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ABSTRACT: In non-diabetic people, insulin levels in the liver are two-fold higher than those in the systemic circulation. In contrast, patients with type 1 diabetes have similar hepatic and systemic insulin levels because insulin is administered peripherally. The aim of this study was to compare the effects of systemic (SI) and pre-portal (PI) insulin administration on energy, glucose and protein metabolism in chronic insulin-dependent ketosis-prone diabetic dogs.
We applied glucose-controlled insulin infusion, indirect calorimetry and stable isotope and radioisotope techniques to measure energy, protein and glucose metabolism. We maintained near-normoglycaemia at identical levels under both study conditions for 20 h.
SI was associated with lower oxygen consumption (130+/-13 vs 161+/-8 ml/min), CO(2) production (99+/-10 vs 130+/-8 ml/min), respiratory quotient (0.76+/-0.02 vs 0.81+/-0.01) and energy expenditure (870+/-90 vs 1089+/-60 kcal/24 h) (p<0.05 for all differences). PI increased the respiratory quotient from the insulin-deprived state, whereas SI did not. Glucose kinetics were similar for SI and PI, whereas leucine oxidation (36+/-4 vs 54+/-5 micromol kg(-1) min(-1)) and the fractional synthesis rates of liver tissue protein (0.68+/-0.6 vs 0.83+/-0.07%/h), albumin (0.55+/-0.06 vs 0.68+/-0.4%/h), and fibrinogen (1.73+/-0.23 vs 2.59+/-0.25%/h) were all lower during SI than PI (p<0.05).
The route of insulin administration did not alter glucose metabolism but did affect protein synthesis in the liver. The potential impact of this altered liver protein metabolism on chronic complications needs careful evaluation. A similar decrease in energy expenditure resulting from systemic insulin administration during tight glycaemic control is a potential cause of weight gain.
Diabetologia 03/2006; 49(3):543-51. · 6.81 Impact Factor
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ABSTRACT: The appearance of Fas receptor at the surface of pancreatic beta-cells affected by progressive insulitis strongly suggests that Fas-mediated beta-cell apoptosis plays an important role in the pathogenesis of type 1 diabetes. In support of this concept, the present study has shown that islet cells from NOD mice and the beta-cell line NIT-1 respond to the proinflammatory cytokines IL-1beta and IFN-gamma with Fas surface expression in a dose- and time-dependent manner. Moreover, the prevention of cytokine-induced surface Fas expression by actinomycin D, cycloheximide, and brefeldin A demonstrated that trafficking of Fas to the beta-cell surface requires RNA and protein synthesis and, in addition is critically dependent on intracellular protein transport. Compared with total cellular Fas protein, the amount of Fas at the cell surface was relatively small and indicated that Fas is preferentially expressed in cytoplasmic compartments of NIT-1 cells. It is concluded that inflammatory insults specifically induce translocation of Fas to the beta-cell surface and that interference with cell surface Fas expression is a new strategy to improve beta-cell survival in inflamed islets.
