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M J Müller

Publications and source records attributed to M J Müller.

At least 145 records · Page 8Linked to original sources
PubMed1992

Jasmonic acid is a signal transducer in elicitor-induced plant cell cultures.

To deter pathogenic microorganisms and herbivores, plants have developed an inducible chemical defense system. It is known that the induced synthesis of low molecular weight compounds can be provoked by exposing cultured cells to fungal cell wall fragments. In this study we show that endogenous jasmonic acid and its methyl ester accumulate rapidly and transiently after treatment of plant cell suspension cultures of Rauvolfia canescens and Eschscholtzia californica with a yeast elicitor. Thirty-six plant species tested in cell suspension culture could be elicited with respect to the accumulation of secondary metabolites by exogenously supplied methyl jasmonate. Addition of methyl jasmonate initiates de novo transcription of genes, such as phenylalanine ammonia lyase, that are known to be involved in the chemical defense mechanisms of plants. These data demonstrate the integral role of jasmonic acid and its derivatives in the intracellular signal cascade that begins with interaction of an elicitor molecule with the plant cell surface and results, ultimately, in the accumulation of secondary compounds.

Journal Article↗
PubMed1992

Energy expenditure and substrate oxidation in patients with cirrhosis: the impact of cause, clinical staging and nutritional state.

Many clinicians subjectively feel that cirrhotic patients frequently have clinical signs of hypermetabolism. However, it is unknown whether hypermetabolism is a constant feature of chronic liver disease, corresponds to liver destruction and repair or is of prognostic value. This article is about resting energy expenditure and substrate oxidation rates in 123 patients with biopsy-proven cirrhosis differing with respect to cause, duration of the disease, biochemical parameters of parenchymal cell damage, cholestasis, liver function, number of complications, clinical staging and nutritional state. Resting energy expenditure varied between 1,090 and 2,300 kcal/day and differed from the predicted values in 70% of the patients. Resting energy expenditure was closely related to fat-free mass, and 52% of the variability could be explained by fat-free mass, age and sex. Of all the patients, 18% were hypermetabolic and 31% were hypometabolic. Hypermetabolism showed no strict association with the cause of cirrhosis, the duration of the disease, liver function, cholestasis, cell damage, clinical staging, blood hemoglobin, plasma thyroid hormone levels or human leukocyte antigens. An increased resting energy expenditure was associated with significant losses of muscle, body cell mass and extracellular mass at unchanged body fat, whereas fat and fat-free mass were increased in hypometabolic patients when compared with normometabolic patients. Lipid oxidation was increased, but glucose oxidation was reduced in nearly all patients with cirrhosis. This was most pronounced at advanced stages of liver disease. Although similar with respect to liver function and clinical staging, 76.2% of hypermetabolic patients had transplants within the observation period, compared with only 16.7% and 8.1% in the normometabolic group and hypometabolic group, respectively. Posttransplantation mortality was independent of pretransplantation resting energy expenditure, but it increased significantly in patients with losses in body cell mass. In conclusion, hypermetabolism is not a constant feature of cirrhosis and results more from extrahepatic than from hepatic factors. It may cause malnutrition and contributes to the clinical outcome of patients with chronic liver disease.

Adult↗
PubMed1992

[Significance of preoperative weight loss for perioperative metabolic adaptation and surgical risk in patients with tumors of the upper gastrointestinal tract].

