bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quality, Efficiency, and Cost of a Physician-Assistant-Protocol System for Managment of Diabetes and Hypertension
Authors: Komaroff Anthony L , Flatley Margare , Browne Christina , Sherman Herbert , Fineberg S Edwin , Knopp Robert H 
Published: September 2013

Briefly trained physicians assistants using protocols (clinical algorithms) for diabetes, hypertension, and related chronic arteriosclerotic and hypertensive heart disease abstrated information from the medical record and obtained history and physical examination data on every patient-visit to a city hospital chronic disease clinic over a 18-month period. The care rendered by the protocol system was compared with care rendered by a “traditional” system in the same clinic in which physicians delegated few clinical tasks.
Increased thoroughness in collecting clinical data in the protocol system led to an increase in the recognition of new pathology. Outcome criteria reflected equivalent quality of care in both groups. Efficiency time-motion studies demonstrated a 20 per cent saving in physician time with the protocol system. Coct estimates, based on the time spent with patients by various providers and on the laboratory-test-ordering patterns, demonstrated equivalent costs of the two systems, given optimal staffing patterns. Laboratory tests were a major element of the cost of patient care,and the clinical yield per unit cost of different tests varied widely.
Suppression and Stimulation Mechanisms Controlling Glucagon Secretion in a Case of Islet-Cell Tumor Producing Glucagon, Insulin, and Gastrin
Authors: Tiengo Antonio , Fedele Domenico , Marchiori Elisa , Nosadini Romano , Muggeo Michele 
Published: September 2013

The mechanisms controlling secretion of glucagon and other pancreatic hormones were studied in a patient affected with multihormone-secreting islet-cell tumor.
Fasting glucagon levels (3,000 pg./ml.) rose to 10 ng./ml. following arginine stimulation. While oral glucose load and intravenous glucose infusion did not suppress glucagon secretion, insulin administration induced a prompt depression in glucagon levels. Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase.
It is suggested that only some of the stimulation-inhibition mechanisms were conserved in this case of glucagon-secreting pancreatic tumor.
Evaluation of a ‘True’ Fractional Removal Rate of Glucose in Man by Bolus and Simulated-ramp Increase of Glucose
Authors: Rosenqvist Urban , Ličko Vojtech , Karam John H 
Published: September 2013

An infusion method designed to produce a gradual ramplike rise in plasma glucose levels in man showed that the observed slope of the ramp was not significantly different from the calculated slope only when both of the following parameters were used:
1. When the glucose disappearance rate coefficient (k) was calculated by an incremental method in which the fasting plasma glucose level was subtracted from each plasma glucose value obtained during a standard rapid intravenous glucose tolerance test. This proved to be superior to a contrasting method in which absolute glucose values are used for the semilogarithmic plot of glucose concentration versus time.
2. When the dilution technic was used to estimate directly the volume distribution of glucose rather than relying on standard reference tables that predict glucose distribution space in man.
By using these two parameters obtained during standard intravenous glucose tolerance testing, we have shown that it is possible to calculate the rate of glucose infusion required to achieve successfully in man a ramp of plasma glucose of any desired steepness and to characterize the consequent insulin secretion. This simulated ramp increase of glucose provides a potentially useful tool for investigation of the dynamics of islet-cell function in man.
Insulin Response to Oral Glucose in Patients with a Previous Myocardial Infarction and in Patients with Peripheral Vascular Disease: Hyperinsulinism and Its Relationships to Hypertriglyceridemia and Overweight
Authors: Sorge Franco , Schwartzkopff Wolfgang , Neuhaus Günter A 
Published: September 2013