Biochemical and Biophysical Research Communications 02/2002; 290(1):443-51. · 2.48 Impact Factor
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ABSTRACT: A pharmacological concentration of glucagon-like peptide-1 (GLP-1) in the insulin-deficient state clearly decreases the blood glucose level. Therefore, this study was designed to evaluate a putatively relevant effect of the gastrointestinal peptide as an adjuvant to insulin replacement therapy. GLP-1 (GLP-1(7-36) amide 10 pmol x kg(-1) x min(-1)) was infused intravenously over 8 hours in nine fasting, C-peptide-negative diabetic dogs. The animals were under normoglycemic control by glucose-controlled insulin infusion (GCII) during the night before and during GLP-1 administration. During the paired control tests, the animals received saline infusion instead of GLP-1. In addition to the insulin infusion rates required to maintain normoglycemia, hormones, metabolites, and the turnover rates for glucose (6-3H-glucose), alanine (U-14C-alanine), and urea (15N2-urea) were measured during the final 2 hours of GLP-1 administration. Circulating plasma GLP-1 levels increased from 3+/-1 to 17+/-7 pmol/L. There was no significant difference in the insulin infusion rate between the experimental and control groups (0.43+/-0.05 v. 0.40+/-0.05 mU x kg(-1) x h(-1), average over the entire interval). Glycemia was maintained at a practically identical level (4.9+/-0.3 v. 4.8+/-0.4 mmol/L). Also, the concentration of plasma insulin-which was not hyperinsulinemic--and pancreatic glucagon remained unaltered. We found no appreciable effect of GLP-1 on glucose production and metabolic clearance, alanine turnover and the formation of glucose from alanine (1.8+/-0.2 v. 1.4+/-0.2 micromol x kg(-1) x min(-1), or the urea production rate as a measure of overall amino acid catabolism (4.1+/-0.4 v. 4.1+/-0.4 micromol x kg(-1) x min(-1)). Thus, no conclusive adjuvant effect of GLP-1 was ascertained in insulin-treated diabetic dogs under normoglycemic control.
Metabolism 02/1999; 48(1):134-7. · 2.66 Impact Factor
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ABSTRACT: To establish potential effects of glucagon-like peptide I (GLP-I) on blood glucose control in insulin-deficient states, GLP-I [GLP-I(7-36) amide; 10 pmol x kg(-1) x min(-1)] was infused intravenously in six fasting, canine C-peptide-negative, chronically diabetic dogs for 8 h. Blood samples were saved for the analysis of hormones, metabolites, and turnover rates of glucose (6-(3)H-glucose), alanine (U-(14)C-alanine), and urea ((15)N(2)-urea) starting 22 h after the last subcutaneous dose of exogenous insulin. Circulating plasma GLP-I levels rose under infusion from 2.9 +/- 0.8 to 41.4 +/- 10.1 pmol/l. This was efficient to significantly reduce the preexisting diabetic hyperglucagonemia. Since in the utilized model functioning pancreatic beta-cells are lacking, GLP-I had no insulinogenic effect. Compared with control experiments in the same animals receiving saline infusion, glycemia dropped from 20.8 +/- 1.9 to 16.2 +/- 1.0 mmol/l (P < 0.05). This was in parallel to the infusion of GLP-I and was most likely caused by a decrease of elevated glucose production since overall glucose turnover decreased with no alteration in glucose metabolic clearance. Alanine turnover was significantly reduced, obviously reflecting a decline in alanine production in relation to changed muscle glucose uptake under conditions of lower glycemia and overall glucose turnover. There was, however, neither an effect of GLP-I on alanine conversion into circulating glucose nor an effect on urea production rate, indicating unchanged gluconeogenesis from amino acid precursors. We conclude that the blood glucose-lowering effect of GLP-I in an animal model of insulinopenia was shown to be due to a reduction in hepatic glucose output, possibly secondary to reduction in glucagon concentrations leading to decreased glycogenolysis. Whether GLP-I might be therapeutically useful in clinical insulin-deficient diabetes needs to be verified.