Body composition and energy expenditure were investigated before and 10-14 days after surgery in 44 patients with upper gastrointestinal cancer (23 esophageal and 21 gastric cancer) in order to assess the impact of preoperative weight loss on metabolic adaptation to the surgical trauma and on postoperative complications. Patients were divided in three groups with I: 0-5%, II: 5-10% and III: greater than 10% preoperative weight loss related to the usual body weight. 50% of the patients presented with no or just minor weight loss. Even in case of weight loss greater than 10% no decrease below the ideal body weight was observed. Body cell mass and fat mass were significantly (p less than 0.05) reduced in group III when compared with I. Since energy expenditure and substrate oxidation rates were rather normal in most patients weight loss was considered to be due to tumor related stenosis and dysphagia. More than 50% of the energy requirements were gained from fat oxidation. General criteria of malnutrition were not fulfilled. Perioperative weight loss was lowest (1.6 +/- 4.9 kg) in patients of group III related to group I (2.9 +/- 1.7 kg) and II (5.0 +/- 6.9 kg). Similar elevation of energy expenditure and lipid oxidation with concomitant reduction in glucose oxidation was observed in all groups of patients. This led to a similar decrease of body cell mass. Independent of preoperative weight loss major complications occurred in 8 cases--pneumonia in 6 and leakage of the anastomosis in 2 patients; no patient died. From this study can be concluded that with regard to perioperative weight loss the metabolic response to surgical trauma is adequate even in patients with marked preoperative weight loss. These patients remain compensated and preoperative weight loss is without major effect on postoperative complication rate.

Adult↗
PubMed1992

Protein-calorie malnutrition in liver cirrhosis.

The purpose of this article is to present detailed data on the nutritional assessment in cirrhotic patients. The exact frequency and types of malnutrition, its associations with the aetiology of liver disease, liver dysfunction and clinical staging in liver cirrhosis are unknown. A new classification system is presented which may help to suggest some interventional guidelines. Physical (anthropometry, 24-h urinary creatinine excretion, bioelectrical impedance analysis (BIA), total body potassium counting, ultrasound examination) and metabolic (indirect calorimetry) assessment of nutritional status was therefore performed in 123 patients with liver cirrhosis, who were considered as potential candidates for liver transplantation. Data were related to the clinical, biochemical, histological and prognostic data of liver disease. Of our patients 65% showed some signs of protein-calorie malnutrition as indicated by low body cell mass, reduced serum albumin concentrations or abnormal skinfold thickness. Of these 34% were considered as "kwashiorkor-like" (normal body composition, serum albumin less than 35 g/l), and 18% were "marastic" (reduced body weight, body cell mass, and fat mass). However, 49% of the malnourished group had reduced body cell mass in association with increased fat mass and frequently presented with a normal body weight ("mixed" or "obese" type). Protein-calorie malnutrition did not correlate with the aetiology of the disease and biochemical parameters of liver function. Malnutrition was observed at all clinical stages but was more frequently seen at advanced stages. We conclude that malnutrition associated with liver cirrhosis is not a clear phenomenon. Its clinical presentation is heterogenous and not reflected by the histological or biochemical parameters of liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Mechanism of insulin resistance associated with liver cirrhosis.

Insulin-induced glucose metabolism was investigated in 26 patients with biopsy-proven liver cirrhosis and 10 control subjects. Two glucose clamp protocols together with continuous indirect calorimetry were performed to examine whether reduced rates of glucose oxidation and/or nonoxidative glucose metabolism explain insulin resistance in liver cirrhosis. Using a 4-hour, two-step protocol (0-2 hours, plasma glucose 5.2 mmol/L, plasma insulin 92 mU/L to test the half-maximum response; 2-4 hours, hyperglycemia 10.0 mmol/L, plasma insulin 442 mU/L to test the maximum cellular glucose disposal) liver cirrhosis reduced glucose disposal to 45% and 60% of control values, respectively. Simultaneously, insulin-induced increases in glucose oxidation, plasma lactate levels, and lipogenesis were normal, whereas nonoxidative glucose metabolism was reduced (-82% and -47% of controls, respectively). To determine whether reduced nonoxidative glucose metabolism was caused by reduced glucose disposal, glucose disposal was "matched" to normal values in a subgroup of cirrhotic patients. Nonoxidative glucose metabolism values were normal, but plasma lactate concentrations disproportionally increased (+96%) after "matching" glucose disposal. Insulin resistance was independent of the etiology of the cirrhosis, the biochemical parameters of parenchymal cell damage and liver function, and the clinical and nutritional state of the patients. It is concluded that liver cirrhosis impairs insulin sensitivity and maximum cellular glucose disposal. Reduced glucose disposal is caused by defective glucose storage. Insulin resistance is independent of the etiology of liver cirrhosis and of the clinical and nutritional state of the patient.