The insulin response to an oral glucose load (100 gm.) in 127 patients with a previous myocardial infarction (MI) (six months to one year) and in 65 patients with surgically treated or arteriographically identified peripheral vascular disease (PVD) was compared with that of 89 controls after matching the three collectives for age, glucose tolerance, and per cent ideal body weight (% IBW). The insulin response was of greater magnitude in MI and PVD groups than in respective control groups also in the absence of hyperglycemia, hypertriglyceridemia, and obesity. This finding suggests that hyperinsulinism may represent an early metabolic alteration associated with the development of MI and PVD. The insulin secretion pattern was prevalently of the delayed type in association with impaired glucose tolerance and with hypertriglyceridemia but not with overweight.
Correlations between serum insulin, triglyceride (TG) levels, and % IBW were also investigated. We found a strong correlation (p &lt; 0.001) between stimulated insulin levels and % IBW in MI patients and none in PVD patients; conversely, the correlation between serum insulin and TG levels was very high (p &lt; 0.001) in PVD patients and only weak (p &lt; 0.05) in MI patients. No correlation was found between cholesterol (CH) levels and any of the other parameters studied. According to these results, it seems likely that hyperinsulinism plays a major role as a closely associated factor to obesity in those subjects who develop an MI, whereas in PVD patients the raised insulin levels may favor lipid accumulation in the arterial intima and accelerate the progress of atherosclerosis.
Studies on Streptozotocin Diabetes
Authors: Ganda Om P , Rossini Aldo A , Like Arthur A 
Published: September 2013

Both alloxan and streptozotocin produce β-cell necrosis in the rat. Previous studies have shown protection against alloxan toxicity by D-glucose, D-mannose, and the nonmetabolized analogue 3-0-methyl-D-glucose and removal of this protective effect by D-mannoheptulose. The effect of several agents (i.v. infusion) against the β-cell toxic effect of streptozotocin (60 mg./kg. i.v. in 24-hour-fasted 200-gm. male rats) was studied. Protection was determined by plasma glucose concentrations 24 and 48 hours later and, in certain experiments, by histologic examination of the islets.
D-glucose and D-mannose provided no protection. Similarly, D-galactose, D-fructose, α-methyl-D-glucoside, D-L-glyceraldehyde, D-xylose, and D-glucosamine had no effect. However, 3-0-methyl-D-glucose administered immediately before streptozotocin resulted in progressive inhibition of β-cell toxicity with complete protection at 0.83 mMoles per rat. The protective effect of 3-0-methyl-D-glucose was not altered by mannoheptulose. 2-Deoxy-D-glucose, which has no effect against alloxan, provided nearly complete protection against streptozotocin at 2.2 mMoles per rat. The effects of 3-0-methyl-D-glucose and 2-deoxy-D-glucose were additive and were not altered by glucose. Furthermore, the 3-0-methyl-D-glucose as well as 2-deoxy-D-glucose protective effects were still present, albeit attenuated, when these agents were given following the administration of streptozotocin. This is in contrast to alloxan, against which 3-0-methyl-D-glucose provides protection only when given before alloxan.
3-0-Methyl-D-glucose is the only carbohydrate protective against both streptozotocin and alloxan in the rat. However, several silent differences seem to exist between the mechanisms of beta-cytotoxic effects of these two diabetogenic compounds.
Immunopathology of Renal Extracellular Membranes in Kidneys Transplanted into Patients with Diabetes Mellitus
Authors: Mauer S Michael , Miller Kenneth , Goetz Frederick C , Barbosa Jose , Simmons Richard L , Najarian John S , Michael Alfred F 
Published: September 2013

Kidneys of patients with severe diabetic nephropathy demonstrate marked linear immunofluorescent staining of extracellular membranes, including the tubular and glomerular basement membranes (TBM and GBM) and Bowman's capsule. Immunofluorescent studies were carried out on kidney tissue obtained from 12 diabetic and 17 nondiabetic patients from two to 12 years following renal transplantation. The frequency and intensity of IgG and albumin staining of these membranes were significantly greater in the diabetic than in the nondiabetic patients (P &lt;0.0005). TBM, GBM, and Bowman's capsule staining did not occur in any of the seven kidneys studied at the time of their transplantation into diabetic recipients.
Thus, the abnormalities leading to the deposition or trapping of proteins in renal extracellular membranes occur early after the placement of normal kidneys into the abnormal metabolic environment of the diabetic transplant recipient. The present study supports the concept that basement membrane alterations in diabetes are a consequence of the biochemical perturbations of diabetes rather than a separately inherited genetically linked disorder.
Glucose and 3-0-Methylglucose Protection Against Alloxan Poisoning of Pancreatic Alpha and Beta Cells
Authors: Pagliara Anthony S , Stillings Susan N , Zawalich Walter S , Williams Ann D , Matschinsky Franz M 
Published: September 2013

