Search PubMed⌕ Search

Biomedical subjects

U Keller

Publications and source records attributed to U Keller.

At least 109 records · Page 6Linked to original sources
PubMed1996

[Reproducibility of fasting serum cholesterol and triglycerides in ambulatory patients with mixed hyperlipidemia].

Intraindividual variability of serum lipid concentrations in normal volunteers and in patients with hyperlipidemia is substantial. The aim of this study was to investigate prospectively the reproducibility of fasting serum triglyceride and total cholesterol concentrations in primary health care patients with combined hyperlipidemia, i.e. under conditions of daily medical practice. Secondary forms of hyperlipidemia were excluded. 19 general medical outpatients with primary combined hyperlipidemia were studied. Serum total cholesterol and triglyceride concentrations were measured after an overnight fast at 08.00 h 4 times at weekly intervals. To study the influence of alcohol intake on serum lipid concentrations, total cholesterol and triglycerides were measured without alcohol influence and 12 hours after consumption of a mean of 100 g alcohol in the evening. In 19 patients (10 males, 9 females, mean age 55 years, body mass index 27.9 +/- 4.4 kg/m2), mean +/- SD of serum triglycerides was 3.97 +/- 1.8 mmol/l and of total cholesterol 7.9 +/- 1.8 mmol/l. The combined intraindividual and interassay coefficient of variation was 18.7 +/- 8.2% for triglycerides and 5.1 +/- 2.5% for total cholesterol. Fasting serum triglycerides (3.5 +/- 1.1 vs. 3.7 +/- 1.4 mmol/l) and total cholesterol (7.6 +/- 1.4 vs. 7.8 +/- 1.0 mmol/l) did not significantly change 12 hours after acute alcohol consumption. Patients with primary combined hyperlipidemia in a primary health care setting show small intraindividual variations of overnight fasted serum triglyceride and total cholesterol concentrations. Moderate alcohol consumption 12 hours before blood sampling does not significantly affect triglyceride and cholesterol values.

Adult↗
PubMed1996

[Nutritional recommendations for diabetic patients: adaptation of the recommendations defined by the Diabetes and Nutrition Study Group of EASD].

Nutritional recommendations for diabetics are nowadays more flexible and better adapted to the individual patient. They resemble those offered to the public at large. Caloric intake is determined by body size and weight as well as physical activity. Approximately 60% of the energy should be consumed in the form of carbohydrates and monounsaturated fatty acids. The proportion of fatty acids and carbohydrates is fixed according to the individual nutritional habits. The intake of saturated and polyunsaturated fatty acids should be restricted. Meals and carbohydrates should be distributed over the day as three main meals with two to three snacks in between. Recommendations should always be adapted to the practical possibilities of the individual and to his particular metabolic situation.

Diabetes Mellitus↗
PubMed1996

D-Lysergyl peptide synthetase from the ergot fungus Claviceps purpurea.

The ergot fungus Claviceps purpurea produces the medically important ergopeptines, which consist of a cyclol-structured tripeptide and D-lysergic acid linked by an amide bond. An enzyme activity capable of non-ribosomal synthesis of D-lysergyl-L-alanyl-L-phenylalanyl-L-proline lactam, the non-cyclol precursor of the ergopeptine ergotamine, has been purified about 18-fold from the ergotamine-producing C. purpurea strain D1. Analysis of radioactively labeled enzyme-substrate complexes revealed a 370-kDa lysergyl peptide synthetase 1 (LPS 1) carrying the amino acid activation domains for alanine, phenylalanine, and proline. The activation of D-lysergic acid is catalyzed by a 140-kDa peptide synthetase (LPS 2) copurifying with LPS 1. LPS 1 and LPS 2 contain 4'-phosphopantetheine and bind their substrates covalently by thioester linkage. Kinetic analysis of the synthesis reaction revealed a Km of approximately 1.4 microM for both D-lysergic acid and its structural homolog dihydrolysergic acid, which is one to two orders of magnitude lower than the Km values for the other amino acids involved. The Km values for the amino acids reflect their relative concentrations in the cellular pool of C. purpurea. This may indicate that in in vivo conditions D-lysergyl peptide formation is limited by the D-lysergic acid concentration in the cell. In vitro, the multienzyme preparation catalyzes the formation of several different D-lysergyl peptide lactams according to the amino acids supplied. Specific antiserum was used to detect LPS 1 in various C. purpurea strains. In C. purpurea wild type, the enzyme was expressed at all stages of cultivation and in different media, suggesting that it is produced constitutively.

