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Biomedical subjects

J Kvetny

Publications and source records attributed to J Kvetny.

At least 37 records · Page 2Linked to original sources
PubMed1990

Different short-term effect of protein and carbohydrate intake on TSH, growth hormone (GH), insulin, C-peptide, and glucagon in humans.

The effect of isocaloric (500 kcal) protein and carbohydrate ingestion was studied in a crossover study in nine healthy humans. Subjects were studied twice after overnight fasting, with an interval of 3 to 7 days. Blood was collected for 240 min after food ingestion. The initial reaction of growth hormone (GH) and thyroid stimulating hormone (TSH) to protein and carbohydrate was identical, with a reduction in both GH and TSH, and nadir occurring after 45-60 min and 120 min, respectively. During the next 120 min TSH returned to starting level after carbohydrate intake but was still reduced after protein intake (p less than 0.04). After both diets GH increased after the initial decline, the increase was greatest after protein intake and maximum was reached at 180 min (p less than 0.02). It has been reported that the 5'-deiodination of T4 is stimulated by insulin and inhibited by glucagon. The physiological increase in insulin after carbohydrate ingestion (p less than 0.05), and the physiological increase in glucagon after protein ingestion (p less than 0.05) was not associated with any changes in TT4, FT4, TT3, FT3, or rT3 that could indicate changes in the 5'-deiodinase activity.

Adult↗
PubMed1990

Alterations of serum concentrations of thyroid hormones and sex hormone-binding globulin, nuclear binding of tri-iodothyronine and thyroid hormone-stimulated cellular uptake of oxygen and glucose in mononuclear blood cells from patients with non-thyroidal illness.

Nuclear tri-iodothyronine (T3) binding and thyroid hormone-stimulated oxygen consumption and glucose uptake were examined in mononuclear blood cells from patients with non-thyroidal illness (NTI) in which serum T3 was significantly (P less than 0.05) depressed (0.62 +/- 0.12 (S.D.) nmol/l) compared with healthy control subjects (1.45 +/- 0.30 nmol/l). Neither serum TSH nor sex hormone-binding globulin differed from that of the control group. Nuclear T3 binding capacity was increased (P less than 0.05) in patients with NTI (10.1 +/- 3.0 fmol/100 micrograms DNA) compared with controls (2.5 +/- 0.9 fmol/100 micrograms DNA). Unstimulated glucose uptake was increased in cells from patients with NTI (2.03 +/- 0.49 mmol/l per mg DNA per h, P less than 0.01) compared with controls (1.13 +/- 0.20 mmol/l per mg DNA per h). Thyroxine-stimulated glucose uptake (stimulated glucose uptake--unstimulated glucose uptake) was increased in cells from patients with NTI (2.06 +/- 1.67 mmol/l per mg DNA per h, P less than 0.01) compared with controls (0.26 +/- 0.12 mmol/l per mg DNA per h), and T3-stimulated glucose uptake was also increased in cells from patients with NTI (1.34 +/- 0.81 mmol/l per mg DNA per h, P less than 0.05) compared with controls (0.24 +/- 0.10 mmol/l per mg DNA per h). In contrast, neither unstimulated nor thyroid hormone-stimulated oxygen consumption differed. We conclude that both increased nuclear T3 binding and increased thyroid hormone-induced glucose uptake may represent counter-regulatory mechanisms which tend to maintain intracellular homeostasis.

Adult↗
PubMed1990

Effect of oral glucose feeding on thyroid hormone action in human mononuclear blood cells.

The effect of glucose feeding on serum concentrations of thyroid hormones, nuclear T3 binding and thyroid hormone stimulated oxygen consumption and glucose uptake was evaluated. Six persons without thyroid diseases were fed exclusively glucose (2500 kcal/day) for two days. Glucose feeding resulted in the following serum hormone levels (before vs after glucose feeding) T3: 1.07 vs 1.16 nmol/l (p less than 0.05); FT4I: 76 vs 102 a.u. (p less than 0.05) and TSH: 1.48 vs 1.14 mU/l (n.s.). Nuclear T3 binding decreased after glucose feeding; before: maximal binding capacity (MBC) 1.3 +/- 0.5 fmol/100 ug DNA, MBC after glucose feeding: 0.8 +/- 0.2 fmol/100 ug DNA (p less than 0.05). The Ka's were identical in both groups before glucose, Ka: 4.2 +/- 1.2 x 10A10 l/mol, after glucose, Ka: 3.5 +/- 1.2 x 10(10) l/mol. Conversely did glucose feeding increase thyroid hormone stimulated oxygen consumption by approximately 100% and thyroid hormone stimulated glucose uptake by approximately 200%. In conclusion, our results show that glucose feeding 1) increases serum T3 levels, 2) decreases nuclear T3 binding, 3) enhances thyroid hormone stimulated oxygen consumption and glucose uptake.

