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P Bratusch-Marrain

Publications and source records attributed to P Bratusch-Marrain.

At least 19 recordsLinked to original sources
PubMed1998

[Preventive iodine administration and iodine excretion in the Vienna area and in the forest quarter].

In order to reduce the still substantial iodine deficiency in the Austrian population, compulsory iodisation of salt was increased in 1990 from 10 mg potassium iodide/kg salt to 20 mg potassium iodide/kg. In this investigation we evaluated the adequacy of iodine supply in Vienna and the Waldviertel, a rural region northwest of Vienna. Daily iodine excretion (which reflects daily iodine intake) was investigated in 92 persons from the Waldviertel (all without thyroid gland pathology) and 110 persons from Vienna (54 with unremarkable thyroid glands, 56 with endemic goiter). Daily iodine excretion was higher in persons from the Waldviertel (161 +/- 90.7 micrograms/24 h, p < 0.05) than in those from Vienna (with healthy thyroid glands 126.4 +/- 42.9 micrograms/24 h and with goiter 117.2 +/- 60.5 micrograms/24 h, resp.). In both populations iodine supply as defined by the WHO (excretion of > 150 ug iodine/day) was inadequate. The recommended level was not achieved in 50% of the persons from the Waldviertel region and in 75% of persons from Vienna (healthy thyroid glands 76%, goiter: 75%). Iodine deficiency (intake < 100 micrograms/24 h) was present in 42% persons from the Waldviertel and in 31% and 24% persons, respectively, from Vienna with unremarkable thyroid glands and goiter. We conclude that although the iodine content of salt was increased, an iodine deficiency was present in a considerable portion of the population of an industrialized country (approximately 40% of persons from a rural region and 30% from the city of Vienna).

Adult↗
PubMed1992

Blood glucose response to stress hormone exposure in healthy man and insulin dependent diabetic patients: prediction by computer modeling.

To establish a qualitative and quantitative model of blood glucose response to stress hormone exposure, healthy subjects (HS) on and off somatostatin (250 micrograms/h) as well as insulin dependent diabetic patients were infused with either epinephrine (E), glucagon (G), cortisol (F), growth hormone (GH) or with a cocktail of these hormones raising plasma stress hormones to values seen in severe diabetic ketoacidosis. The developed input/output model consists of two submodels interconnected in series plus two additional submodels for correction of gains describing both sensitivity of tissue response and utilisation as well as provision of glucose. It was shown and confirmed experimentally that blood glucose response to stress hormones was essentially nonlinear. Furthermore, the mathematical models for healthy subjects and for insulin dependent diabetic patients proved to be of the same structure and differed only in the values of some typical parameters. The model raises the possibility to describe and in part to predict blood glucose response to stress hormone exposure in healthy man and insulin dependent diabetic patients.

Adult↗
PubMed1991

Effect of stress hormones on transsplanchnic balance of exogenous amino acid in healthy man.

The effect of stress hormones on transsplanchnic balance of basal and infused amino acids (AA: Val,Met,Ile,Leu,Phe,Lys,His) was investigated in healthy men without and with added epinephrine (EPI) and dexamethasone (DEX). Concentrations of AA and blood glucose were measured in arterial and hepatic venous blood before and after primed-continuous (t = 120 minutes) AA infusion without (group I: controls; n = 6, 24 +/- 3 years), and with intravenous (IV) EPI infusion (group II: 6 micrograms/min, t = -75 to 120 minutes; n = 6, 26 +/- 5 years) or oral DEX pretreatment (group III: 6 mg/d for 2 days; n = 7, 26 +/- 3 years). In the absence of exogenous AA, EPI was demonstrated to increase estimated hepatic plasma flow (EHPF, mL/min: 1,019 +/- 133 [mean +/- SD] v 737 +/- 153; P less than .01), splanchnic output of glucose (SGO), and splanchnic uptake of total AA (nmol/kg.min: 4,657 +/- 2,014 v 2,802 +/- 704; P less than .05), of Gln (+78%) and of Gly (+100%). DEX did not affect EHPF or SGO, but doubled basal splanchnic AA uptake (5,446 +/- 3,635 nmol/kg.min) and increased that of Gln by 110%. Following AA administration, total splanchnic AA uptake was consistently increased (group I, 8,577 +/- 2,380; II, 8,957 +/- 3,714; III, 10,757 +/- 2,689 nmol/kg.min) as was splanchnic Gln uptake, both of which did not differ versus controls following EPI or DEX exposure. However, metabolic clearance rate (MCR, L/min) of infused AA was elevated by 40% (Met) to 85% (Leu) versus controls in subjects receiving EPI, but unchanged in those receiving oral DEX.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1989