Amino Acids↗
PubMed1996

Metabolic actions of growth hormone: direct and indirect.

GH may exert metabolic effects either directly or indirectly through increased production of IGF-I. GH administration increases circulating IGF-I levels via stimulation of hepatic synthesis and secretion of IGF-I; it may also enhance local IGF-I synthesis, which exerts paracrine or autocrine effects. Figure 2 summarizes the metabolic effects of GH and IGF-I. Administration of GH and IGF-I in adult humans has been demonstrated to enhance protein anabolism. Combined administration of GH and IGF-I was observed to be more anabolic than either IGF-I or GH alone. Evidence is presented that protein accretion results mainly from direct effects of GH on tissues; additional indirect effects via IGF-I production are also likely. Administration of GH has been reported to produce carbohydrate intolerance with elevated plasma insulin levels, resulting from insulin resistance. in contrast, insulin sensitivity increased during administration of IGF-I, which exerts hypoglycaemic effects even with concomitant suppression of insulin secretion. A major direct metabolic effect of GH is to increase fat mobilization and oxidation, and thereby to reduce total body fat; there is no evidence that IGF-I acts directly on adipose tissue in vivo. GH administration results in sodium retention via stimulation of Na-K-ATPase. It is suggested that part of the effects of GH on tubular function (e.g. phosphate reabsorption) are mediated via IGF-I. Energy expenditure may be increased by administration of either GH or relatively high doses of IGF-I. One of the reasons for this phenomenon is an increase in lean body mass; GH may increase energy expenditure additionally be enhancing the production of T3 and by increasing lipid oxidation.

Adult↗
PubMed1996

Effects of growth hormone and IGF-I on glucocorticoid-induced protein catabolism in humans.

The effects of similar increases in total insulin-like growth factor I (IGF-I) plasma concentrations achieved by either recombinant human (rh) growth hormone (GH) or rhIGF-I administration on whole body protein and glucose kinetics were assessed. Twenty-six healthy subjects received methylprednisolone (0.5 mg.kg-1.day-1 orally) during 6 days in combination with either placebo (saline sc), GH (0.3 mg.kg-1.day-1 sc), or IGF-I (80 micrograms.kg-1.day-1 sc) in a double-blind randomized fashion. Glucocorticoid administration resulted in protein catabolism as indicated by an increase in leucine flux and a 62 +/- 13% increase in leucine oxidation ([1-13C]leucine infusion technique); this increase was abolished by GH (-1 +/- 18%) as was statistically insignificant during IGF-I treatment (+53 +/- 25%). GH increased endogenous glucose production by 28 +/- 8%, augmented glucocorticoid-induced insulin resistance of peripheral glucose clearance (euglycemic clamp), and increased circulating lipids. IGF-I administration resulted in both increased endogenous glucose production and increased peripheral glucose clearance such that plasma glucose concentrations remained unchanged by IGF-I. IGF-I lowered circulating GH and insulin and altered IGF binding proteins, which all may have reduced bioactivity of IGF-I. The data demonstrate that, in spite of similar total IGF-I plasma concentrations during treatment, GH and IGF-I exert markedly different effects on whole body leucine, glucose, and lipid metabolism.

Adult↗
PubMed1996

Early glycogenolysis and late glycogenesis in human liver after intravenous administration of galactose.

