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Biomedical subjects

W Kerner

Publications and source records attributed to W Kerner.

At least 91 records · Page 5Linked to original sources
PubMed1980

[The Noonan syndrome (author's transl)].

Noonan's syndrome is a autosomal-dominant inherited clinical condition characterized by nanism, cardiovascular abnormalities, gonadal dysfunction and phenotypical stigmata. The questions of growth, fertility and threat of osteoporosis in the presence of hypogonadism with reference to a case history are discussed.

Adolescent↗
PubMed1979

[Postoperative blood-sugar regulation in pancreatectomized patients using the artificial "beta cell"].

Seven patients who had undergone total duodenopancreatectomy were connected postoperatively to an artificial 'beta cell', which is a computer-regulated, glucose-controlled-insulin-infusion-system. Despite high-calorie parenteral nutrition, the apparatus enabled successful regulation of the diabetes that followed removal of the pancreas in our patients during the immediate postoperative period (7 days). The artificial beta cell is capable of exogenously regulating the carbohydrate metabolism of pancreatectomized diabetics, even in the extreme conditions immediately following operation.

Artificial Organs↗
PubMed1979

D-Trp8-D-Cys14-somatostatin--demonstration of its differential suppressive activity in juvenile diabetics.

In 8 insulin-dependent diabetics, the effect of D-Trp8-D-Cys14-somatostatin on blood glucose, growth hormone, and glucagon levels as well as on insulin requirements from an artificial endocrine pancreas was studied during a balanced meal. The somatostatin analogue was infused at a rate of 25 microgram/h preceeded by a bolus injection of 25 microgram 30 minutes before ingestion of the meal. At this dose the analogue had no effect on glucagon levels and insulin requirements from the artificial pancreas. On the other hand, there was a significant lowering effect on fasting blood glucose levels, possibly indicating a direct inhibition of hepatic glucose production. Furthermore, there might be a slight effect on growth hormone levels, as was demonstrated by a rebound increase after termination of analogue infusion.

Adolescent↗
PubMed1979

Application of an artificial endocrine pancreas in the management of the diabetic surgical patient.

Application of the artificial endocrine pancreas in 12 patients undergoing total duodenopancreatectomy and 3 diabetics in whom different operations were performed proved to be safe for the patients with respect to blood glucose control and prevention of ketosis. In the postoperative period, essentially normal blood glucose values were obtained despite high caloric parenteral nutrition.

Adult↗
PubMed1979

Influence of insulin infusion kinetics of an artificial beta cell on blood glucose control in insulin-dependent diabetics.

The influence of different control modes for insulin infusion with an artificial beta cell was examined in 41 insulin-dependent diabetics. In 21 Patients, oral glucose tolerance tests were performed with control modes characterized either by low dynamic and high static gain (type I, 10 patients) or high dynamic and low static gain (type III, 11 patients). The change from type I to type III control mode effected an increase of initial insulin infusion rates (91 +/- 59 to 313 +/- 81 mU/min 10-20 min after glucose ingestion) and a decrease of infusion rates during the following phase of the 3-hour observation period (28.2 +/- 4.2 to 18.1 +/- 2.8 U) in patients whose blood glucose curves were completely normalized. Suppression of plasma glucagon levels, observed in 5 healthy control subjects, was not fully restored to normal in these patients. In another 20 insulin-dependent diabetics, daily insulin requirements form the artificial beta cell were determined by employing two control modes (types II and III) comparable in static control but different in dynamic control. Gain of dynamic control, especially in the range of falling glucose levels, was higher in type III control mode (15 patients) than in type II mode (5 patients). These insulin requirements were compared to the insulin doses necessary for subcutaneous treatment. While intravenous insulin requirements were much higher when type II control mode was employed (78.2 +/- 10.2%), during application of type III mode, intravenous insulin requirements were only 10.8 +/- 5.5% higher than subcutaneous doses. We conclude from these data that early increases in insulin infusion rates followed by a rapid decrease seem to reduce insulin requirements after glucose ingestion. A high-gain dynamic control is the basis for this insulin infusion profile.

Adolescent↗
PubMed1979

The effect of three days of blood glucose normalization by means of an "artificial endocrine pancreas" on the concentrations of growth hormone, glucagon, and cortisol in juvenile diabetics.

Glucagon, growth hormone, and cortisol secretion was studied in seven male insulin-dependent diabetics under conventional subcutaneous insulin therapy and after three days of blood glucose normalization attained by the artificial endocrine pancreas (Biostator-GCIIS). The diurnal hormonal profiles under the two types of therapy were compared. Six healthy male students served as control group. A three-day period of blood glucose normalization in insulin-dependent diabetic can restore glucagon secretion to normal. Growth hormone secretion is decreased but not completely normalised. Cortisol secretion is slightly decreased. It is concluded that prolonged normoglycemia achieved by means of an artificial endocrine pancreas may completely control endocrine abnormalities in insulin-dependent diabetics.

Adult↗
PubMed1979

Feedback inhibition of insulin in healthy and overweight subjects studied by use of an artificial endocrine pancreas.