Diabetes 05/1997; 46(5):824-8. · 8.29 Impact Factor
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ABSTRACT: To study the ability of interleukin 1-beta (IL-1) to induce apoptosis in the endocrine pancreas, rat islets of Langerhans obtained from 14-day-old BB.1A rats were exposed to 25 U/ml IL-1 for 40 h. In order to prove the role of nitric oxide (NO) in this process islets were exposed either to 1 mmol/l N-nitro-L-arginine methylester (NAME) or to 25 mmol/l nicotinamide (NA) or to a combination of NA or NAME with IL-1. In dispersed cells oligonucleosomes, resulting from cleavage of nuclear DNA due to apoptosis, were identified by enzymatic labelling the free 3'-OH-DNA ends with fluorescein-dUTP and quantified by means of flow cytometry. After exposure to IL-1, the islets were characterized by elevated basal (in response to 2 mmol/l glucose) insulin release while glucose-stimulated (20 mmol/l glucose) insulin secretion was nearly completely abolished. In contrast, glucose-stimulated insulin secretion was well preserved in NAME-exposed islets, but was markedly inhibited after NA treatment. Accordingly, only the IL-1-induced inhibition of glucose-stimulated insulin secretion was significantly restored in the presence of NAME but was reinforced by NA. IL-1 exposure resulted in a significant increase in the percentage of apoptotic cells (untreated controls 3.8 +/- 0.5% IL-1 18.8 +/- 1.8%, P < 0.01). This effect was significantly reduced in the presence of NA and NAME. Nitrite production which was assayed as an equivalent of NO generation of islets was highest under the influence of IL-1 (16.48 +/- 1.40 versus 2.89 +/- 0.37 pmol/islet for control islets) which was correlated with the percentage of apoptotic cells. IL-1-stimulated nitrite production was reduced to 9.25 +/- 0.48 and 3.41 +/- 0.36 pmol/islet in the presence of NA or NAME, respectively. The results demonstrate the potency of IL-1 to induce apoptosis in rat islets. Since inhibition of NO production was always paralleled by a reduced ability of IL-1 to induce programmed cell death, this radical appears to be involved in this process. Remarkably, the near-complete prevention of NO generation as demonstrated under the influence of NAME was able to prevent the IL-1-induced deterioration of glucose-stimulated insulin secretion in parallel to the prevention of apoptosis-related appearance of DNA double-strand breaks. It is concluded that the elimination of damaged beta cells due to IL-1 exposure is partly achieved by induction of apoptosis.
Journal of Autoimmunity 06/1996; 9(3):309-13. · 7.37 Impact Factor
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ABSTRACT: In IDDM, the gluconeogenic turnover of amino acids is increased even if glycemia is well controlled and may be restored to normal by means of prehepatic insulin substitution. Therefore, the present study was designed 1) to investigate the influence of route of insulin administration (portal versus peripheral) on the urea production rate, which is considered to measure amino acid catabolism, and 2) to elucidate the impact of different food-protein intake. Paired studies were conducted in chronic insulin-dependent diabetic dogs maintained normoglycemic. Diabetic animals and nondiabetic controls were fed either a high-protein diet (46% of energy intake provided by proteins; study 1) or a low-protein carbohydrate-supplemented diet (20% of energy intake provided by protein; study 2) for 2 days, and flux rates of glucose and urea were measured using isotope dilution techniques. In both studies, the diabetic animals were maintained normoglycemic by glucose-controlled insulin infusion delivered either systemically or portally. In study 1 versus study 2, the animals showed lower alpha-amino nitrogen levels and concentrations of gluconeogenic amino acids, predominantly alanine. There were no significant differences in plasma glucose and glucose turnover between the experimental groups on either systemic or portal insulin infusion versus controls; however, peripheral insulin levels were higher for diabetic animals maintained with systemic versus portal insulin delivery (P < 0.05). No significant differences in glucagon, lactate, pyruvate, nonesterified fatty acids, or beta-hydroxybutyrate were observed. Urea production was significantly higher in study 1 compared with study 2: 7.48 +/- 0.83 vs. 5.97 +/- 0.59 micromol / kg / min (normal dogs); 12.97 +/- 1.86 vs. 5.54 +/- 0.60 micromol / kg / min (diabetic dogs on portal insulin); 16.11 +/- 2.59 vs. 6.82 +/- 0.70 micromol / kg / min (diabetic dogs on systemic insulin infusion); P < 0.05 for all. The diabetic dogs maintained normoglycemic with systemic insulin infusions had significantly higher rates of urea synthesis than those with portal insulin infusion (P < 0.05). It is concluded that in IDDM, even if normoglycemia is managed, there is significantly increased amino acid catabolism with posthepatic systemic insulin treatment. This increased catabolic rate is more pronounced during high-protein nourishment.