Alloxan infused into the isolated perfused rat pancreas caused transient insulin secretion and permanent suppression of amino-acid-stimulated glucagon release. Alloxan poisoning also prevented subsequent induction of glucose-mediated insulin release and also prevented the inhibition of glucagon release by glucose. Glucose or 3-0-methylglucose infused simultaneously with alloxan protected the α-and β-cell, allowing subsequent glucose inhibition of glucagon secretion and stimulation of insulin release. The above alloxan effects were dose-related, the α-cell being one fourth as sensitive to alloxan as the β-cell.
The data indicate-that (1) alloxan and glucose suppression of amino-acid-stimulated glucagon secretion is independent of concomitant insulin secretion; (2) alloxan, like glucose, affects α-and β-cells directly, stimulating the β-cell and inhibiting the α-cell; and (3) alloxan acts on a glucoreceptor system with comparable physicochemlcal characteristics common to both cell types.
Insulin Antibodies and Clinical Complications in Diabetics Treated for Five Years with Lente or Sulfated Insulin
Authors: Little J A , Lee R , Sebriakova M , Csima A 
Published: September 2013

The antigenlcity of two types of insulin and their effect on diabetic control and complications were studied for 66 months in two groups of diabetics not treated previously with insulin. The groups were similar in age, weight, duration of the disease, and other biochemical and clinical findings. None of the patients developed brittle diabetes or became insulin-resistant, and both groups were controlled initially on an average of 30 U. of insulin daily. Plasma insulin antibodies and their avidities were measured by a modification of the insulin radioimmunoassay. Sulfated insulin was found to be less antigenic than lente throughout the treatment (p &lt; 0.001). In the sulfated group the antibody index averaged 22 μU/ml. over the five years and did not change significantly with time. In the lente group there was a peak at six months of 2,161 μU./ml. and then a gradual and significant decrease to 88 μU./rnl. at 66 months.
The avidity of the antibodies in the sulfated group was initially higher than in the lente group (2.491 vs. 1.972, p &lt; 0.001). In the sulfated group it did not change with time, whereas in the lente group the avidity increased with time and became similar to that in the sulfated group. In both groups there was a significant negative correlation between antibody index and avidity throughout the study, ranging from −0.510 to −0.927 (p &lt; 0.05 to &lt; 0.001). In the sulfated group the insulin dose decreased with time (b = −2.56, p &lt; 0.001), whereas in the lente group it tended to increase. The incidence of local skin reactions at the injection sites was lower throughout the study in the sulfated group (p &lt; 0.01). Low levels of insulin autoantibodies (0.03 to 4 μU./ml.) were found in 4 per cent of untreated diabetics and in 6 per cent of normal subjects (0.46 to 0.52 μU./ml.).
The Regulation of Plasma Ketone Body Concentration by Counterregulatory Hormones in Man I. Effects of Norepinephrine in Diabetic Man
Authors: Schade David S , Eaton R Philip 
Published: September 2013

Previous studies have attributed norepinephrine's ketogenic activity to its ability to mobilize peripheral fat stores. This study was designed to determine whether norepinephrine has ketogenic activity independent of its lipolytic effect in diabetic man.
Six insulin-dependent diabetic subjects were infused with pathophysiologic concentrations of norepinephrine (0.08 μg./kg./ min.). As a control for norepinephrine's lipolytic effect, a separate heparin-induced free fatty acid generation study was performed on each subject. The results demonstrate, for the first time in man, that norepinephrine has ketogenic activity independent of its lipolytic effect. Furthermore; physiologic elevations of norepinephrine concentration were also demonstrated to increase plasma glucagon concentration. Our data are consistent with the possibility that the rise in concentration of glucagon may have a participated in the catecholamine-augmented ketogenesis.
Plasma Androgen Concentrations in Diabetic Women
Authors: Szpunar Walter E , Blair A James , McCann Daisy S 
Published: September 2013

