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Biomedical subjects

R Prager

Publications and source records attributed to R Prager.

At least 109 records · Page 6Linked to original sources
PubMed1990

[Diurnal variations of fructosamine in patients with type II diabetes mellitus].

During the last years fructosamine has been presented as a measurement of diabetic long term control, particularly a shorter half life of fructosamine was seen as an advantage over HbAlc (half life of fructosamine: 16 days, half life of HbAlc: 28 days). Due to diurnal variations of fructosamine levels especially in dependence of variations of the albumin-and protein concentrations the interpretation of this parameter was somewhat limited. Recently a new colorimetric fructosamine-assay was developed. We investigated the diurnal variations of fructosamine in 28 patients with type II diabetes. Fructosamine, glucose, albumin, total protein and creatinine were measured at the times towards 3, 6, 9, 12 a.m. and 3, 6, 9, and 12 p.m. In relation to the 6 a.m. fructosamine value (= 100%) the fructosamine levels showed a daily variation from -4% at 3 a.m. to +11% at 9 a.m. Correcting fructosamine levels with total protein or with albumin reduced the variations to -1% to +6% or -3% to +9%. Daily profiles of the new fructosamine assay show a daily variation which can be minimized by correcting with protein-or with albumin concentrations. For clinical routine the daily variations especially of the corrected fructosamine levels are neglectible.

Adult↗
PubMed1989

Metabolic effects of biosynthetic human proinsulin in type 2 diabetes mellitus.

Due to a longer plasma half-life and half-time of action on glucose metabolism biosynthetic human proinsulin was thought to be an alternative to long-acting insulin preparations. To test this hypothesis we studied 23 type 2 diabetic patients who could no longer be treated sufficiently with oral hypoglycaemic agents. After an initial 1 week phase during which all patients received protamine bound insulin twice daily, the patients either continued on NPH insulin (Group A, n = 11) or were randomly switched to human proinsulin (Group B, n = 12). Glucose profiles and peripheral and hepatic insulin sensitivity (euglycaemic clamp: 120 mU m-2 min-1) were measured at the end of the initial period (Time 1) and 1 week later (Time 2). The insulin-mediated glucose disposal (RD) was not changed after either treatment (group A: 176 +/- 18 vs. 192 +/- 19 mg m-2 min-1; group B: 175 +/- 15 vs. 174 +/- 12 mg m-2 min-1 for times 1 and 2, respectively, NS). Suppression of hepatic glucose output (HGO) was complete in both groups at both times. Fasting blood glucose levels (FBG) and basal HGO were equally low at times 1 and 2 (group A: FBG 118 vs. 123 mg dl-1, BHGO 81 vs. 79 mg m-2 min-1; group B: FBG 118 vs. 106 mg dl-1, BHGO 87 vs. 84 mg m-2 min-1; NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[Treatment of hyperlipidemia with HMG-CoA reductase inhibitors].

HMG-CoA-reductase inhibitors represent an interesting new class of cholesterol-lowering substances. At the moment there is only one of these substances, lovastatin (Mevacor), registered in Austria. HMG-CoA-reductase inhibitors act primarily through an increase of the expression of the LDL-receptors presumably in the liver. By this mechanism they cause a marked reduction of LDL-cholesterol-levels and thus should markedly reduce the risk of coronary heart disease. The once daily dosage of these drugs, their effectiveness in low doses and the low incidence of side effects facilitate the patient's compliance. With the exception of rhabdomyolysis which occurs very rarely when avoiding a combination therapy with fibrate-analoges or cyclosporin, this kind of treatment is relatively free of serious side effects. Results from long-term studies indicate that the hypocholesterolemic effect of these drugs is maintained during prolonged therapy; possible drug-related side effects did not differ from those reported in short-term studies.

Adult↗
PubMed1988

Mixtures of human intermediate and human regular insulin in type 1 diabetic patients. Evaluation of free insulin levels and insulin action on glucose metabolism after combined and separate subcutaneous administration.

Recent resorption studies in healthy subjects suggest that intermediate human zinc insulin preparations might diminish the absorption and activity of human short-acting insulin when the two insulins are administered as a single, combined preparation. This study was designed to investigate whether combined and separate administration of human zinc or human NPH insulin with soluble human insulin have different pharmacokinetic characteristics, as evaluated by glucose clamp studies and determination of free insulin levels. Eight type 1 diabetic patients received, in random order, four different, subcutaneously injected preparations of human insulin. Zinc insulin (Monotard HM, Novo-M) and protamine insulin (Protaphan HM, Novo-P) were each given with short-acting insulin (Actrapid HM, Novo-A). These insulins were administered either as a single combined preparation (MA;PA) or as two separate injections (M + A; P + A). Prior to the insulin injection euglycemia was achieved by an overnight intravenous insulin infusion. After the subcutaneous injection of insulin, glucose was monitored at 10-min intervals and euglycemia was maintained by a variable glucose infusion rate for 6 h. The total glucose infusion rate during this period was significantly lower following MA compared with M + A (total glucose infusion: 643 +/- 117 vs. 817 +/- 130 mg/kg, P = 0.009) whereas the glucose infusion rate did not differ between PA and P + A (878 +/- 122 vs. 914 +/- 118 mg/kg, NS(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Pathogenesis and therapy of type I and type II diabetes mellitus].