Diabetes 05/1996; 45(5):667-74. · 8.29 Impact Factor
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ABSTRACT: The most advanced glucose sensors are measuring amperometrically the hydrogen peroxide generated in a stoichiometric relation to the prevailing glucose concentration during glucose oxidase-mediated glucose oxidation. They proved useful in commercially available glucose analysers and in experimental subcutaneous (sc) monitoring. Here it is shown (a) that under steady state conditions the s.c glucose concentration is nearly identical to that in blood, (b) that sc. inserted glucose electrodes do mirror the intracorporal glucose concentration both under hypo-, normo-, and hyperglycaemic conditions with a clinically relevant accuracy, (c) that automated feedback control of intracorporal glucose concentration is possible applying the output of sc. glucose sensor as an input to the computer that controls the insulin pump, and (d) that stable function of sc. sensor may be accomplished over intervals up to one day; in some cases applications over up to ten days have been reported. The underlying problem consists in an insufficient functional biostability which is a function of biocompatibility and size of the sensor, of its sterility, and of the permanent skin penetration. The latter is still required to get the device in place, to keep it in function, and to make use of the data under any condition. At this time, sc. glucose electrodes to be employed as hypoglycaemia-warning systems over one day are considered clinically important and technically achievable.
Acta anaesthesiologica Scandinavica. Supplementum 02/1995; 104:21-9.
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Artificial Intelligence Medicine, 5th Conference on Artificial Intelligence in Medicine in Europe, AIME'95, Pavia, Italy, June 25-28, 1995, Proceedings; 01/1995
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ABSTRACT: Biosensors are miniaturized analytical tools which comprise a biological detection element providing specificity to the analyte, and a physical transducer which guarantees an output signal, e.g. an electric current the size of which is proportional to the concentration of the analyte. They provide the unique possibility of continuous in vivo monitoring. Glucosensors were in fact the first biosensors under study. Among them, the most advanced devices are measuring amperometrically the hydrogen peroxide generated in a stoichiometric relation to the prevailing glucose concentration during glucose oxidase-mediated glucose oxidation. They proved useful in commercially available glucose analyzers and in experimental subcutaneous monitoring. Here it is shown (a) that under steady state conditions the s.c. glucose concentration is nearly identical to that in blood, (b) that s.c. inserted glucose electrodes do mirror the intracorporal glucose concentration both under hypo-, normo-, and hyperglycaemic conditions with a clinically relevant accuracy, (c) that even stable feedback control of intracorporal glucose concentration is possible employing s.c. glucosensor signal as an input to automated insulin pump controller, and (d) that stable function of s.c. sensor is usually accomplished over intervals up to one day but in some cases applications over up to ten days could be realized. The underlying problem consists in an insufficient functional biostability which is a function of biocompatibility and size of the sensor, of its sterility, and of the permanent skin penetration. The latter is still required to get the device in place, to keep it in function, and to make use of the data under any condition.(ABSTRACT TRUNCATED AT 250 WORDS)
Hormone and Metabolic Research 12/1994; 26(11):515-22. · 2.19 Impact Factor
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ABSTRACT: After subcutaneous implantation of glucose sensors into LEW.1A rats, antibodies could be detected by means of enzyme-linked immunosorbent assay against the outer membrane (cellulose acetate) but not against either the inner membrane (polyethylene) or glucose oxidase (GOD). The kinetics of humoral immune response were investigated implanting different polymeric membranes such as polyurethane, cellulose acetate, regenerated cellulose. The highest antibody titer was detected against regenerated cellulose. There was no cytotoxic effect in vitro by any of the tested materials as examined on monolayer cultures of the mouse fibroblast cell line L-929. Thus immunogenicity is suggested to be considered as a parameter in biocompatibility testing of implantable medical devices.
Hormone and Metabolic Research 12/1994; 26(11):534-7. · 2.19 Impact Factor
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ABSTRACT: This paper presents a simple procedure to assess the amount of hydrogen peroxide arising in amperometric glucose oxidase sensors. At an external glucose concentration of 30 mmol/l, which represents the linear range of calibration, a hydrogen peroxide concentration of approximately 0.18 mmol/l is generated. Taking into consideration that in medical applications the main range of interest would be within euglycaemia which is between 4 and 9 mmol/l, it is concluded that in the type of glucose electrode investigated, hydrogen peroxide produced during enzymatic glucose measurement does not appreciably damage the enzyme glucose oxidase.
