 +/- 33 and 452 +/- 31 mg/dl) of diabetic subjects when insulin deficient were decreased by intensive insulin therapy to values (82 +/- 6 and 193 +/- 10 mg/dl, P less than 0.01) that approximated those of nondiabetic subjects (93 +/- 3 and 140 +/- 15 mg/dl, respectively). Total and endogenous rates of glucose appearance (3,091 +/- 523 and 1,814 +/- 474 mg/kg per 8 h) in the diabetic subjects were significantly (P less than 0.02) greater than those in non-diabetic subjects (1,718 +/- 34 and 620 +/- 98 mg/kg per 8 h, respectively), whereas meal-derived rates of glucose appearance did not differ. Intensive insulin therapy decreased (P less than 0.01) both total (1,581 +/- 98 mg/kg per 8 h) and endogenous (478 +/- 67 mg/kg per 8 h) glucose appearance to rates that approximated those observed in the nondiabetic subjects, but did not alter meal-related glucose appearance. Thus, excessive entry of glucose into the peripheral circulation in insulin-deficient diabetic patients after ingestion of a mixed meal resulted from a lack of appropriate suppression of endogenous glucose production rather than impairment of initial splanchnic glucose uptake. Intensive insulin therapy restored postprandial suppression of endogenous glucose production to rates observed in nondiabetic subjects.

Adult↗
PubMed1984

Gastric inhibitory polypeptide in obesity and diabetes mellitus.

Gastric inhibitory polypeptide (GIP) concentrations may be influenced by obesity, diabetes, and glucagon deficiency and be under feedback inhibition by insulin. To assess these factors, insulin-dependent diabetic, totally pancreatectomized diabetic, and lean and obese noninsulin-dependent diabetic patients were studied twice, once during partial insulin withdrawal and again when euglycemia was achieved before and after mixed meal ingestion, using an artificial endocrine pancreas. The results were compared to those from weight-matched lean and obese nondiabetic subjects. No significant differences in postprandial GIP responses were found between lean and obese nondiabetic subjects. Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. In contrast, lean and obese noninsulin-dependent diabetic patients had reduced GIP responses compared to weight-matched nondiabetic subjects (mean +/- SE, 37.9 +/- 5.4 vs. 67.1 +/- 10.8 ng ml-1 240 min-1, respectively; P less than 0.05). This difference was entirely due to the reduced GIP responses in obese noninsulin-dependent diabetic patients compared to those in obese nondiabetic subjects (32.1 +/- 7.9 vs. 76.9 +/- 18.2 ng ml-1 240 min-1, respectively; P less than 0.05); the postprandial GIP responses were not significantly different between lean noninsulin-dependent diabetic patients and lean nondiabetic subjects. Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes.

Adult↗
PubMed1983

Effects of size, time of day and sequence of meal ingestion on carbohydrate tolerance in normal subjects.

The effects of size, time of day and sequence of meal ingestion were determined in healthy subjects using a Latin square design. Plasma glucose, insulin and gastric inhibitory polypeptide, but not glucagon, were correlated with meal size. Plasma glucose, but not insulin, gastric inhibitory polypeptide or glucagon, were greater later in the day. The progressive decline in carbohydrate tolerance from 08.00 to 18.00 h was associated with impaired insulin secretion estimated by C-peptide, and with impaired insulin action.

Adult↗
PubMed1983

Effect of graded intraduodenal glucose infusions on the release and physiological action of gastric inhibitory polypeptide.

Gastric inhibitory polypeptide (GIP) is the leading candidate for gut hormonal augmentation of insulin release. The release of its subspecies (mol wt, 5000 and 7500) and the physiological action of total immunoreactive GIP (IR-GIP) were investigated during isotonic glucose infusions at 75, 225, and 465 mg/min in nine volunteers. Each dose was infused intraduodenally and iv in the same volunteer. Intestinal augmentation of insulin release occurred during the high dose intraduodenal glucose infusion (P less than 0.001) but not during the lower doses. An elevation of 17-20 mg/dl in plasma glucose was required before this insulinotropic effect occurred (P less than 0.001). At increments of plasma glucose above 17 mg/dl, the augmentation of gut-mediated insulin release was dependent on the degree of hyperglycemia (r = 0.81; P less than 0.01). At each dose of intraduodenally administered glucose, IR-GIP was elevated within 20-40 min (P less than 0.01), remaining at a steady level until the infusion was stopped. The release of IR-GIP was elevated within 20-40 min (P less than 0.01), remaining at a steady level until the infusion was stopped. The release of IR-GIP was proportional to the intestinal glucose load but was unchanged from the basal level during iv glucose studies. The attained IR-GIP levels remained constant in each study despite large variations over time in plasma glucose and insulin concentrations. During intestinal glucose infusion, 58.7 +/- 4.1% of IR-GIP was accounted for by the 5000 mol wt subspecies and 17.3 +/- 3.5% was accounted for by the 7500 mol wt subspecies, with the remaining immunoreactivity found in the void volume of a Sephadex G-50 column. Relative proportions remained constant throughout the 4-h study. Thus, during glucose stimulation, the total IR-GIP released 1) is proportional to the absorbable luminal stimulus, 2) is independent of ambient plasma insulin and glucose levels, 3) is composed predominantly of the 5000 mol wt form, and 4) requires an elevation in plasma glucose of 17-20 mg/dl before it augments insulin release, but then stimulates insulin release in a fashion linearly dependent upon the increment in plasma glucose.