Galactose is incorporated by a different metabolic pathway than glucose. Its contribution to glycogen synthesis has not been studied in humans. We administered galactose (0.5 g/kg iv) to overnight-fasted normal human volunteers and examined its effects on hepatic glycogen synthesis and hepatic glucose output (HGO). Hepatic glycogenesis was assessed noninvasively, determining glycogen concentration by 13C magnetic resonance spectroscopy (MRS) and liver volume by magnetic resonance imaging. HGO was determined by [6,6-2H2]glucose and gluconeogenesis calculated by adding the amount of hepatic glycogenesis to the HGO. After galactose administration, liver glycogen concentration (baseline 254 +/- 11 mmol/l) decreased in the first 45 min to 207 +/- 15 mmol/l (P < 0.05) and increased thereafter to 313 +/- 7 mmol/l (P < 0.01). Net hepatic glycogenesis was 101 +/- 12 mmol over 150 min. HGO (baseline 14.3 +/- 1.9 mumol.kg-1.min-1) increased threefold in the first 15 min and then returned to baseline. The average rate of gluconeogenesis was 12.3 mumol.kg-1.min-1. Intravenous galactose leads to an increase in hepatic glycogen and hepatic glucose output in normal humans. Competitive inhibition of UDP-glucose pyrophosphorylase by UDP-galactose could explain the apparent glycogenolysis observed early after galactose administration. 13C MRS in combination with a stable isotope tracer is a noninvasive and safe method to study hepatic carbohydrate metabolism in humans.

Adult↗
PubMed1996

Incidental adrenal mass hampers the diagnosis of an extra-adrenal phaeochromocytoma.

This report describes a 65-year-old woman with a history of phaeochromocytoma and a right-sided adrenal mass. Biochemical findings and localisation procedures suggested an extra-adrenal phaeochromocytoma which was confirmed by surgery. We conclude that an extra-adrenal tumour should be considered in the evaluation of a phaeochromocytoma even if an adrenal tumour is present--the latter may represent an 'incidental' adrenal mass.

3-Iodobenzylguanidine↗
PubMed1996

Effects of glucocorticoids and of growth hormone on serum leptin concentrations in man.

Recent data suggest an involvement of the ob gene and its product leptin in the regulation of body fat. To assess the effects of glucocorticoids and growth hormone (GH) on serum leptin and body fat, 30 normal subjects received methylprednisolone (0.5 mg.kg-1.day-1) per os for 7 days and 15 subjects received in addition sc injections of GH (0.15 IU.kg-1.day-1) twice daily (combination group). Serum leptin levels increased both in the glucocorticoid group (p < 0.02) and in the combination group (p < 0.002). When body fat was estimated by bioelectrical impedance analysis it decreased during combined treatment and remained unchanged in the glucocorticoid group. Plasma insulin concentrations increased in both groups. Resting energy expenditure (indirect calorimetry) increased in the combination group and remained unchanged in the glucocorticoid group. The finding of increased serum leptin concentrations during treatment with glucocorticoid and GH suggests that serum leptin is regulated by glucocorticoids, possibly though changes in insulin secretion, independently of changes of body fat mass.

Adult↗
PubMed1996

[Malnutrition in the hospital].

It can be expected that every fifth patient in an internal medical ward in our hospitals is malnourished. Reasons for this are consuming underlying diseases as well as psychological and social factors. The association of malnutrition and hypoalbuminemia is a marker of poor prognosis; malnutrition associated with hypoalbuminemia has also been named "protein malnutrition". However, this term is misleading and "dysproteinemic malnutrition" would be more appropriate, because hypoalbuminemia is usually not caused by protein malnutrition but rather by an underlying severe illness. The nutritional state should be assessed in all patients with suspected malnutrition; not only body composition but also body function should be determined. Elderly patients have an increased prevalence of malnutrition; among individual micronutrients vitamin D, B12 and B6 in particular are frequently diminished. Nutritional therapy should be a component of all comprehensive treatment programmes for diseases which may lead to malnutrition.

Age Factors↗
PubMed1995

[Do Type-I diabetics eat a diet in accordance with recommendations?].