Biosensors and Bioelectronics 02/1994; 9(1):65-71. · 5.60 Impact Factor
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ABSTRACT: Education and training in self-management of blood glucose control has become a permanent task for all people involved in the care of diabetic patients. Since this may be facilitated by applying state-of-the-art information technology, we have developed the decision support system KADIS (Karlsburg Diabetes Management System). It comprises computer-aided tools for (1) the evaluation (selection, aggregation, storage, statistics, graphics) of therapeutic data, e.g. from patients' logbooks, and (2) the simulation of daily profiles of glycaemia and insulinaemia on the basis of a mathematical model of the glucose-insulin regulatory system, parameters of which can be adapted to the characteristics of individual patients. The latter tool allows the patient to predict his response to any modification in the therapeutic regime and to learn how variations in timing, formulation and doses of insulin, in carbohydrate equivalents and absorption characteristics of meals, and in exercise may influence the daily pattern in glycaemia. This procedure has been well accepted as an educational tool by those patients who were 'self-managing' their metabolic control.
Computer Methods and Programs in Biomedicine 02/1994; 41(3-4):205-15. · 1.52 Impact Factor
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ABSTRACT: To assure health care quality requires a tool for establishing the feedback between parameters of patient management and related standards. To assess the current situation and to evaluate the DIABCARE system as a potential monitoring instrument, a retrospective study was performed in 85 randomly assigned insulin-treated patients (72% type 2) who were regularly attending the diabetes outpatient unit (total of 3,595 patients) in a township of approximately 90,000 inhabitants. 1,195 records of sequential medical visits during the years 1987 and 1990 were analyzed. -Selected results (averages in 1987 vs. 1990): (1) Visits per year 6.9 vs 7.1; (2) intensified insulin treatment in 14 vs. 27% of all patients, they were on 4.0 vs. 4.5 injections per day applying doses of 0.8 vs. 0.6 IU kg-1 d-1; (3) glycaemic control: random blood glucose 6.0 vs. 5.8 mmol/l on conventional and 6.4 vs. 5.7 mmol/l on intensified regimes, HbA1 regular measurements in 2 vs. 21% of the patients; (4) body mass index 26.4 vs. 26.6 (conventional) and 24.7 vs. 25.9 (intensified) kg/(m)2; (5) retinopathy prevalence 30 vs. 29%, in 4 vs. 29% of the patients no information; (6) nephropathy prevalence 7 vs. 11%, in 75 vs. 68% of the patients no information; (7) foot complications prevalence 6 vs. 9%, in 91 vs. 84% of the patients no pathological findings. -The DIABCARE monitor proved appropriate but too laborious. The general level of care showed a tendency towards improvement between the two investigated periods but dit not yet meet the standards which must be attained to attain the St. Vincent Declaration.
Diabète & métabolisme 02/1993; 19(1 Pt 2):188-94.
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ABSTRACT: At present in Germany, data on the prevalence of diabetes can only be obtained by modelling health insurance data. The National Diabetes Register of the former (East) German Democratic Republic which, between 1960 and 1990, monitored approximately 98% of all diabetic subjects, provides a tool for evaluating epidemiological estimates from other data sources. Therefore, the following data bases were compared for the year 1988: (1) a 5% random-sample (n = 6478) of all subjects insured at a local statutory health insurance company in the city of Dormund; (2) related data from the population-based diabetes register of former East-Berlin and (3) of the former German Democratic Republic. All data were standardized by sex and age according to the 1988 population statistics of the Federal Republic of (West) Germany thus resulting in the apparent diabetes prevalence of the Western part of Germany at that time. Results: total prevalence rates were (1) 4.8%, (2) 4.9%, and (3) 4.4% (p < 0.05). The percentages of insulin-treated patients were (1) 18%, (2) 19%, and (3) 16%, respectively. 54% (1), 37% (p < 0.05) (2), and 42% (p < 0.05) (3), of the patients received oral antidiabetic drugs. It is concluded that the three samples are comparable and that the diabetes prevalence rates as estimated from health insurance data and from the two population-based registers give corresponding conclusions. Sample-based health insurance data may provide a useful and reliable tool for epidemiological studies on diabetes mellitus.