Plasma androgen levels were determined in women assigned to the following groups: idlopathically hirsute, diabetic, both idiopathkally hirsute and diabetic, and normal. The androgens examined were androstenedione (AD), dihydrotestosterone (DHT), testosterone (T), and dehydroepiandrosterone (DHEA). We And statistical differences between young (&lt;38 years) and older (≥38 years) controls at confidence levels of p≤ 0.01 for AD, DHT, and T and of p≤ 0.05 for DHEA. The results indicate that peak circulating androgen levels occur prior to age 30-35 years for women. There are no significant differences between the young controls and young idiopathkally hirsute subjects, but a statistical difference exists between older hirsute and older controls for all four androgens (p≤ 0.05).
When a comparison is made among the diabetic, hirsute dia-betk, and older control groups (all groups ≥38 years), the diabetic group is significantly higher than the control in plasma AD (p≤ 0.01) and DHEA (p≤ 0.05). These same two steroids are also higher in the diabetk group than in the hirsute diabetic group (p≤ 0.05), while the latter differs from controls only in testosterone levels (p≤ 0.05). DHT levels are similar for all three groups.
Rapid Conversion by Insulin of Hepatic Intermediary Metabolism from Glucose Production to Glucose Utilization in the Liver of Alloxan-diabetic Rats
Authors: Seitz H J , Müller M J , Krone W , Tarnowski W 
Published: September 2013

The concentration of free fatty adds in the blood, the tissue concentrations of hepatic cyclic AMP, long-chain acyl-CoA (LCA), adenine nucleo tides, inorganic phosphate, the intermediates of the Embden-Meyerhof pathway and the citric acid cycle (including acetyl-CoA and free CoA), and the cytoplasmic and mitochondrial redox couples were determined in alloxan-diabetic rats 15, 30, 60, and 90 minutes after insulin injection. From the meared values, the energy state of the adenine nucleotide system in the liver, the redox state of the NAD system, and the concentrations of malate, oxaloacetate, citrate, and α-ketoglutarate were estimated for the cytoplasmic and mitochondrial compartment by the use of established calculation methods.
Insulin injection into alloxan-diabetic rats caused a rapid decline in the concentration of serum free fatty acids and a coordinate decline in hepatic LCA concentration. The latter alteration was accompanied by an increase in the cytoplasmic and a synchronous decrease in the mitochondrial ATP/ADP×P ratio. Simultaneously, the redox state of the cytoplasmic NAD system was shifted towards the oxidized state. When the appropriate data were plotted against each other, a highly significant correlation between the concentration of free fatty acids in the blood and that of LCA in the liver, between the hepatic LCA concentration and the cytoplasmic energy state, and between the cytoplasmic energy state and the cytoplasmic redox state was obtained. These findings are interpreted to support the hypothesis derived from in-vitro experiments that insulin, because of the concentration of hepatic LCA, might affect the translocation of adenine nucleotides between the cytoplasmic and the mitochondrial compartment, thereby regulating the cytoplasmic energy state and, consequently, the redox state of the cytoplasmic NAD system.
Insulin injection into alloxan-diabetic rats provoked rapid, coordinate changes in the concentration of the intermediates of both the citric acid cycle and the Embden-Meyerhof chain, indicating the altered substrate flow through these pathways. Thosemetabolit s known to modulate the activity of key regulatory enzymes in vitro were analyzed with respect to their proposed regulatory function. As to the insulin-induced shift from pyruvate carboxylatlon to pyruvate decarboxylatIon, the data reveal that the decrease in pyruvate carboxylase activity can be attributed to the decrease in the intramitochondrial ATP/ADP ratio and the simultaneous fall in acetyl-CoA concentration, while the coordinate increase in pyruvate dehydrogenase activity can be ascribed to the decline in the concentration of LCA and, consequently, in the ratios of ATP/ADP, NADH/NAD, and acetyl-CoA/CoA within the mitochondria.
Cholinergic Blockade in Reactive Hypoglycemia
Authors: Permutt M Alan , Keller David , Santiago Julio 
Published: September 2013