The nutritional habits regarding intake of calories, carbohydrates, fat and protein of 25 nonobese type-I diabetic subjects were compared with the recommendations given at onset of diabetes by a dietician and with the official recommendations of the American Diabetes Association. Food questionnaires indicated that the subjects currently ate 39% more calories than originally recommended by the dietician. The carbohydrate part of total energy was 4 +/- 7% and thereby lower than recommended by the dietician and officially by the professional society (55%). Fat consumption was 38 +/- 7% of total energy and therefore higher than recommended (30%). 17.2% of total energy was fat with saturated fatty acids (recommendation: maximum 8 to 10%). Protein consumption was 1.25 +/- 0.35 g/kg BW/d and thereby above the recommended amounts (0.8 g/kg BW/d). Thus, dietary counseling of type-I diabetic subjects at disease onset is frequently hypocaloric, probably because of lack of appetite. Patients show a tendency to add fat and protein calories thereafter, instead of increasing carbohydrate intake. Dietary habits of type I diabetic subjects should therefore be re-evaluated periodically by a dietician and adjusted to the individual requirements and to the official guidelines.

Adult↗
PubMed1995

[Hypercholesterolemia in children and young adults: should screening be done?].

Risk factors such as hypercholesterolemia, hypertension and smoking are already operative in children and during adolescence; it has been demonstrated that they favour the development of early atherosclerosis lesions in young adults. This fact poses the question of diagnosis and treatment of risk factors. There is still controversy whether hypercholesterolemia should be searched for by universal or by selective screening, or by no screening at all. Several professional organizations favour a selective screening strategy, i.e. determination of serum cholesterol if one parent has premature coronary heart disease (before age 55 yr) or if the family has familial hyperlipidemia, in particular familial hypercholesterolemia. This strategy is advocated here: cholesterol should be measured early, i.e. between age 6 and 8 yr. A total serum cholesterol of > 5.2 mmol/l is elevated (approx. 75th percentile) and should be further evaluated and possibly treated. The presence of familial hypercholesterolemia should be looked for in particular: such individuals can now be diagnosed with molecular genetic tools, and they are particularly prone to develop premature coronary heart disease. Treatment of hypercholesterolemia is mainly of a dietary nature, or possible with a bile acid binding resin (cholestyramine). Other drugs have not been sufficiently evaluated for efficacy and safety; they may be indicated in special cases such as patients with a very high risk. Young people with familial hypercholesterolemia should be particularly counselled to avoid other risk factors such as smoking.

Adolescent↗
PubMed1995

[Practical guidelines for the administration of artificial nutrition at home (home nutrition) (SAEPE; Swiss Work Group for Enteral and Parenteral Nutrition)].

The number of outpatients with major difficulties in feeding themselves is constantly growing. This results into severe malnutrition resulting in increased infection rate, physical disabilities, skin sores, increased therapeutic costs and poor quality of life. Home nutritional support can cover all nutritional needs but requires appropriate indications, optimal technical management and cautious ethical evaluation. In addition, the overall costs should be covered by an insurance at the time of home nutritional support prescription. Swiss home nutritional support recommendations for practising physicians are presented.

Enteral Nutrition↗
PubMed1995

Peptidolactones.

Explore the source record for details and available documents.

Amino Acid Sequence↗
PubMed1995

Comparative effects of recombinant human insulin-like growth factor I and insulin on whole-body and forearm palmitate metabolism in man.

