PubMed Health⌕ Search

Biomedical subjects

M J Müller

Publications and source records attributed to M J Müller.

At least 163 records · Page 9Linked to original sources
PubMed1990

Evidence that hyperglycaemia per se does not inhibit hepatic glucose production in man.

The effect of hyperglycaemia on hepatic glucose production (Ra) was investigated in nine healthy men using sequential clamp protocols during somatostatin infusion and euglycaemia (0-150 min), at plasma glucose levels of 165 mg x dl-1 (9.2 mM, 150-270 min) and during insulin infusion (1.0 mU x kg-1 x min-1, 270-360 min) in study 1 or during hypo-insulinaemia and plasma glucose levels of 220 mg x dl-1 (12.2 mM; 270-390 min) in study 2. Somatostatin decreased Ra and glucose disposal rate (Rd) but increased plasma free fatty acids (FFA) and lipid oxidation during euglycaemia. Increasing plasma glucose to 165 mg x dl-1 (9.2 mM) and hypo-insulinaemia increased Rd, but no suppressive effects on Ra, plasma FFA and lipid oxidation were observed. By contrast hyperinsulinaemia (study 1), as well as a further increase in plasma glucose (study 2), both decreased Ra. However, more pronounced hyperglycaemia increased insulin secretion despite somatostatin resulting in a fall in plasma FFA and lipid oxidation. Our data questions the accepted dogma that hyperglycaemia inhibits Ra independently of insulin action.

Adult↗
PubMed1990

Thyroid hormone action on lipid metabolism in humans: a role for endogenous insulin.

The effects of moderate hyperthyroidism on lipid metabolism were investigated in six healthy subjects before and after thyroxine treatment (300 micrograms/d). T4-treatment increased basal metabolic rate (+8%) and glucose oxidation (+87%), without affecting lipid oxidation, plasma free fatty acids, glycerol, and beta-hydroxybutyrate. During euthyroidism, a hypoinsulinaemic-euglycaemic 150-minute clamp protocol increased energy expenditure (+3%), lipid oxidation (+42%), plasma free fatty acids (+254%), glycerol (+232%), and beta-hydroxybutyrate (+343%), but decreased glucose oxidation (-20%). Similar effects were observed after T4-treatment, but hyperthyroidism induced disproportionate increases in energy expenditure (+7%), plasma glycerol (+310%), and ketone body levels (+436%). We conclude that moderate hyperthyroidism enhances hypoinsulinemia-induced increases in lipolysis, free fatty acid recycling, and ketogenesis without affecting lipid oxidation. Thus basal insulin may camouflage some of thyroid hormone action on lipid metabolism.

3-Hydroxybutyric Acid↗
PubMed1990

Thermogenic effect of thyroid hormones: interactions with epinephrine and insulin.

The interactions between thyroid hormones, epinephrine, and insulin in the regulation of energy expenditure were investigated in a group of healthy young men before and after thyroxine (T4) treatment (300 micrograms/day for 14 days) at basal plasma insulin concentrations and during hypoinsulinemia with and without epinephrine infusion (0.05 micrograms.kg fat-free mass-1.min-1). T4 treatment induced moderate hyperthyroidism and increased resting energy expenditure (RMR). The effect was more pronounced during short-term hypoinsulinemia, but hypoinsulinemia by itself did not influence RMR. Epinephrine infusion caused a significant increase in energy expenditure. The effect was most pronounced at hypoinsulinemia and with T4 treatment. Hypoinsulinemia and T4 treatment were not additive in their effects. We conclude that basal insulin concentrations mask some of the thermogenic effects of thyroid hormones and epinephrine. Thus insulin antagonism may suppress some of the thermogenic actions of thyroid hormones and epinephrine.

Adult↗
PubMed1990

Increased resting energy expenditure in malnourished patients with cystic fibrosis.

Two recent studies (Shepherd 1988, Buchwals 1988) suggest that the malnutrition of CF may be associated with an energy-requiring defect leading to increased resting energy expenditure (REE). We investigated REE in relation to lean body mass (LBM) in 8 malnourished children with CF prior to the insertion of a gastrostomy tube. Two groups of age-matched (N1, n = 6) and weight-matched (N2, n = 5) healthy children served as controls. REE was measured by indirect calorimetry (Deltatrac Metabolic Monitor, Datex Instruments, Finland); FFM was determined by means of bioelectric impedance (BIA 103, RJL Systems, Detroit, U.S.A.). Malnourished patients with CF had higher expenditures than predicted by the Harris-Benedict equation (+32.7%). REE per kg LBM per day was markedly increased (+38.5%) compared to weight-matched controls. These results suggest that malnourished patients with CF have higher energy requirements than would be expected by the use of standard equations for caloric expenditure.