The diuretic and natriuretic action of human atrial natriuretic peptide in humans: lack of effect of exogenous insulin.

The interaction of exogenous, synthetic human atrial natriuretic peptide [(hANP) (ANF 99-126)] and of exogenous insulin was investigated in six healthy men and in seven type I diabetic patients using the euglycemic clamp technique. A primed-continuous (1.0 mU/kg x min) infusion of biosynthetic human insulin was administered to acutely raise and maintain plasma insulin concentrations at approximately 75 to 100 microU/mL during four hours while plasma glucose concentrations were maintained constant at the fasting level by a variable infusion of glucose. In healthy men a decrease in natriuresis (P less than .01) was seen during a euglycemic clamp study without exogenous hANP. No changes in diuresis and natriuresis were seen during a control experiment without exogenous insulin and glucose. Both in healthy men and in the type I diabetics sequential IV bolus doses of hANP of 100, 200, and 400 micrograms induced an increase in urine flow (P less than .01) and in natriuresis (P less than .01). In healthy men these effects were comparable to those achieved by hANP in the absence of induced hyperinsulinemia. It is concluded that the antinatriuretic action of insulin is of no major relevance in counteracting the pharmacologic action of hANP in healthy men. The effects of pharmacologic doses of hANP on diuresis and natriuresis in patients with type I diabetes mellitus is comparable to that in healthy men.

Adult↗
PubMed1989

Effect of hyperosmolality on basal and hormone-stimulated hepatic glucose metabolism in vitro.

To understand better impairment of glucose utilization in diabetics during a hyperosmolal state, in vitro models were established to evaluate the effects of hyperosmolality on basal glucose uptake as well as glucagon dependent glucose release by isolated hepatocytes. In these studies simulating a hyperglycaemic (40 mmol glucose) and hyperosmolal (up to 500 mosm kg-1, NaCl as added solute) state basal hepatic glucose uptake was reversibly suppressed by 19% when osmolality was increased by as little as 10 mosm kg-1. No such effects on glucose uptake by isolated hepatocytes could be attained when the incubation's fluid osmolality was augmented by the addition of urea or mannitol. Estimations of the transport rates of 3-O-methylglucose and uptake of 2-deoxyglucose at 400 vs. 300 mosm kg-1 revealed that impaired intracellular enzymatic activity but not the transport rate of glucose into the cell were responsible for the hyperosmolal defect as uptake was more reduced (P less than 0.025) by increased osmolality for 2-deoxyglucose (16%) than for 3-O-methylglucose (13%). Glucagon dependent glucose release from isolated hepatocytes was diminished by 17.8% when the osmolality was raised to 400 mosm kg-1 by NaCl as added solute. These data obtained in vitro support the clinical contention that a hyperosmolal state, which corresponds to a loss of fluid in excess of solutes, is able to impair basal hepatic glucose uptake as well as glycogenolytic glucagon action on the liver.

3-O-Methylglucose↗
PubMed1988

[Conventional or functional insulin therapy?].

The main difference between "conventional" and "functional" insulin replacement is that the former requires meals to be taken at set times throughout the day to avoid hypoglycaemic insulin reactions, while the latter separates insulin replacement in the basal ("fasting") state from that required with food intake. Such strategy reverses conventional insulin treatment (namely balancing the action of administered insulin by a fixed dietary intake), by substitution with a functional control of hyperglycaemia on the basis of tailored insulin doses. To this end blood glucose self control and systemic blood glucose correction are a must during functional insulin substitution, but not necessarily so during conventional insulin therapy. From this it is apparent that "conventional" and "functional" insulin therapy refer to different strategies, both of which may be intensified by more strict rules, although the term "intensified" remains without any conceptional meaning per se. However, whatever the therapeutic recommendation, the attending physician has to be aware that he must appropriately inform and train the insulin-deficient patient (a) on how to deal with a proposed treatment schedule, and (b) to the point that he fully understands the available therapeutic possibilities and the difference in their quality. Experience has shown that a majority of informed patients opt for functional therapy.