Adult↗
PubMed1992

Thermic effect of epinephrine: a role for endogenous insulin.

The contribution of the basal insulin concentration to the metabolic response to epinephrine was measured in eight, postabsorptive, healthy volunteers before and during epinephrine (0.05 micrograms/kg fat-free mass [FFM] x min) and somatostatin (500 micrograms/h) infusion with and without insulin (0.1 mU/kg body weight [BW] x min) replacement. At basal plasma insulin concentrations, epinephrine increased oxygen consumption, heart rate, heart work, hepatic glucose production, glycogen breakdown in liver and muscle, and glucose oxidation, and the arterial plasma concentrations of glucose, lactate, and free fatty acids. Similar effects were observed during hypoinsulinemia, but epinephrine's actions on oxygen consumption and plasma concentrations of free fatty acids were disproportionally enhanced. We conclude that epinephrine-induced thermogenesis is partially inhibited by basal plasma insulin concentrations.

Adult↗
PubMed1992

Metabolic responses to lipid infusions in patients with liver cirrhosis.

Energy expenditure, whole body substrate oxidation rates and arterial substrate concentrations were measured in 14 patients with liver cirrhosis and 13 control subjects before and during sequential infusions of a long chain (LCT) or a medium chain triglyceride emulsion (MCT) without and with concomitant insulin plus glucose infusions. Resting energy expenditure, basal substrate oxidation rates and the arterial concentrations of glucose, lactate, triglycerides and ketones were normal, whereas plasma free fatty acids and glycerol were both increased in patients with liver cirrhosis. The arterial plasma triglyceride and free fatty acid concentrations as well as whole body lipid oxidation rate rose in response to LCT in both groups and the maximum lipid oxidation rate was 1.1 or 1.3 mg/kg fat free mass x min in controls and in cirrhotics, respectively (n.s.). Concomitantly, glucose oxidation rate fell to 65% of basal values in controls (p < 0.01), but remained nearly unchanged in the cirrhotic group (89% of the basal value; n.s.). The increase in plasma ketones was reduced to 67% of control values in liver cirrhosis (p < 0.01). Only a slight effect on energy expenditure was observed in both groups. When compared to controls, liver cirrhosis impaired insulin-induced increases in glucose disposal (-30%, p < 0.01) and in non oxidative glucose metabolism (-93%, p < 0.01). Concomitantly, normal increases in energy expenditure, glucose oxidation rate and the arterial plasma lactate concentrations and normal decreases in lipolysis, lipid oxidation and ketogenesis were observed in patients with liver cirrhosis. When lipids were given together with glucose, energy expenditure and lipid oxidation increased in controls, but glucose was the preferred fuel oxidised and lipid-induced thermogenesis was reduced in the cirrhotic group. Using a 50% MCT-emulsion, plasma free fatty acid concentrations further increased, but energy expenditure and lipid oxidation remained unchanged in both groups and further increases in plasma ketones were only observed in controls. Infusing glycerol in a subgroup of patients showed no thermogenic effect and a reduced glycerol clearance in liver cirrhosis.

Journal Article↗
PubMed1992

Resting energy expenditure and the thermic effect of adrenaline in patients with liver cirrhosis.