Administration, Oral↗
PubMed1989

The influence of caloric deprivation and food composition on TSH, thyroid hormones and nuclear binding of T3 in mononuclear blood cells in obese women.

In vivo changes in thyroid-stimulating hormone (TSH), thyroxin (T4), triiodothyronine (T3) and nuclear binding of T3 (NBT3) in mononuclear blood cells were studied in obese women during seven days of caloric deprivation (maximum 1,100 kcal/d). In seven women given a high protein diet (80% protein, 7% carbohydrates, 7% fat) and in two women who fasted (group 1), total T3 (TT3) decreased from 1.66 +/- 0.43 nmol/L to 1.11 +/- 0.32 nmol/L (P less than .01), free T3 (FT3) decreased from 5.7 +/- 1.1 pmol/L to 4.3 +/- 1.6 pmol/L (P less than .01), and free T4 (FT4) increased from 17.8 +/- 2.3 pmol/L to 21.1 +/- 2.0 pmol/L (P less than .01). In five women given a carbohydrate diet (Dextrin-maltose 100%) (group 2), thyroid hormones were unchanged, TT3 was at start 1.66 +/- 0.24 nmol/L and after seven days 1.43 +/- 0.26 nmol/L (NS), FT3 changed from 6.4 +/- 1.8 pmol/L to 6.0 +/- 2.1 pmol/L (NS) and FT4 changed from 20.4 +/- 5.1 pmol/L to 20.6 +/- 3.1 pmol/L (NS). The caloric intake and the weight reduction was the same in the two groups. Basal TSH and TSH after thyrotropin-releasing hormone (TRH) (TSH+30min) declined in both groups. In group 1, basal TSH declined from 1.88 +/- 1.07 microU/mL (P less than .03), and TSH+30min declined from 12.44 +/- 7.49 microU/mL to 9.38 +/- 5.97 microU/mL (P less than .03). In group 2, basal TSH declined from 2.09 +/- 0.87 microU/mL to 1.66 +/- 0.92 microU/mL (P less than .03), and TSH+30min declined from 15.63 +/- 7.90 microU/mL to 11.93 +/- 7.20 microU/mL (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Nuclear thyroid hormone receptor binding in human mononuclear blood cells after goitre resection.

Nuclear thyroxine and triiodothyronine receptor-binding in human mononuclear blood cells were examined in 14 euthyroid persons prior to and 1, 6, 24 and 53 weeks after goitre resection. One week after resection decreased serum T3 from 1.47 nmol/l to 1.14 nmol/l (P less than 0.05), FT4I from 103 a. u. to 94 a. u. and SHBG from 80 nmol/l to 69 nmol/l (P less than 0.05) followed after 6 weeks by a rise in serum TSH from 1.2 mU/l to 11.0 mU/l (P less than 0.05) suggesting an initial slight hypothyroidism. Nuclear receptor-binding of T4 and T3 increased within one week and eventually decreased to preresectional values. We conclude that the expected alteration of the metabolic state caused by resection of the gland is opposed by increased nuclear binding of T4 and T3.

Adult↗
PubMed1989

Thyroid hormone stimulated glucose uptake in human mononuclear blood cells from normal persons and from patients with non-insulin-dependent diabetes mellitus.