Adult↗
PubMed1983

Prandial insulin requirements in insulin-dependent diabetics: effects of size, time of day, and sequence of meals.

To assess the effects of size, time of day, and sequence of meals on insulin requirements determined by an artificial endocrine pancreas, eight insulin-dependent diabetics ate meals of 12.5%, 25%, and 50% of total calories (30 Kcal/kg) at 0800, 1300, and 1800 on each of 3 separate days in a randomized order in one of two sequences in a three by three Latin square design. Plasma glucose and free insulin concentrations and amounts of insulin infused by the artificial endocrine pancreas were associated with meal size (P less than 0.001) but not with time of day of meal ingestion (analysis of variance). The sequence of meal ingestion did not alter integrated plasma glucose responses, but did influence the meal-related amounts of insulin infused. Thus, consideration should be given to meal size and sequence of meal ingestion but not time of day of meal ingestion when determining prandial iv insulin requirements.

Adult↗
PubMed1983

Effect of blood glucose control on peripheral nerve function in diabetic patients.

A prospective, stratified, randomized 3-year clinical trial was conducted on the effect of rigorous versus conventional glucose control on peripheral nerve function in 33 insulin-treated diabetic patients with a duration of diabetes of less than 2 years. The goals for conventional glucose control were the mean of fasting and 80-minute postprandial plasma glucose of 150 mg/dl for non-insulin-dependent diabetes and 200 mg/dl for insulin-dependent diabetes. The goal of rigorous glucose control was an approximation of nondiabetic glucose control. No significant difference in glucose control or peripheral nerve function was observed between the rigorously and the conventionally controlled groups. Eight patients in the conventional-control group spontaneously achieved glucose control in the range that was the objective for the rigorous-control group, and five patients in the rigorous-control group never achieved the desired glucose control. In the remaining 20 patients, with similar baseline glucose control and peripheral nerve function characteristics, observed over a median of 2 years, improved blood glucose control (P less than 0.01) was not associated with any significant improvement in peripheral nerve function. Nevertheless, a significant (P less than 0.05) correlation was found between the degree of abnormal nerve function at entry into the study and change in nerve function during the study. If control of hyperglycemia benefits peripheral nerve function of diabetic patients, its demonstration may require a closer approximation of normoglycemia, a larger difference in glucose control between the two study groups, a longer duration of treatment, and the use of patients with more advanced peripheral nerve function abnormalities than those in this study.

Adult↗
PubMed1983

Oral glucose tolerance test compared with a mixed meal in the diagnosis of reactive hypoglycemia. A caveat on stimulation.

Reactive hypoglycemia is being diagnosed with increasing frequency. We compared plasma glucose, insulin, glucagon, epinephrine, and norepinephrine responses to an oral glucose tolerance test and to a mixed meal containing equivalent carbohydrate in 33 patients who had been referred to our institution with a presumed diagnosis of reactive hypoglycemia and in 2 patients who had insulinomas. In addition, a control group of 36 normal volunteers underwent the meal study. During the meal studies, electroencephalograms were obtained. Despite provocation of hypoglycemia by the oral glucose tolerance test, no consistent relationship between hypoglycemia and symptoms was observed. Despite similar symptoms, hypoglycemia did not develop after the meal test in the 33 patients without insulinomas. Both patients with insulinoma became hypoglycemic after ingestion of the meal. When a physiologic stimulus such as a meal is used to duplicate the daily dietary experience of patients, reactive hypoglycemia in the absence of a pancreatic pathologic lesion is an uncommon occurrence.

Adolescent↗
PubMed1982

Subcutaneous versus intraperitoneal administration of insulin on post-prandial hyperglycaemia and glucose turnover in alloxan diabetic dogs.

The effects of subcutaneous and intraperitoneal insulin delivery by a closed-loop insulin infusion device on post-prandial hyperglycaemia and rates of glucose appearance and disappearance were compared in alloxan diabetic dogs. No differences in basal or post-prandial values or patterns of response were observed between the two routes of insulin delivery. In addition, the amounts of insulin infused and the plasma insulin concentrations achieved were not different for the two routes of insulin administration. These studies demonstrate that in the dog there appears to be no difference in the pattern of disposal of glucose from a mixed meal when insulin was administered intraperitoneally or subcutaneously at the rates of insulin infusion used in these experiments.

Alloxan↗