Insulin self-inhibition is still a controversial subject. The majority of data is in favour of an inhibition; however, whether this mechanism is of physiologic relevance in the regulation of insulin secretion is open to discussion. We examined the effect of exogenous insulin on beta cell secretion in 16 volunteers, including 3 who were overweight. Blood glucose (BG) was clamped by means of the dextrose infusion unit of the artificial beta cell, and the secretion of the pancreatic beta cell was monitored by immunomeasureable C-peptide (IMCP) before, during, and after infusion of insulin. The subjects were divided into 3 experimental groups. The inhibition of the basal insulin secretion was examined in group I by clamping BG at the fasting level. The inhibition of the glucose-stimulated insulin secretion was examined in group II by clamping BG at a raised level. The stimulation of insulin secretion by glucose during insulin infusion was examined in group III by stepwise BG rises from the fasting level. An inhibition of the basal insulin secretion was observed in all volunteers examined according to the protocol for group I (n = 9, including 3 overweight volunteers). The lowest insulin infusion rate applied was 1.75 U/h. An inhibition occurred at this low infusion rate corresponding to 44 mu U immunomeasurable insulin (IMI) per ml of serum. However the inhibition was impaired in the overweight participants, who, in addition, were the only ones showing a rebound rise of IMCP after stopping the insulin infusion. An inhibiting effect of exogenous insulin appeared as likely in only 1 of 5 participants examined according to the protocol for group II. Sudden rises of BG abolished the inhibition, while a total or partial inhibition was found at a constantly raised BG level in both participants examined according to protocol III. We conclude that exogenous insulin inhibits beta cell secretion, depending on the BG level, the mode of glucose stimulation, and the time relation between glucose and insulin application. Physiologically occuring IMI levels in peripheral serum were sufficient to cause an inhibition. A disturbance of the negative feedback inhibition of insulin should be discussed as a pathogenetic factor of adipositas.

Adult↗
PubMed1977

[Insulin treatment of decompensated diabetes mellitus with a new artificial endocrine pancreas (author's transl)].

During the past decades insulin has been given in relatively high doses when treating diabetic coma. Recently low-dose insulin treatment has been proposed by several groups. In the reported investigation insulin was initially given in moderate to high doses (12-200 U/h) with a steady reduction in dose during the course of treatment. Insulin infusion was regulated either manually with an adjustable infusion pump (7 patients) or automatically with an artificial endocrine pancreas (glucose-controlled insulin infusion system; 11 patients). Thus 18 patients with decompensated diabetes mellitus (coma or precoma) were treated. In 14 patients with ketoacidotic decompensation laboratory data on hospital admission were: blood glucose 7.35 +/- 0.61 g/l, serum potassium 4.7 +/- 0.4 mmol/l, pH 7.1 +/- 0.04, base excess - 19,7 +/- 2.2 mmol/l (x +/- SEM). The other patients had hyperglycaemic or hyperosmolar non-ketotic decompensation. In all patients controlled reduction of blood glucose levels was achieved within 2.3 to 18 hours. The amounts of insulin infused during this ranged from 17 to 320 units, but in one instance was 1950 units. There were no complications.

Adolescent↗
PubMed1976

Human C-peptide. Part II: Clinical studies.

Human C-peptide is determined by radioimmunoassay. On gel filtration of serum from a healthy subject and from a patient with islet cell carcinoma, C-peptide (MW 3025) appears ahead of insulin (MW 5808) and shows much higher molar concentrations than the hormone. Human proinsulin cross-reacts with our antiserum to synthetic human C-peptide. On direct determination of immunomeasurable C-peptide (IMCP) in fasting serum of 25 healthy subjects we find an average of 1.8 (+/- 0.4) ng/ml, corresponding to 60.4 X 10(-11) Mol/l. The molar concentration is about five-fold as compared to IMI (immuno-measurable insulin). IMCP and IMI patterns are not identical on stimulation of beta-cell secretion in healthy subjects by i.v. glucose or glucose-glibenclamide. This is probably due to differences in peripheral metabolism of both compounds. We conclude from our results that C-peptide determined in peripheral venous serum is a better indicator of beta-cell secretion than is insulin. Among 26 insulin-treated juvenile diabetics 15 show not measurable and 11 subnormal IMCP levels in fasting serum. No rise in IMCP is found 1-2 h following breakfast. Four juvenile patients receiving no insulin in a phase of total diabetes remission have normal or raised fasting IMCP concentrations. Only 2 out of 24 adult diabetics (16 treated with insulin and 8 with tablets) show non-measurable fasting IMCP concentrations, in another 4 patients values are below and in the remaining 18 cases above 1 ng/ml serum. Stimulation of beta-cell secretion through glucose-glibenclamide is more or less impaired in all adult diabetics compared to the healthy subjects.

C-Peptide↗
PubMed1976

Attempts at perfect normalization of glucose tolerance test of severe diabetics by artificial beta cell.

The artificial beta cell is a Glucose Controlled Insulin (and dextrose) Infusion System (GCIIS) for maintaining normoglycemia in diabetic conditions and other disturbances of metabolism. The insulin and dextrose infusion rates are calculated by a microcomputer according to the static glucose concentration (proportional control) and to its rate of change (dynamic control). The algorithms controlling the computer can be adapted to the subjects' requirements. It has already been shown, that the artificial beta cell is able to maintain blood sugar values in diabetics within physiological ranges during the course of the day. In our present study we examined the response of the artificial beta cell using a 100 gm oral glucose load in severe diabetics. The first type of control algorithms applied effected a rather small initial insulin infusion following OGTT in 8 juvenile diabetics connected with the artificial beta cell. The glucose responses thus obtained were similar to latent diabetes. In contrast, when the computer was controlled by the second type of algorithms with a more responsive dynamic control and a consequently higher initial insulin infusion, in one diabetic OGTT was fully normalized, whereas an improvement was achieved in another diabetic patient. Furthermore it was shown that control algorithms must be varied individually, depending on residual beta cell function and glucose regulatory mechanisms.

Blood Glucose↗