Diabète & métabolisme 01/1993; 19(1 Pt 2):89-95.
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ABSTRACT: The replacement of insulinogenic function in insulin-dependent diabetes has to restore the feedback between intracorporal glucose and insulin. This has been accomplished by the following approaches: (a) the so-called open-loop insulin treatment by means of injections or pumps, employing laboratory or other extracorporal analytical devices and closing the feedback at large intervals only; (b) transplantation of insulin producing tissue and the bioartificial pancreas, employing the natural beta-cell both for glucose sensing and insulin delivery; (c) implanted artificial drug delivery systems providing chemical feedback between intracorporal glucose and insulin release from a nonrefillable reservoir of limited capacity; (d) the intracorporal or paracorporal artificial beta-cell comprising a glucose sensor (electrochemical or other type) that permanently delivers the signal to the computer-controlled insulin pump. This artificial device works on the basis of an algorithm of glucose-dependent insulin provision, compensating for the lack of other regulators, for the site of insulin administration, which is usually posthepatic, and for the kinetic properties of sensing system, e.g., a subcutaneous inserted amperometric electrode. Present experimental studies show that the pharmacodynamics of peritoneally applied insulin may be implemented into a mathematical model of the overall glucose-insulin system. They include absorption nearly as fast as after intravenous application, predominant portal inflow and approximately 30% hepatic removal. Feedback-controlled peritoneal insulin administration by means of an artificial beta-cell working on peripheral-venous blood glucose monitoring results in normal glycemic profiles under basal conditions and during oral glucose loads, if the pharmacodynamic properties of the peritoneal route are implemented into the insulin dosage algorithm.
Artificial Organs 05/1992; 16(2):151-62. · 2.00 Impact Factor
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ABSTRACT: Amperometric glucose oxidase/hydrogen peroxide sensors were inserted subcutaneously into the neck of normal and diabetic dogs (n = 10), to elucidate the conditions for stable long-term functioning. Their output current was observed in parallel with measurements of plasma glucose concentrations and their function was checked by means of induced alterations in glycaemia. After between 14 and 96 h the experiments were terminated due to losses in the apparent sensitivity of implanted sensors and/or increasing oscillations following stable measurements. This was accompanied by an inflammatory reaction which was analysed on the basis of the clinical picture and histology. In most cases there was a bacterial ingrowth from the normal skin flora of dogs. The inflammatory exsudate contained only 23 +/- 17% of the simultaneous steady state plasma glucose concentration, which was significantly different from the glucose level in the fluid obtained from non-irritate subcutaneous tissue (95 +/- 12%, separate set of experiments). The in vitro calibration of sensors exhibited essentially comparable sensitivities before and after the in vivo application. No differences in reported findings related to the biomaterials used (polyurethane versus cellulose acetate), the presence of diabetes, the history of individual electrodes and the effective duration of a given experiment were discernible. We conclude that the functional bioinstability of subcutaneous glucose sensors is largely due to the inflammatory tissue reaction which alters the effective glucose concentration within the measuring compartment of the electrodes; these drawbacks may be overcome by further miniaturization including implantable telemetric devices allowing the closure of the skin.
Journal of Biomedical Engineering 02/1992; 14(1):33-40.