The effects of cholinergic blockade on the plasma glucose and insulin responses during oral and intravenous glucose administration were studied. Propantheline (30 mg.) was given by mouth 45 minutes before standard glucose tolerance testing to produce symptomatic cholinergic blockade. In 10 normal subjects a flattening of the over-all plasma glucose response to oral glucose was observed compared with the control test, whereas insulin secretion was not different. In seven patients with repeated episodes of symptomatic reactive hypoglycemia, cholinergic blockade eliminated both symptomatic and chemical hypoglycemia in each, raising the mean nadir glucose from 44 ± 4 mg./dl. to 84 ± 8 mg./dl. (p&lt;0.01) and significantly reducing insulin secretion. In contrast, following intravenous glucose challenge, cholinergic blockade produced no significant difference in the rate of glucose utilization or insulin secretion in either group.
These results are compatible with the hypothesis that excessive vagal stimulation may contribute to the hypoglycemia seen in patients with reactive hypoglycemia but suggest that the predominant effect is on the gastrointestinal tract rather than on pancreatic islets directly. These studies confirm that anticholinergic drugs may be useful adjuvants in treating these patients.
Blood Glucose, Insulin, and Free Fatty Acid Levels During Oral Glucose Tolerance Tests in 158 Obese Children
Authors: Deschamps I , Giron B J , Lestradet H 
Published: September 2013

In 158 obese children, aged from three months to 15 years, blood glucose, immunoreactive insulin, and free fatty acid levels were measured during a standard oral glucose tolerance test carried out prior to treatment. The results were analyzed for the total sample as well as for three age groups: 0–5 years, 6–10 years, and 11–15 years and compared with those of 70 normal-weight children matched for age and sex.
Glucose tolerance is normal in the obese children. It is different from the controls only two hours after glucose loading, when a slight but significant elevation is found. The glucose levels at one and two hours are significantly higher in the obese children of group III than in the younger ones.
Fasting F.F.A. levels are similar in normal and obese children, but the F.F.A. decrease following glucose absorption is significantly diminished in the obese. The F.F.A. levels of the youngest obese are significantly higher than those of the older ones.
A constant and important hyperinsulinism, fasting and postabsorptive, is demonstrated in obese children of all ages, even before five years and at the beginning of obesity. Age- and sex-related differences in insulin secretion are much more marked in the obese than in normal children. The degree of hyperinsulinemia is related to the degree of obesity, but not to its duration.
The results suggest that hyperinsulinism is associated with obesity from its onset rather than being a long-term consequence of overweight. However, the origin of hyperinsulinism in obesity and the mechanism of insulin resistance still remain obscure.
Relation of Fasting Plasma Glucose Concentration to Plasma Insulin and Glucagon Concentrations: Studies in Latent Diabetics and Women Who Have Produced Large-for-dates Babies
Authors: Turner R C , Harris E , Bloom S R , Uren C 
Published: September 2013

Mothers who have had gestational diabetes (latent diabetics—LD), as well as those who have produced a large-for-dates baby (LFD) but who were not known to have been diabetic, have raised fasting plasma glucose levels, and these may induce fetal overnutrition. The increased birth weight of babies of obese mothers may also be due to their raised fasting plasma glucose levels.
LD and LFD have normal or raised fasting plasma insulin levels even though they have both decreased insulin secretion to small changes in plasma glucose and normal or increased insulin sensitivity. The high fasting plasma glucose probably results from the decreased insulin-secretory response to glucose. Normal subjects have little day-to-day variation of their fasting plasma glucose, whereas subjects with a high fasting plasma glucose have less precise control.
Although LD and LFD had abnormal insulin responses, they have normal plasma glucagon concentrations that do not correlate with glucose tolerance or insulin sensitivity. The reported abnormalities of glucagon in diabetes are probably a secondary, not a primary, event.