1. The effects of intravenous infusions of recombinant human insulin-like growth factor I and insulin on palmitate kinetics, lipolysis and on serum triacylglycerol were compared. Overnight-fasted normal subjects received high doses of insulin-like growth factor I (30 micrograms h-1 kg-1) and insulin (0.23 nmol h-1 kg-1; group 1), low doses of insulin-like growth factor I (5 micrograms h-1 kg-1) and insulin (0.04 nmol h-1 kg-1; group 2) or saline (control group). The doses of insulin-like growth factor I and insulin were equipotent with regard to increases in glucose uptake during 8 h euglycaemic clamping. 2. Whole-body palmitate flux (measured by continuous infusions of [2,2-D2]palmitate) was lowered dose-dependently by 68% +/- 6% during insulin-like growth factor I and by 82% +/- 2% during insulin after 8 h of infusions of high doses (insulin-like growth factor I versus insulin; not significant). Plasma palmitate, glycerol and triacylglycerol concentrations had decreased to a similar extent at the end of the infusions of both peptides at either dose. 3. The present results demonstrate that insulin-like growth factor I and insulin infused at doses which result in identical increases in glucose uptake during euglycaemic clamping are equipotent inhibitors of lipolysis.

Adult↗
PubMed1995

Insulin sensitivity in obese hypertensive dyslipidemic patients treated with enalapril or atenolol.

We evaluated the effects of enalapril [angiotensin converting enzyme (ACE) inhibitor] in comparison with atenolol (beta-blocker) on insulin sensitivity and serum lipoprotein concentration in obese hypertensive dyslipidemic patients. Twenty-eight hypertensive [mean blood pressure (MAP) 152 +/- 3/103 +/- 1 mm Hgl], obese [mean body mass index (BMI) 30 + 1 kg/m2A], dyslipidemic [total triglycerides 2.0 +/- 0.2 mM and/or high density lipoprotein (HDL) cholesterol 1.1 +/- 0.1 mM and low density lipoprotein (LDL) cholesterol 4.5 +/- 0.2 mM] outpatients were randomized in two groups receiving enalapril or atenolol for 12 weeks, in an investigator-blinded, parallel, comparative two-center trial. Insulin sensitivity was assessed by a modified insulin suppression test. Blood pressure (BP), insulin sensitivity, and serum lipoprotein concentrations were compared before and after each treatment and between the two treated groups. BP decreased significantly and comparably during enalapril and atenolol treatment (p < or = 0.01). The sensitivity to insulin improved by 15% (p = 0.03) in the enalapril group and worsened by 17% (p < or = 0.01) in the atenolol group. Serum lipoprotein concentrations were not modified by any treatment. The improvement in insulin sensitivity caused by enalapril treatment appears to be an advantage as compared with atenolol treatment in hypertensive obese and dyslipidemic patients, whereas the BP-lowering efficacy of the two drugs is similar. Because this effect has been reported with other ACE inhibitors, it appears to be characteristic of the entire class of ACE inhibitors.

Adrenergic beta-Antagonists↗
PubMed1995

Protein content of the evening meal and nocturnal plasma glucose regulation in type-I diabetic subjects.

The effect of two isocaloric evening meals (low protein-high fat vs. high protein-low fat content) on plasma glucose regulation during the night were compared. Eight C-peptide-deficient type-I diabetic subjects without autonomic neuropathy were treated with fixed doses of continuous infusions of insulin during 2 nights. At 7 p.m. they received in random order either a low protein-high fat (5% of total energy protein, 60% fat, 35% carbohydrate) or a high protein-low fat (35% protein, 30% fat, 35% carbohydrate) evening meal. Venous plasma samples were drawn hourly thereafter. Plasma glucose concentrations were similar postprandially during the 2 nights between 7 p.m. and 11 p.m., but they were higher in the early morning hours after the high protein meal (p < 0.02 vs. the low protein meal). Two subjects developed symptomatic hypoglycemia after the low protein meal. Plasma glucagon concentrations were higher (p = 0.023) and serum free insulin lower (p < 0.05) after the high protein-low fat meal. Plasma cortisol and growth hormone were not significantly different between the two diets. Therefore, an increase in the protein content of the evening meal (fat content diminished) increases plasma glucose concentrations several hours later in the night, possibly due to protein-induced glucagon secretion and to lower plasma free insulin levels. Patients with type-I diabetes with a tendency to develop hypoglycemia during the night may avoid this problem by increasing the protein content of the evening meal.

Blood Glucose↗