1. Resting energy expenditure and the metabolic responses to adrenaline (infusion rate: 0.03 micrograms min-1 kg-1 fat-free mass for 1 h) were investigated in 25 patients with liver cirrhosis. The patient group was heterogeneous and varied with respect to the aetiology of cirrhosis, the clinical condition (i.e. Child A or B), the nutritional status and the degree of hyperinsulinaemia. 2. When compared with 10 healthy control subjects the basal plasma adrenaline and noradrenaline concentrations were both increased in cirrhosis and remained elevated during adrenaline infusion (+39% and +31%, respectively; P < 0.05). Concomitantly, the peripheral plasma insulin concentration and the molar C-peptide/insulin ratio were increased in liver cirrhosis (+96% and +30%, respectively; P < 0.05). Hyperinsulinaemia was more pronounced in patients with ethanol-induced liver cirrhosis. 3. When expressed per kg fat-free mass, resting energy expenditure was enhanced in liver cirrhosis (+21%; P < 0.05) and was more pronounced (i.e. resting energy expenditures of +35% to +49% above estimated values) in patients with ethanol-induced cirrhosis, at advanced stages of the disease and in association with decreased body cell mass. 4. Infusion of adrenaline increased heart rate, O2 consumption and the plasma concentrations of glucose, lactate, free fatty acids, glycerol and 3-hydroxybutyrate, and similar transient increases and subsequent decreases in the respiratory quotient were observed in both groups. However, the lipolytic, ketogenic and thermic responses were reduced in cirrhotic patients. Reduced metabolic responses were more pronounced in hyperinsulinaemic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The Norcoclaurine Pathway is Operative in Berberine Biosynthesis in Coptis japonica.

The commercially used cell suspension culture of COPTIS JAPONICA Makino (Ranunculaceae) incorporates [beta- (13)C]tyrosine into both halves of the berberine molecule (isoquinoline and benzyl portion) while L-[3'- (18)O]DOPA only labels the isoquinoline portion of this molecule. This labelling pattern indicates that different C (6)-C (2) units derived from tyrosine form this molecule. This result and the incorporation of ( S)-[1- (13)C] norcoclaurine into berberine demonstrates that the biosynthesis of protoberberine alkaloids in COPTIS involves the norcoclaurine but not the norlaudanosoline pathway.

Journal Article↗
PubMed1992

Thermogenesis and fructose metabolism in humans.

Resting metabolic rate was measured in 10 healthy volunteers (25 yr, 73 kg, 182 cm) for 1 h before and 4 h during intravenous (iv) fructose administration (20% at 50 mumol.kg-1.min-1) with (+P) or without (-P) propranolol (100 micrograms/kg, 1 microgram.kg-1.min-1) during the last 2 h. Some subjects were studied a further 2 h with fructose infusion and +P or -P in hyperinsulinemic (2.9 pmol.kg-1.min-1) euglycemic conditions. Glucose turnover ([3-3H]glucose, 20 muCi bolus and 0.2 muCi/min) was calculated over 30 min at 0, 2, 4, and 6 h. The thermic effect of iv fructose was approximately 7.5% and decreased to 4.9 +/- 0.4% (P less than 0.01) +P. During the euglycemic clamp the thermic effect was 6.2 +/- 0.9% (-P) and 5.3 +/- 0.9% (+P). Hepatic glucose production (HGP) was 11.7 mumol.kg-1.min-1 (0 h) and did not change after 2 h iv fructose (11.8 +/- 0.5 and 9.8 +/- 0.6 mumol.kg-1.min-1 -P and +P, respectively) but increased to 13.8 +/- 0.9 (-P) and 12.9 +/- 0.8 mumol.kg-1.min-1 (+P) (P less than 0.01) after 4 h. HGP was suppressed to varying degrees during the euglycemic clamp. It is concluded that 1) the greater thermic effect of fructose compared with glucose is probably due to continued gluconeogenesis (which is suppressed by glucose or glucose-insulin) and the energy cost of fructose metabolism to glucose in the liver. 2) There is a sympathetically mediated component to the thermic effect of fructose (approximately 30%) that is not mediated by elevated plasma insulin concentrations similar to those observed with iv glucose.

Adrenergic beta-Antagonists↗
PubMed1991

Malnutrition and immune dysfunction in patients infected with human immunodeficiency virus.