Diabetes mellitus is a heterogenous syndrome. Insulin dependent type I diabetes is characterised by progressive beta-cell-loss, resulting in a deterioration of insulin secretion. Cause of the beta-cell-destruction is a chronic autoimmune process, which starts already months to years before manifestation of the disease. New advances in the diagnosis of the autoimmune mechanisms, which are responsible for type I diabetes might help to prevent type I diabetes by immunization or immunosuppressive therapy in the near future. At the moment multiple daily insulin injections are the substitution therapy of the choice in type I diabetes mellitus. This kind of therapy is designed to imitate the physiologic dynamics of insulin secretion in healthy subjects. In non insulin dependent diabetes a defect in insulin action seems to be the primary cause of the disease although there are also defects in insulin secretion in type II diabetes mellitus. Most type II diabetics are overweight at the beginning of the disease and the primary goal of therapy in these patients is normalization of bodyweight and improvement of peripheral and hepatic insulin sensitivity. Regular exercise is seen as a cornerstone in the treatment of type I and type II diabetes. Besides the acute blood glucose lowering effect of exercise, regular exercise has beneficial effects on the circulatory system and muscle system, leads to an increase in insulin sensitivity, to a decrease of the daily insulin dosage and to a stabilization of metabolic control. Furthermore beneficial effects of exercise on plasma lipids and lipoproteins are reported. In overweight diabetics regular exercise facilitates normalization of body weight.

Diabetes Mellitus, Type 1↗
PubMed1988

[The status of managing the type I diabetic patient in Austria. Organization].

During the Annual Meeting of the Austrian Diabetes Association various diabetic centres presented their success and failure rates with respect to metabolic control and prevention of late complications in diabetic patients on a country-wide basis. The analysis revealed that only 30% of all type I diabetic patients are adequately controlled. Intensive education in diabetes self-management, capable of leading to optimal metabolic control in up to 50% of the instructed patients, is however available only to a small minority of the diabetic patients to date. Despite the enormous improvement which has been achieved in the management of pregnant diabetic women, intensive specialized care is often commenced far too late. In rural areas, in particular, even conventional therapy is not fully implemented and late complications are, thus, inevitable.

Austria↗
PubMed1988

DNA fingerprinting of conjugative plasmids incompatible with R6K (IncX).

14 conjugative plasmids originated from different bacterial hosts and geographical sources were identified as members of the incompatibility group IncX with R6K as the reference plasmid. In spite of their close genetic relatedness (transfer and incompatibility properties), their molecular sizes ranged between 39 and 77 kb and DNA fingerprinting with endonucleases such as EcoRI, EcoRV, BamHI, BglI, BglII, PstI and SalI revealed a great variety of fragment patterns.

Conjugation, Genetic↗
PubMed1988

Cardiopulmonary effects of Intralipid infusion in critically ill patients.

Cardiopulmonary effects of 500 ml of 20% iv fat emulsion (Intralipid) infusion in two groups of patients who required mechanical ventilation were evaluated in our Critical Care Center. Group 1 included ten patients void of signs or symptoms of sepsis. Group 2 consisted of ten patients exhibiting clinical and laboratory signs and symptoms of sepsis. Data were measured before and immediately after Intralipid infusion and when serum lipemia cleared. Intralipid infusion precipitated a significant increase in venous admixture (Qsp/Qt) from 13.7 +/- 3.6 (SEM) to 18.0 +/- 6.5% and from 22.0 +/- 4.8 to 25.8 +/- 7.0% in groups 1 and 2, respectively. Mean pulmonary artery pressure (MPAP) increased from 22.7 +/- 4.2 to 29.2 +/- 8.1 mm Hg and 26.4 +/- 6.8 to 28.0 +/- 4.0 mm Hg in groups 1 and 2, respectively. When serum lipemia cleared, Qsp/Qt and MPAP returned to preinfusion levels. We conclude that Intralipid infusion increases pulmonary artery pressure and venous admixture in critically ill patients. These changes are temporary and coincidental with serum lipemia rather than presence or absence of sepsis. Adequate levels of oxygenation should be confirmed during Intralipid infusion in patients with borderline oxygenation.