Blood Glucose↗
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

Detrimental effect of hyperosmolality on insulin-stimulated glucose metabolism in adipose and muscle tissue in vitro.

To better understand impairment of glucose utilization in diabetics during a hyperosmolal state, in vitro models were established to evaluate the interdependence of hyperosmolality on basal as well as insulin-dependent glucose uptake by rat epididymal fat pads and diaphragms. Using the epididymal fat pad it was shown that NaCl and urea induced hyperosmolality of 400 and 500 mOsm/kg diminished insulin-stimulated glucose uptake by 35 and 90%, as well as 29 and 68%, respectively. Using rat diaphragm as target tissue for insulin action instead a transient rise in basal (non-insulin-dependent) glucose uptake was seen at 400 but not at 500 mOsm/kg. Associated impairment of insulin-dependent glucose uptake was 30 and 79%, respectively. These in vitro data support our previous clinical contention that a hyperosmolal state, which corresponds to a loss of fluid in excess of solutes, is able to impair basal glucose utilization as well as hormone action on glucose metabolism.

Adipose Tissue↗
PubMed1988

Effect of verapamil on basal and glucagon-dependent splanchnic glucose metabolism and insulin secretion in man.

To determine the effect of verapamil on basal and glucagon-induced changes in splanchnic glucose metabolism and insulin secretion, six healthy men were studied during a primed-continuous infusion of verapamil (2.5 micrograms/kg/min). After a basal period of 30 min, glucagon was infused at a rate of 12 ng/kg/min for an additional 60 min. Splanchnic exchange of glucose, lactate, alanine and beta-hydroxy-butyrate, as well as splanchnic C-peptide release, reflecting insulin production rate, were determined by means of the liver vein catheter technique. Intraindividual control trials without verapamil were performed. Basal and glucagon-stimulated arterial glucose and insulin concentrations as well as insulin production rate were not significantly altered by verapamil, which also had no influence on basal splanchnic glucose output or on the glucagon-induced initial (0-30 min) increment in splanchnic glucose output. However, the gradual decline in splanchnic glucose output was delayed at 30-60 min (verapamil: 55.85 +/- 6.31 control: 39.73 +/- 5.6 mmol/30 min; mmol/30 min, mean, s.e.m., p less than 0.02). Splanchnic lactate-alanine- and beta-hydroxy-butyrate exchange were also unchanged by verapamil. We conclude that verapamil attenuates glucagon's evanescent effect on splanchnic glucose output without interfering with the exchange of gluconeogenic precursors or beta-hydroxy-butyrate or insulin production rate.

Adult↗
PubMed1988

[Proteinuria in diabetes mellitus].

A third of all Type 1 diabetic patients will develop proteinuria as a clinical sign of diabetic nephropathy. A 100-fold increase in relative mortality is observed in patients with persistent proteinuria. Proteinuria is preceded by a microproteinuric phase, which is reversible upon optimized metabolic control. Thereby, progression towards clinically manifest nephropathy can be delayed. Macroproteinuria and progressive renal insufficiency are not influenced by metabolic control, but by aggressive antihypertensive therapy.

Diabetes Mellitus, Type 1↗
PubMed1987

[Hepatic and peripheral insulin resistance as a cause of hyperglycemia in non-insulin-dependent (type 2) diabetes mellitus: a review].