Thyroxine and T3 induced oxygen consumption and glucose uptake were studied in vitro in mononuclear blood cells isolated from patients with non-insulin-dependent diabetes mellitus (NIDDM) and from non-diabetic control persons. Cellular oxygen consumption and glucose uptake were promptly increased by physiological and supraphysiological concentrations of T3 and T4 in a dose-dependent manner (50-5000 nmol/l), whereas rT3 and T2 had no stimulatory effect. The effect of T3 and T4 was independent of new protein synthesis in that it was not blocked by tunicamycin (1 mg/l) and tiothepa (75 mg/l). Examination of stimulation of cells from control subjects and patients with NIDDM revealed an identical oxygen consumption, whereas the thyroid hormone-induced glucose uptake was significantly increased in cells from patients with NIDDM. T4 (5 mumol/l) stimulation in controls: 1.34 +/- 0.23 mmol.l-1 (mg DNA)-1.h-1, in NIDDM: 3.24 +/- 0.77 mmol.l-1.(mg DNA)-1.h-1, P less than 0.05 (mean +/- SD). These studies indicate that T4 as well as T3 increases cellular oxygen consumption and glucose uptake and that this stimulation is independent of new protein synthesis. Examination of cells from patients with NIDDM revealed an increased thyroid hormone induced glucose uptake, indicating increased thyroid hormone sensitivity. This observation contrasts the well known insulin insensitivity, suggesting separate mechanisms for glucose uptake elicited by insulin and thyroid hormones.

Adolescent↗
PubMed1989

Thyroid hormone induced oxygen consumption and glucose-uptake in human mononuclear cells.

Cellular oxygen consumption and glucose metabolism were examined in human mononuclear blood cells. The cellular oxygen consumption and glucose uptake were dependent on the number of cells, the temperature and the duration of incubation. Stimulation of the cells by T4 and T3 led to a dose dependent increase of oxygen consumption and glucose uptake, whereas T2 and rT3 had no effect. Thyroxine as well as T3 stimulated the cellular glucose metabolism, but lactate production was independent of T3 and T4 stimulation. The data suggested a direct effect of T4 and T3 on oxidative phosphorylation. Further thyroid hormones and insulin exerted an additive effect on glucose uptake. Our study indicates a direct intracellular effect of T4 independent of its conversion to T3 and a different mechanism for insulin dependent and thyroid hormone glucose uptake.

Adult↗
PubMed1989

TSH, thyroid hormones and nuclear-binding of T3 in mononuclear blood cells from obese and non-obese women.

The specific nuclear-binding of T3 (NBT3) in mononuclear blood cells, and the concentrations of TSH, thyroid hormones, and binding proteins were measured after overnight fasting in 12 obese and in 14 non-obese women, none of the subjects were taking any medicine. The concentrations of TSH and free plus bound-T3 (TT3) were significantly higher in the obese (p less than 0.05), concentrations of T4 and binding proteins did not differ. The NBT3 was significantly lower in the obese women; the maximal binding capacity (MBC) was 34.5 +/- 11.6 fmol/mg DNA in the obese subjects and 50.0 +/- 11.6 fmol/mg DNA in the non-obese subjects (p less than 0.02). The binding affinities did not differ. We have previously shown that increasing T3 concentrations within the physiological range down-regulates NBT3. Therefore, the reduced NBT3 in the obese women was probably secondary to the increased TT3 concentration and was not caused by a primary tissue resistance. The higher TSH and TT3 in the obese women could be caused by a greater caloric intake.

Adult↗
PubMed1988

Triiodothyronine stimulates urinary excretion of calcium and hydroxyproline in autosomal dominant osteopetrosis.

Six patients with autosomal dominant osteopetrosis were treated orally with 100 mcg. triiodothyronine (T3) daily for seven days. The effect of T3 on bone remodelling was monitored. T3 treatment increased serum T3 from day 1 to 7 (p less than 0.02) with a corresponding fall in serum T4 (p less than 0.01) and serum TSH (p less than 0.02). The levels of thyroid hormones returned to initial levels within the observation period. The renal excretion of calcium and hydroxyproline increased significantly (p less than 0.05) on day 7 and 14 respectively, while there was no significant increase in phosphate excretion. No significant changes were observed in serum calcium, phosphate, or osteocalcin during the study. The observed changes suggest that bone resorption in autosomal dominant osteopetrosis is stimulated by exogenous administration of T3.

Adult↗
PubMed1988

Thyroid hormone resistance in blood monocyte cells and elevated serum T3 in patients with autosomal dominant osteopetrosis.