Aged↗
PubMed1987

Equivalence of the insulin sensitivity index in man derived by the minimal model method and the euglycemic glucose clamp.

Studies were done to determine whether the minimal model approach and the glucose clamp measure equivalent indices of insulin action. Euglycemic glucose clamps (glucose, G: 85 mg/dl) were performed at two rates of insulin (I) infusion (15 and 40 mU/min per m2) in 10 subjects (body mass index, BMI, from 21 to 41 kg/m2). Insulin sensitivity index (SI) from clamps varied from 0.15 to 3.15 (mean: 1.87 +/- 0.36 X 10(-2) dl/[min per m2] per microU/ml), and declined linearly with increasing adiposity (versus BMI: r = -0.97; P less than 0.001). SI from modeling the modified frequently sampled intravenous tolerance test varied from 0.66 to 7.34 X 10(-4) min-1 per microU/ml, and was strongly correlated with SIP(clamp) (r = 0.89; P less than 0.001). SI and SIP(clamp) were similar (0.046 +/- 0.008 vs. 0.037 +/- 0.007 dl/min per microU/ml, P greater than 0.35); the relation had a slope not different from unity (1.05 P greater than 0.70) and passed through the origin (P greater than 0.40). However, on a period basis, SI exceeded SIP(clamp) slightly, due to inhibition of hepatic glucose output during the FSIGT, not included in SIP(clamp). These methods are equivalent for assessment of overall insulin sensitivity in normal and insulin-resistant nondiabetic subjects.

Adult↗
PubMed1987

Somatostatin does not increase insulin-stimulated glucose uptake in humans.

Somatostatin (SRIF) has been widely used in the study of in vivo carbohydrate metabolism to suppress pancreatic hormone secretion and thereby interrupt the glucoregulatory feedback loops between insulin, glucagon, and glucose. A critical assumption in the use of SRIF is that it has no effect on hepatic or peripheral glucose metabolism other than those mediated through the inhibition of hormone secretion. To assess whether doses of SRIF commonly used in human investigation have any effect on insulin-stimulated glucose disposal rates, we measured the rate in 6 normal subjects (mean fasting serum glucose level, 93 +/- 2 mg/dl) during euglycemic (approximately equal to 85 mg/dl) hyperinsulinemic (40 mU X m-2 X min-1) clamp studies both with and without the concomitant infusion of SRIF (600 micrograms/hr). The steady-state insulin levels achieved were 85 +/- 6 microU/ml and 74 +/- 8 microU/ml with and without SRIF, respectively (difference not significant). Glucose disposal rates between 120 and 180 min of the clamp were 7.11 +/- 0.10 and 7.35 +/- 0.10 mg X kg-1 X min-1 with and without SRIF, respectively (difference not significant). We concluded that in doses commonly used in human investigation, SRIF does not increase glucose disposal.

Adult↗
PubMed1987

Hyperinsulinemia does not compensate for peripheral insulin resistance in obesity.

Based on previous steady-state measures of the biologic activity of insulin, it was thought that postprandial hyperinsulinemia in obesity compensated for insulin resistance. However, we recently demonstrated kinetic defects in insulin action in insulin-resistant nondiabetic obese subjects: activation of insulin-stimulated glucose disposal was slower and deactivation was faster in obese than in normal subjects. In view of these kinetic defects in peripheral insulin action and of the fact that insulin is normally secreted in a phasic manner after meals, we postulated that the hyperinsulinemia of obesity does not compensate for insulin resistance and that the abnormal kinetics of insulin action in obesity are functionally important. To test this hypothesis, oral glucose tolerance tests (OGTTs) were performed in five control (mean age, 33 +/- 2 yr) and five obese (mean age, 41 +/- 5 yr) subjects. All controls had normal glucose tolerance; two obese subjects had normal and three had impaired glucose tolerance. After the results of the OGTTs were available, euglycemic clamp studies were performed in which insulin was infused in a phasic stepped fashion to mimic the rise and fall of mean peripheral insulin levels during the OGTTs. Each subject was clamped at both the "normal" and "obese" OGTT insulin profiles. During the OGTT, glucose and insulin levels were significantly elevated in the obese subjects compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Direct and indirect effects of insulin to inhibit hepatic glucose output in obese subjects.