STUDY OBJECTIVE: To determine forms of malnutrition and basal metabolism at different stages of immunological impairment in clinically stable patients infected with Human Immunodeficiency Virus (HIV). DESIGN: Cross sectional study. SETTING: 53 outpatients with HIV-infection classified according to the Walter Reed staging system (WR1 to WR6). MEASUREMENTS AND MAIN RESULTS: 87% of the patients showed some evidence of malnutrition. Reduced body weight was found in 53%, 68% and 25% had decreases in fat and body cell mass, 17% had visceral protein deficiency, whereas extracellular mass and serum triglyceride concentrations were increased in 58% and 30%, respectively. Reduced serum albumin and transferrin closely paralleled immunological depression, whereas alterations in body composition were manifest early during HIV-infection (WR3) and remained unchanged during the transition to the Acquired Immune Deficiency Syndrome itself. Resting metabolic rate increased from WR1 to WR3; it remained within the expected range during later stages (WR4-WR6), but was not appropriately reduced in response to the loss in body cell mass. CONCLUSIONS: HIV-infected patients display both, calorie and protein malnutrition. Immunological depression was independent of loss of body mass, but was closely associated to decreases in serum albumin values. Nutritional assessment and intervention should therefore be performed at an early stage of HIV-infection.

Adult↗
PubMed1991

Pathophysiology and clinical basis of prevention and treatment of complications of chronic liver disease.

Chronic liver failure is characterized by the appearance of jaundice, ascites, encephalopathy and/or gastrointestinal bleeding. Acute episodes of hepatic decompensation are frequently precipitated by additional events, e.g. septicaemia, diuretic therapy or excessive protein intake. Identification, correction and treatment of these precipitating factors are first steps in the management of chronic liver failure. Nutritional support is important in the treatment of cirrhotic patients, because malnutrition is one of the major determinants of patient outcome. Management of encephalopathy reduces the appearance of gut-derived nitrogenous toxins and corrects imbalances in amino acid metabolism. Treatment of ascites is salt restriction supported by gentle and incremental administration of diuretics. Ursodesoxycholic acid has become a new and promising modality in the management of cholestatic liver diseases. If conservative therapy fails to recompensate liver function, liver transplantation may be indicated.

Ascites↗
PubMed1991

Thermogenic effect of adrenaline: interaction with insulin.

The contribution of insulin (3.6 pmol.kg body mass-1.min-1) to adrenaline-induced (0.164 nmol.kg fat free mass-1.min-1) thermogenesis was studied in ten postabsorptive healthy volunteers using two sequential protocols. Variables considered were oxygen consumption as well as carbon dioxide production, heart rate, blood pressure, plasma concentrations of glucose, insulin, glycerol, free fatty acids, beta-HO-butyrate and lactate. Adrenaline increased plasma concentrations of glucose, glycerol, free fatty acids, and beta-HO-butyrate, and heart rate and metabolic rate during normo-insulinaemia [61.3 (SEM 6.6) pmol.l-1]. Similar effects were observed during hyperinsulinaemia [167.9 (SEM 18.7) pmol.l-1], but the effect of adrenaline on oxygen consumption was reduced. On average, metabolic rate increased by 12.9% during normo-insulinaemia and by 8.9% during hyperinsulinaemia. We concluded that relative hyperinsulinaemia resulted in decreased adrenaline-induced thermogenesis and therefore increased whole body anabolism.

3-Hydroxybutyric Acid↗
PubMed1991

Energy expenditure and substrate metabolism in ethanol-induced liver cirrhosis.