In diabetic patients, fasting hyperglycaemia is attributed to both, reduced clearance by peripheral tissues and augmented endogenous glucose release. In normal-weight, non-insulin-dependent diabetic patients, basal hepatic glucose production (HGP) was determined by means of tracer kinetic analysis. HGP was enhanced to 3.00 +/- 0.20 mg/kg X min as compared to 1.90 +/- 0.05 in healthy, non-diabetic subjects, even though hyperglycaemia and fasting hyperinsulinaemia prevailed. HGP correlated positively with fasting blood glucose (r = 0.577; P less than 0.01). Glucose clearance rate was reduced by 20%. Marked hyperinsulinaemia during an isoglycaemic (0.75 mU/kg X min) insulin clamp study suppressed HGP by only 82% as compared to greater than 95% in healthy subjects. Furthermore, significant residual HGP was also observed when hyperglycaemia was augmented by exogenous glucose administration. Thus, in the fasting state, HGP is increased and directly correlated with severity of hyperglycaemia. Due to a reduction in glucose clearance, blood glucose concentration rises until glucose utilization rate equals HGP. Under conditions of hyperinsulinaemia and hyperglycaemia, suppressibility of HGP is diminished. Thereby, HGP and diminished glucose clearance by peripheral tissues contribute to basal as well as postprandial hyperglycaemia in type 2 diabetic patients.

Blood Glucose↗
PubMed1987

Effect of stress hormones on splanchnic substrate and insulin disposal after glucose ingestion in healthy humans.

To compare cortisol and epinephrine action on oral glucose tolerance, healthy humans were infused with either cortisol (0.1 mg X kg-1 X h-1), epinephrine (5.4 micrograms X kg-1 X h-1), or saline before and after a 75-g glucose load, thereby elevating the respective plasma hormone concentrations into the pathophysiologic range. In the basal state, epinephrine increased arterial concentrations of glucose, beta-hydroxybutyrate, and free fatty acids (FFA) as well as splanchnic output of glucose and beta-hydroxybutyrate and splanchnic FFA more than cortisol. Postprandially, C-peptide release and hyperinsulinemia were blunted by epinephrine initially and increased less thereafter than during cortisol infusion. The rise in arterial glucose after glucose ingestion as calculated by the area under the curve was more marked (P less than .01) after epinephrine [( 1.90 +/- 0.08 M) 150 min] and cortisol [( 1.41 +/- 0.05 M) 150 min] than in the control study [( 1.07 +/- 0.04 M) 150 min]. In parallel, the stress hormones induced an almost identical 24 and 31% rise in mean splanchnic glucose output versus control values (normal, 44.8 +/- 2.5; cortisol, 55.3 +/- 3.3; epinephrine, 58.9 +/- 6.9 g/150 min). The associated rise in arterial concentrations and splanchnic output of insulin above control values was considerably greater during cortisol but unchanged during epinephrine exposure. Epinephrine but not cortisol induced a rise versus the control study in splanchnic uptake of lactate and FFA, as well as in pyruvate output, whereas plasma beta-hydroxybutyrate and acetoacetate remained unchanged. The postprandial splanchnic glucose output-to-splanchnic C-peptide output ratio did not differ from normal during epinephrine but was reduced (P less than .01) during cortisol administration.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗
PubMed1986

Effect of hyperketonemia on renal ammonia excretion in man.

The effect of DL-sodium beta-hydroxybutyrate (Na BOHB) on urinary ammonia excretion was studied in seven chronically acidemic human subjects. Metabolic acidosis was induced by the ingestion of 0.1 g/kg body weight of ammonium chloride for three days. On the morning of day 4, baseline blood and urine samples were collected during three 30-minute periods. Na BOHB (1 mmol/kg, pH = 7.4) was then infused over 20 minutes, and this was followed by a continuous infusion at the rate of 10 mumol/kg min for 160 minutes. Urinary ammonia excretion decreased by 35% (P less than 0.001) while urine pH rose slightly from 5.49 to 5.82 (P less than 0.002). Venous pH increased from 7.31 to 7.38 (P less than 0.005) and bicarbonate concentration from 19 to 25 mEq/L (P less than 0.002). Four subjects were restudied with an infusion of Na beta-OHB (pH adjusted to 4.4 with the addition of HCI). Venous pH and bicarbonate concentration did not change significantly while urine pH decreased from 5.25 to 4.90 (P less than 0.001). Urinary ammonia excretion fell by 34% (P less than 0.01) despite the decline in urine pH and the absence of change in blood pH and bicarbonate concentration. Three subjects were restudied with sodium bicarbonate (0.52 to 0.85 mEq/min) infusion. Despite similar increases in blood pH and plasma bicarbonate concentration as observed with Na beta-OHB at pH = 7.4, urinary ammonia excretion did not fall significantly. In an attempt to simulate the change in redox potential and NAD+ to NADH ratio that occurred during the metabolism of beta-hydroxybutyrate to acetoacetate, sodium lactate was given to four subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1986