The effects of small increases in plasma insulin on hepatic glucose production are incompletely understood. To partially elucidate this issue we have studied seven obese subjects with the euglycemic clamp technique with a low-dose insulin infusion rate of 15 mU X m-2 X min-1 over 3 h. Basal insulin levels were 24 +/- 7 microU/ml and increased to steady-state levels of 35 +/- 3 microU/ml during insulin infusion. Endogenous insulin secretion, quantitated by C-peptide measurements, decreased by 58% of the basal value after peripheral insulin infusion. Based on C-peptide measurements and the contribution of the peripheral insulin infusion to the circulating insulin concentrations, calculated portal insulin levels either decreased or remained unchanged during the clamp studies. Basal glucagon levels were 165 +/- 18 and did not change during the insulin infusion. The basal glucose disposal rate was 86 +/- 2 mg X m-2 X min-1 and did not increase significantly during the clamp studies. In contrast, hepatic glucose output (HGO) was suppressed by 82 +/- 5% of the basal value. In summary, in a group of insulin-resistant obese subjects, glucose-clamp studies were performed at peripheral insulin levels of 35 +/- 3 microU/ml; glucose disposal did not increase, whereas HGO was suppressed by 82%. At the same time, glucagon levels remained constant and estimated portal insulin levels either decreased or remained unchanged. These findings suggest that insulin can suppress HGO through indirect extrahepatic actions.

Adult↗
PubMed1986

Value of fluoroscopic assistance during transpyloric intubation.

Blind insertion of a weighted nasoenteric tube (NET) has a low chance of immediate duodenal intubation and may cause serious complications. This study used fluoroscopic assistance to facilitate the passage of an NET to the duodenum. The success rate and complications were compared to those for NET insertion without fluoroscopy. Blind passage of a weighted feeding tube was associated with a 15% success rate in 13 patients; by contrast, fluoroscopic assistance allowed 95% of 20 patients to be intubated successfully in an average of 14 +/- 12 min. Although blind insertion caused intrabronchial intubation in two patients, there were no complications associated with fluoroscopy.

Adolescent↗
PubMed1986

In vivo kinetics of insulin action on peripheral glucose disposal and hepatic glucose output in normal and obese subjects.

To determine whether abnormal kinetics of insulin's biologic actions contribute to the overall insulin resistance in obesity, we compared the rate of activation and deactivation of insulin's effects to stimulate glucose disposal rate (Rd) and inhibit hepatic glucose output (HGO) in 12 nonobese and 10 obese subjects using the euglycemic clamp technique at insulin infusion rates of 15, 40, 120, and 1,200 mU/M2 per min. In both groups, stimulation of Rd was faster the higher the insulin infusion rate and the time to reach half maximal stimulation (A50 value) in normals was 52 +/- 4, 44 +/- 2, 29 +/- 3, and 21 +/- 2 min at infusion rates of 15, 40, 120, and 1,200 mU/M2 per min, respectively. In the obese subjects, the rate of activation was slower (higher A50 values) with A50 values of 74 +/- 6, P less than 0.001 (compared to normal), 64 +/- 8 min, P less than 0.001, and 28 +/- 3 min, P less than 0.01, at the 40, 120, and 1,200 mU/M2 per min insulin infusions. Deactivation of the insulin effect to stimulate glucose disposal rate (Rd) was faster in the obese group compared with normal individuals after all comparable insulin infusions. In summary: for both groups, the higher the insulin infusion rate, the higher the steady state Rd value, the faster the rate of activation and the slower the subsequent rate of deactivation. In insulin-resistant obese subjects, the rate of activation of insulin action was slower and the rate of deactivation faster at comparable insulin infusion rates. The rate of suppression of HGO was comparable in normal and obese subjects, but the rate of recovery of HGO back to basal values was faster in the obese group. And in view of the phasic manner in which insulin is normally secreted following meals, steady state insulin action is not normally achieved. Therefore, the abnormal kinetics of insulin action in insulin-resistant obese individuals may represent functionally important manifestations of the insulin resistance in this condition.

Adult↗
PubMed1986

Influence of acute experimental hypercalcemia on peripheral insulin sensitivity in healthy subjects.

Since hypercalcemia is thought to have a modifying effect on glucose metabolism, the possible influence of experimental hypercalcemia on peripheral insulin reaction was investigated in 6 healthy control subjects by the euglycemic clamp technique. Each of these subjects was randomly tested twice, in the normocalcemic as well as in the hypercalcemic state (infusion of calcium gluconate 15 mg/kg body wt. over a period of 180 min). Infusion of calcium gluconate caused a 27% increase in plasma calcium levels, whereas the plasma phosphate levels were not significantly changed during the eucalcemic and hypercalcemic clamp protocol. Steady state plasma insulin levels and plasma glucose levels were nearly identical between the 2 clamp protocols. Exogenous hypercalcemia had no significant influence on peripheral glucose utilization measured by the M-value (M = 4.83 +/- 0.6 mg/kg body wt./min in the eucalcemic state, 4.77 +/- 0.7 mg/kg body wt./min in the hypercalcemic state, n.s.). The present data indicate that at least acute experimental hypercalcemia has no significant influence on peripheral glucose utilization.

Adult↗