Basal Metabolism↗
PubMed1990

Nutritional consequences of total gastrectomy: the relationship between mode of reconstruction, postprandial symptoms, and body composition.

Body composition, postprandial symptoms, and social performance were assessed in 41 patients who were free of tumors 16 to 63 months (median, 41 months) after total gastrectomy with Roux-en-Y esophagojejunostomy (n = 15) or jejunal interposition (n = 26). There were no significant differences with respect to age, sex, initial tumor stage, interval since operation, and premorbid weight/height2 (body mass index). The lowest postoperative body mass index (BMI) was 72% +/- 3% of the preillness BMI in patients with Roux-en-Y reconstruction and 79% +/- 2% in patients with jejunal interposition (p less than 0.05). At the time of the study the relative BMI was 88% +/- 2% of the preillness BMI in patients with jejunal interposition but only 81% +/- 3% in patients with the Roux-en-Y reconstruction (p less than 0.01). Muscle mass and lean body mass estimated from anthropometric and bioelectric impedance measurements were correlated with sex (p = 0.0001) and with the mode of reconstruction (p = 0.02) independently, which was confirmed by multiple linear regression. The postprandial symptoms were not significantly associated with changes in body composition except for an inverse relationship between Sigstad's dumping score and the extracellular mass/body cell mass ratio (r = 0.553; p = 0.0002). Of the patients under 60 years of age, 10 of 15 patients with jejunal interposition and two of eight patients with Roux-en-Y reconstruction were back at work (p = 0.057). The persons who had resumed their work had a significantly higher relative BMI (90% +/- 2% vs 82% +/- 3%), lean body mass (53 +/- 3 kg vs 46 +/- 3 kg), and muscle mass (25 +/- 2 kg vs 21 +/- 1 kg) than persons in early retirement. We concluded that preserving the duodenal transit should be a main objective of gastric replacement after total gastrectomy.

Anastomosis, Roux-en-Y↗
PubMed1989

Energy expenditure in children with type I diabetes: evidence for increased thermogenesis.

The aim of the study was to assess whether increased energy expenditure causes the negative energy balance (tissue catabolism) commonly seen in children with insulin dependent (type I) diabetes. Resting metabolic rate and thermogenesis induced by adrenaline were measured in five healthy children and 14 children with type I diabetes who were all free of clinical signs of late complications of diabetes mellitus but differed in their degree of glycaemic control (in eight glycated haemoglobin concentration was less than 10% and in the six others greater than or equal to 10%). When compared with the control subjects children with type I diabetes had normal resting metabolic rates but their urinary nitrogen excretion was significantly raised (11.5 (SD 5.4) mg/min in those with glycated haemoglobin concentration less than 10%, 11.6 (5.2) mg/min in those with concentration greater than or equal to 10% v 5.4 (3.0) mg/min in control subjects). During the infusion of adrenaline the diabetic children showed a threefold and sustained increase in thermogenesis and disproportionate increases in the work done by the heart, in lipid oxidation rate, and in plasma concentrations of glucose, free fatty acids, and ketone bodies. The increased thermogenic effect of adrenaline did not correlate with the degree of glycaemic control. Increased thermogenesis may explain the tissue wasting commonly seen in children with type I diabetes during intercurrent stress.

Adolescent↗
PubMed1989

Glucoregulatory function of thyroid hormones: evidence for an insulin-independent effect.

The effect of hyperglycemia on glucose kinetics was investigated in normal and T4-treated miniature pigs. 1. T4-treatment increased basal plasma glucose (G) (+ 20%) and glucose turnover (+36%). 2. Glucose infusion (2 mg/kg x min) in controls increased insulin and glucose utilization (Rd), but decreased glucagon and hepatic glucose production (Ra). After T4-treatment glucose increased insulin, decreased glucagon and Ra but only a slight effect on G and Rd were observed. 3. Infusing glucose + somatostatin resulted in hyperglycemia in both groups due to an initial fall in Ra and Rd followed by an increase in Rd, where total Ra (endogenous + exogenous exceeded Rd. Glucose intolerance was more pronounced in controls, due to a T4-induced increase in Rd. During this non-steady state the increment in Rd per increment in G was calculated and showed 1.5 in controls and 2.5 after T4-treatment. These data give evidence that thyroid hormones increase glucose utilization during hypoinsulinemia.

Animals↗
PubMed1989

Glucoregulatory function of thyroid hormones: role of pancreatic hormones.