Inhibition by proinsulin of endogenous C-peptide release in healthy man.

To determine the role of proinsulin on endogenous insulin release, splanchnic output and arterial concentrations of C-peptide were measured in healthy subjects before and during infusion of human (HPI) and porcine (PPI) proinsulin at increasing rates for 70 min each (HPI, 328 and 656 micrograms X m-2 X h-1; PPI, 54, 134, and 268 micrograms/m-2 X h-1), while euglycemia was maintained by variable glucose infusion. By using this approach splanchnic C-peptide output was reduced by human proinsulin infusion from 143 +/- 16 (mean +/- SE) pmol/min to 111 +/- 18 and 75 +/- 11 pmol/min (P = 0.01). Simultaneously, arterial concentrations of C-peptide decreased from 716 +/- 40 pmol/l by 23 and 32%. Similar inhibition was induced by porcine PPI of splanchnic C-peptide output at an infusion rate of 268 micrograms X m-2 X h-1. Mean metabolic clearance rate was 2.7 and 3.7 ml X kg-1 X min-1 for HPI and PPI, respectively. Splanchnic glucose output was almost completely suppressed by human and porcine proinsulin at maximal infusion rates. This effect preceded both inhibition by proinsulin of splanchnic C-peptide output and stimulation of peripheral glucose utilization. We conclude that human and porcine proinsulin suppress endogenous insulin secretion at pharmacological concentrations. The observed constancy of the metabolic clearance rate of HPI demonstrates that its clearance remains a nonsaturable process up to supraphysiological HPI concentrations, while clearance of PPI appears to be subject to saturation. Furthermore, it appears that splanchnic glucose output responds earlier to proinsulin exposure than suppression of C-peptide release or stimulation of peripheral glucose utilization.

Adult↗
PubMed1986

Superior efficacy of pulsatile versus continuous hormone exposure on hepatic glucose production in vitro.

To elucidate the potency of continuous vs. intermittent exposure to hormonal stimuli, hepatic glucose production of isolated perfused rat livers was monitored in response to glucagon and insulin infusion. Using a nonrecirculating perfusion system, continuous exposure to glucagon (35 pM) induced a rise in hepatic glucose production from basal 0.33 +/- 0.03 mmol/(96 min X 100 g BW) to 0.65 +/- 0.02 mmol/(96 min X 100 g BW), while intermittent exposure (3 min on/off intervals; total dose 50%) to the same glucagon concentration elicited an almost identical rise in hepatic glucose production to 0.59 +/- 0.12 mmol/(96 in X 100 g BW). Insulin (100 mU/liter) given continuously and intermittently (3 min on/off intervals) inhibited glucagon-stimulated (70 pM) hepatic glucose production to the same extent, i.e. by 37.4% and 41.1%, respectively. Doubling the off period to 6 min and thereby reducing the total hormone dose to 33% did not diminish insulin's suppressive effect on glucagon-stimulated hepatic glucose release (34.6%). When the latter infusion protocol was applied with insulin at 300 mU/liter, hepatic glucose production during the first 40 min of glucagon infusion was more restrained (P less than 0.01) than during continuous delivery of 100 mU/liter, although the same amount of insulin was infused per period of time. In parallel, glucagon-stimulated cAMP release was similarly suppressed by insulin in all experiments. From this we conclude that the effect on hepatic glucose production of pulsatile administration of glucagon as well as of insulin, depending on the applied time interval of hormone exposure, is equipotent or even superior to the respective hormones' continuous infusion even if the hormone load is significantly reduced.

Animals↗