Energy expenditure and substrate metabolism were investigated in 10 patients with alcoholic liver cirrhosis (EtOH-Ci) and 10 healthy controls (C). Resting metabolic rate (RMR) varied from 1,269 to 2,467 kcal/day in C and from 1,228 to 2,098 kcal/day in EtOH-Ci. RMR was significantly related to fat-free mass (FFM) in both groups, but EtOH-Ci decreased FFM and increased RMR when expressed per kilogram FFM (+33%). Glucose intolerance, hyperinsulinemia, and a decreased C-peptide-to-insulin ratio were observed in EtOH-Ci after a test meal. Concomitantly, nonoxidative glucose metabolism was reduced in association with normal increases in glucose oxidation. EtOH-Ci reduced insulin sensitivity (-59%) and maximal insulin-dependent glucose disposal (-40%) during a sequential two-step glucose clamp protocol (phase 1: 1 mU.kg body wt-1.min-1 insulin infusion rate + euglycemia; phase 2: 4 mU.kg body wt-1.min-1 insulin infusion rate + 165 mg/dl plasma glucose concentration). This was explained by reduced glucose storage (-99%, -51%) in association with normal responses in glucose oxidation rate, plasma lactate concentration, lipid oxidation rate, and rate of lipogenesis. Defective glucose storage was independent of reduced FFM. EtOH-Ci increased glucose-induced thermogenesis by 57%. We conclude that increased resting metabolic rate, enhanced thermogenesis, defective glucose storage, and normal glucose oxidation together result in increased energy needs and favor negative energy balance in patients with alcoholic cirrhosis.

Adult↗
PubMed1991

The role of omeprazole (40 mg) in the treatment of gastric Helicobacter pylori infection.

The efficacy of omeprazole in the elimination of Helicobacter pylori was investigated in a prospective randomized-controlled trial. 50 patients with upper gastrointestinal symptoms and chronic active H. pylori-associated gastritis were allocated to one of the following four therapeutic schedules: 1) omeprazole 40 mg/d for 4 weeks (n = 13); 2) bismuth subsalicylate (BSS) 3 x 600 mg for 4 weeks (n = 12); 3) omeprazole plus BSS for 4 weeks (n = 13); 4) triple therapy (BSS for 4 weeks, amoxicillin 3 x 750 mg and metronidazole 3 x 400 mg for 10 days) (n = 12). Clinical symptoms, endoscopic and histologic findings, and H. pylori status were reassessed immediately after therapy, and 1 and 6 months later. After cessation of therapy bacterial clearance rates were: 1) omeprazole 2/13 (15%); 2) BSS 6/12 (50%); 3) omeprazole plus BSS 5/13 (38%); 4) triple therapy 10/12 (83%). The degree of density of gastric mucosal infestation with H. pylori and the degree of activity of gastritis was reduced in all treatment groups but was most prominent after triple therapy. Clinical symptoms improved in all treatment groups. One and six months after completion of therapy H. pylori eradication rates were: 1) omeprazole 0/13 (0%); 2) BSS 1/12 (8%); 3) omeprazole plus BSS 1/13 (8%); 4) triple therapy 10/12 (83%). Our study shows that 40 mg/d omeprazole is ineffective in eradicating H. pylori. Dual therapy with omeprazole and bismuth subsalicylate does not improve bacterial elimination. Only triple therapy effectively eradicates H. pylori.

Adult↗
PubMed1991

[Lipolysis and lipid oxidation of weight stable patients with malignant tumors of the digestive system].

Tumor-caused weight loss is frequently associated with a high rate of lipolysis and fat oxidation. In order to differentiate the effect of weight-loss from the tumour-dependent regulation of fat metabolism, we studied weight-stable and well nourished patients (ideal body weight 109 +/- 4% (+/- SEM), body mass index 25.1 +/- 0.9 kg/m2). Parameters of lipolysis (glycerol-, fatty acid concentrations) and the calorimetric determined fat oxidation rate of five male tumor patients were examined before and during an euglycaemic insulinclamp (0.2 mU insulin/kg/min). Concomitant with a high rate of lipolysis (glycerol concentration 112 +/- 20 mumol/l, free fatty acid concentration 0.72 +/- 0.13 mmol/l) and fat oxidation (60% of energy expenditure) there was a low normal insulin level (5.9 +/- 0.5 mU/l). Insulin reduced lipolysis and fat oxidation and stimulated glucose oxidation. Weight-stable tumor patients have a high basal rate of lipolysis and fat oxidation; yet the insulin dependent regulation of the fat metabolism is intact, as we have already shown for weight-losing cancer patients.

Adult↗