Glucose metabolism was investigated in humans before and 14 days after 300 micrograms L-thyroxine (T4)/day using a sequential clamp protocol during short-term somatostatin infusion (500 micrograms/h, 0-6 h) at euglycemia (0-2.5 h), at 165 mg/dl (2.5-6 h), and during insulin infusion (1.0 mU.kg-1.min-1, 4.5-6 h). T4 treatment increased plasma T4 (+96%) and 3,5,3'-triiodothyronine (T3, +50%), energy expenditure (+8%), glucose turnover (+32%), and glucose oxidation (Glucox +87%) but decreased thyroid-stimulating hormone (-96%) and nonoxidative glucose metabolism (Glucnonox, -30%) at unchanged lipid oxidation (Lipox). During somatostatin and euglycemia glucose production (Ra, -67%) and disposal (Rd, -28%) both decreased in euthyroid subjects but remained at -22% and -5%, respectively, after T4 treatment. Glucox (control, -20%; +T4, -25%) fell and Lipox increased (control, +42%; +T4, +45%) in both groups, whereas Glucnonox decreased before (-36%) but increased after T4 (+57%). During somatostatin infusion and hyperglycemia Rd (control, +144%; +T4, +84%) and Glucnonox (control, +326%; +T4, +233%) increased, whereas Glucox and Lipox remained unchanged. Insulin further increased Rd (+76%), Glucox (+155%), and Glucnonox (+50%) but decreased Ra (-43%) and Lipox (-43%). All these effects were enhanced by T4 (Rd, +38%; Glucox, +45%; Glucnonox, +35%; Ra, +40%; Lipox, +11%). Our data provide evidence that, in humans, T3 stimulates Ra and Rd, which is in part independent of pancreatic hormones.

Adult↗
PubMed1989

[The value of computer-assisted sonographic tissue characterization in focal lesions of the thyroid].

Thyroid lesions are a common observation in ultrasound examination. In most cases the differentiation of malignant and benign tissue is difficult. In this study 133 thyroid lesions were examined by an ultrasonographic tissue characterization system prior to surgery. The pathologic findings (29 cancers, 31 adenomas, 46 nodular goiters, 27 cysts) were examined with reference to the quantitative evaluation of the ultrasonic images (ROI method). The selected regions of interest (ROI) were analyzed with regard to the three most discriminating parameters. The overall accuracy of differentiation between malignant and benign thyroid nodules was 83.9%.

Adenocarcinoma↗
PubMed1988

Glucoregulatory function of glucagon in hypo-, eu- and hyperthyroid miniature pigs.

The glucoregulatory function of glucagon was investigated in hypo-, eu- and hyperthyroid miniature pigs. Infusion glucagon, (3 ng x kg body weight-1.min-1) transiently increased blood glucose (p less than 0.01) and hepatic glucose production (p less than 0.01) in euthyroidism, but was without effect in hyperthyroidism. Infusing glucagon plus somatostatin (2 ng x kg body weight-1.min-1 and 0.2 microgram x kg body weight-1.min-1) transiently increased blood glucose (delta 3.0 to 4.3 mmol/l) and hepatic glucose production (delta 3.3 to 7.7 mumol x kg body weight-1.min-1) in all thyroid states, the effect was less pronounced in hyperthyroid pigs. By contrast, hypoglucagonaemia (74 to 107 pg/ml) at basal insulin (28 to 35 microU/ml) provoked hypoglycaemia (1.4 to 2.2 mmol/l) and a fall in glucose production (delta 4.7 to 8.3 mumol x kg body weight-1.min-1), which was independent of the thyroid state; the effect was most pronounced in hyperthyroidism (p less than 0.01). Hepatic glycogen content, arterial gluconeogenic precursor concentrations as well as the glycaemic response (delta 0.60 mmol/l) to alanine infusion (23 mumol x kg body weight-1.min-1) were all unaffected by hyperthyroidism. We conclude that moderate experimental hyperthyroidism reduces glucagon action due to reduced glycogen mobilisation. This may in part result from increased insulin sensitivity.

Animals↗
PubMed1988

Regulation of hepatic glucose output by glucose in vivo.

The effect of infusing glucose at a rate estimated to equal hepatic glucose production (2 mg/kg BW X min) was investigated in postabsorptive unrestrained miniature pigs. Glucose turnover was estimated by the use of 3-H-glucose before and during glucose infusion where the contribution of the glucose-induced hormonal changes were estimated by infusing glucose plus somatostatin with or without insulin and/or glucagon substitution. Our data give evidence for an inhibitory effect of glucose on endogenous glucose production in the postabsorptive state. This effect seems to be independent of the hormonal changes induced by glucose infusion.

Animals↗
PubMed1988

Effect of thyroid hormones on oxidative and nonoxidative glucose metabolism in humans.