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ABSTRACT: This study was aimed at validating the in vitro estimated response characteristics of implanted glucose oxidase/H2O2 electrodes with respect to their in vivo function. Monoexponential non-linear regression analysis of sensor current vs. time curves in response to square alterations in glucose concentration gave response times T95 of between 1 and 5 min. Non-primed glucose infusions were applied to dogs with these electrodes implanted subcutaneously. The simultaneously monitored in vivo data were subjected to non-linear regression analysis. The time constants T of increases or decreases after starting or ending the glucose load were (mean +/- SEM) 53 +/- 10 and 26 +/- 4 min (significant difference, p less than 0.05) in sensor current, 28 +/- 8 and 15 +/- 2 min (NS) in whole blood, and 26 +/- 5 and 18 +/- 2 min (NS) in plasma. The in vivo kinetic patterns of sensors were not related to their in vitro response times. Non-linear regression analysis of in vitro responses of glucose sensors under clearly defined conditions is recommended as a basis for further studies. The physiological delay in the subcutaneous glucose system needs more attention in this field of research.
The International journal of artificial organs 09/1991; 14(8):473-81. · 1.86 Impact Factor
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ABSTRACT: To quantitate the degree of glycemic control in relation to insulin doses required on the peritoneal route of administration, insulin dependent diabetic dogs instrumented with chronic peritoneal and venous catheters and with access devices for serial peritoneal injections, were treated with regular insulin at random order as follows: (1) subcutaneous injections, (2) peritoneal injections, (3) continuous intravenous infusion, (4) continuous peritoneal infusion. Metabolic profiles were taken over 24 h after an average duration of treatment of 2 weeks and were compared to data obtained in nondiabetic animals. Insulin doses and postprandial increase in peripheral insulinemia were higher and glycemic control was worse on peritoneal vs. subcutaneous injection therapy. Glycemic control and insulin doses were identical between peritoneal and intravenous infusion regimes. Hyperinsulinemia was only seen during nighttime in intravenously infused animals. It is concluded that in accordance with the fast pharmacokinetics of peritoneally administered insulin, sufficient glycemic and insulinemic control can only be obtained on the peritoneal route, when the insulin is applied by means of pumps.
Experimental and clinical endocrinology 03/1990; 95(1):11-21.
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ABSTRACT: Despite the introduction of new therapeutic aids such as insulin pumps and injectors, blood glucose test tapes, particular insulin formulations, and the physiological basis-bolus principle of insulin dosage regimes, the metabolic care of most insulin-dependent patients is still insufficient. One potential tool of further improving the results in diabetes treatment consists in the application of computer-aided procedures to estimate individually optimal regimes. Employing a validated mathematical model of the glucose/insulin metabolic control system and individual sets of data from patients' self-monitoring, a software package was developed on a micro-computer which allowed both the retrospective analysis of data resulting from the therapeutic process, and the prospective simulation of the outcome of alterations in the regime in terms of glycaemia and insulinaemia. The two parts of the programme provide either for the patient or for the physician an interactive mode of working with the computer. The system is now being validated by means of a long-term follow-up study in type-I diabetic patients. It may be used mainly in diabetic outpatient centers and as a tool of educating, training, and motivating patients.
Experimental and clinical endocrinology 03/1990; 95(1):137-47.
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ABSTRACT: An enzyme electrode (GOD, Pt-Ag/AgCl) is introduced for amperometric measurement of the intracorporal glucose concentration in the subcutaneous tissue. Changes of the glucose concentration in the peripheral blood (PG) were induced by glucose- respectively insulin-infusion in healthy dogs. PG was compared with values found by out means of a sensor implanted in the necks of the dogs (SG). The regression equation SG = 0.81 PG - 1.39 was calculated by analysing 62 steady state levels. The regression delta SG = 0.83 delta PG + 0.22 submitted for the deviation of the normoglycemic base-level. A sensibility loss of the sensor of about 10% appears after an implantation duration of 7.5 hours in medium. Conclusions for the further development of the sensors follows especially with the in vivo functions (biocompatibility, diminution, sterilisation).
Zeitschrift für experimentelle Chirurgie, Transplantation, und künstliche Organe: Organ der Sektion Experimentelle Chirurgie der Gesellschaft für Chirurgie der DDR 02/1990; 23(2):95-8.