The glucoregulatory function of thyroid hormones was investigated in six healthy subjects before and after 14 day 3,5,3',5'-tetraiodothyronine (T4) treatment (300 micrograms/day) using a sequential clamp protocol for 5 h at euglycemia (0-2 h) and hyperglycemia (165 mg/dl, 2-5 h) and different insulin infusion rates (1.0 for 0-3.5 h and 6.5 mU.kg-1.min-1, for 3.5-5 h). T4 treatment increased basal energy expenditure (+8%), glucose disposal (+31%), and oxidation (+87%) but decreased nonoxidative glucose metabolism (-30%) and was without effect on lipid oxidation. During the euglycemic clamp, T4 treatment enhanced insulin-induced glucose disposal (+16%), glucose oxidation (+34%), and inhibition of lipid oxidation (-66 vs. -40%); nonoxidative glucose metabolism was stimulated to a similar extent before and after T4. During hyperglycemia, 3,5,3'-triiodothyronine (T3) did not affect glucose disposal but increased carbohydrate-induced lipogenesis at both insulin infusion rates. We conclude that T4 treatment promotes glucose disposal and oxidation, T3 decreases noninsulin-mediated glucose storage but does not antagonize insulin action.

Adult↗
PubMed1988

Assessment of insulin action in man: role of hyperglycemia.

The effect of hyperglycemia on insulin-induced glucose metabolism (M) was investigated in healthy subjects using sequential clamp protocols at constant insulin + somatostatin infusions and varying plasma glucose. During euglycemia (4.8 mmol/l) M increased from 5.6 to 12.5 mg.kg-1.min-1 with increasing plasma insulin (0.34-3.00 nmol/l). At increasing glucose (6.7 mmol/l), M further increased (9.7 to 19.2 mg.kg-1.min-1) with the plasma insulin level (0.41 to 2.99 nmol/l). At a plasma glucose level of 9.8 mmol/l insulin (0.42 to 3.17 nmol/l) was still effective to increase M (13.7 to 25.2 mg.kg-1.min-1). Regression analysis showed that hyperglycemia does not only increase the maximal insulin-stimulated M, but also decreases the insulin concentration causing a half maximum effect. During prolonged clamp studies M increased by about 10% per h, independent by the plasma glucose level. We conclude that hyperglycemia increases M by increasing insulin responsiveness as well as insulin sensitivity. Data derived from euglycemic clamp studies alone are of limited value with respect to the assessment of insulin action.

Adult↗
PubMed1987

Insulin receptor binding to blood cells: an outdated concept for clinical studies on insulin resistance?

Clinical data on insulin binding to blood cells contribute to our present knowledge of insulin resistance. Binding data have been frequently presented to indicate alterations in insulin action. It is now evident that insulin binding data are of limited value for our understanding of insulin resistance. This is mainly due to the tissue-specific binding of insulin as well as the "pleiotypic" nature of insulin action. As insulin action is determined at (a) the "pre-" receptor level, (b) the receptor, and/or (c) different postbinding sites, it is unlikely that receptor data alone can explain defective insulin action. As knowledge of the molecular biology of insulin receptor morphology and function as well as of the action of insulin on intermediary metabolism increases, clinicians should not be further overloaded with binding data. Nevertheless, binding data on blood cells may be still of some value in investigating patients with severe insulin resistance due to genetic disorders of the insulin receptor or insulin receptor autoantibodies.

Diabetes Mellitus↗
PubMed1987

Interrelation between thyroid state and the effect of glucagon on gluconeogenesis in perfused rat livers.

The effects of different thyroid states on glucagon/dBcAMP-induced gluconeogenesis from alanine or lactate were investigated in the isolated perfused liver from 24-hr starved rats. Gluconeogenesis from alanine varied with the thyroid state, being increased in hyperthyroidism and decreased in hypothyroidism. Both glucagon and dBcAMP increased glucose production from alanine in euthyroid and even less pronounced in hypothyroid livers, the effect was dose dependent; concomitantly alanine and [14C] alpha-amino-isobutyric acid uptake increased. In hyperthyroid liver, both glucagon and dBcAMP stimulated neither hepatic uptake of alanine and [14C] alpha-amino-isobutyric acid nor gluconeogenesis from alanine. Lactate uptake as well as glucose production from lactate varied with the thyroid state, being increased in the hyper- and decreased in the hypothyroid state. Both glucagon and dBcAMP increased lactate uptake as well as gluconeogenesis from lactate: the effect was even more pronounced in hyperthyroid and reduced in hypothyroid liver. We conclude that the glucogenic effect of glucagon/dBcAMP is reduced in the hypo- and--at unlimited substrate supply--stimulated in the hyperthyroid liver.

1-Methyl-3-isobutylxanthine↗