Seven patients with autosomal dominant osteopetrosis from three different families were investigated. They all had the roentgenological type I disease, characterized by universal, symmetrical osteosclerosis and enlarged thickness of the calvarium vault. Serum concentrations of thyroid hormones and the specific nuclear binding of triiodothyronine (T3) in mononuclear blood cells were studied. All patients appeared clinically euthyroid. The serum level of T3 was significantly elevated (serum T3 = 1.89 nmol/l) compared with normal age and sex-matched controls (serum T3 = 1.44 nmol/l, p less than 0.05). The specific maximal nuclear binding capacity of T3 was significantly decreased (MBC = 0.51 fmol T3/mg DNA) in these patients compared with controls (MBC = 1.8 fmol/mg DNA, p less than 0.05) whereas no difference in the equilibrium association constant (Ka) was observed. The decreased specific nuclear binding of T3 and the slightly elevated serum level of T3 might indicate a modest peripheral resistance to T3 in patients with autosomal dominant osteopetrosis type I.

Adult↗
PubMed1986

Treatment of Graves' ophthalmopathy with cyclosporin A.

Six patients with Graves' ophthalmopathy (2 with acute and 4 with chronic alterations) were treated with cyclosporin A (10 mg/kg/day) for 5 weeks. This treatment had no effect on either the ocular manifestations (protrusion, eye muscle function) or subjective well-being of the patients. In contrast, creatinine clearance decreased from 83.5 to 55.5 ml/min during treatment, but normalized (94.9 ml/min) after cessation of the drug. A transient increase in serum 4-androstenedione was observed in 3 patients. We conclude that cyclosporin A has no convincing effect in the treatment of Graves' ophthalmopathy, but rather exerts serious renal effects.

Adult↗
PubMed1986

Nuclear thyroxine binding in human mononuclear blood cells from hyperthyroid and hypothyroid patients before and after treatment.

Nuclear binding of [125I]T4 in human mononuclear blood cells was examined in six hyperthyroid and six hypothyroid patients before and after treatment. In hypothyroid patients the nuclear T4 binding was initially increased and subsequently normalized as the patients became euthyroid suggesting a homeostatic counter-regulation. The thyroid state did not affect the nuclear T4 binding in hyperthyroid patients. Treatment with methimazol however increased the nuclear T4 binding, suggesting either a direct effect of methimazol on the hormone-receptor interaction or that the patients had become slightly hypothyroid during the treatment. The TSH was shown not to affect nuclear T4 binding. The thyroid state of the patients did not significantly affect the nuclear accumulation of the T3 produced intracellularly by deiodination of T4.

Adult↗
PubMed1985

Nuclear thyroxine and triiodothyronine binding in mononuclear cells in dependence of age.

Nuclear binding of thyroxine (T4) and triiodothyronine (T3) in mononuclear blood cells was investigated in 12 young (age 16-30 years) healthy subjects (group A), in 12 middle-aged (age 31-60 years) healthy subjects (group B) and in 12 elderly (61-90 years) healthy subjects. Serum free T3 was depressed in group C as compared to the younger age groups, whereas serum free T4 and TSH did not differ between the groups. Maximal specific nuclear binding capacity for both T4 and T3 decreased with increasing age, T4 group A: 1.2 fmol T4/100 micrograms DNA, group B: 1.2 fmol T4/100 micrograms DNA, group C: 0.7 fmol T4/100 micrograms DNA; T3 group A: 1.7 fmol T3/100 micrograms DNA, group B: 1.0 fmol T3/100 micrograms DNA, group C: 0.9 fmol T3/100 micrograms DNA. The equilibrium association constant (Ka) for T4 increased with age, group A: Ka = 3.3 X 10(9) l/mol, group B: Ka = 3.2 X 10(9) l/mol, group C: Ka = 6.4 X 10(9) l/mol, whereas Ka for nuclear binding of T3 decreased with age group A: Ka = 3.9 X 10(9) l/mol, group B: Ka = 5.9 X 10(9) l/mol, group C: Ka = 1.8 X 10(9) l/mol. We conclude that, whereas the opposite variations of nuclear capacity and binding affinity for T4 tend to preserve the nuclear T4 concentration, the nuclear T3 concentration definitely decreases with age. The unaltered serum levels of TSH suggest that the decrease of both serum levels of free T3 and the nuclear T3 concentration might represent physiologically changes in old age.

Adolescent↗
PubMed1985

Prediction of the course of Graves' disease after medical antithyroid treatment.

The course of thyrotoxicosis in 33 patients with Graves' disease was evaluated clinically and biochemically (free thyroxine index, serum triiodothyronine, thyroid stimulating antibodies, (TSAb), thyroid stimulating hormone binding inhibiting immunoglobulins (TBII)). Relapse of the disease was found to be correlated to anamnestic information of thyrotoxicosis among first degree relatives (predictive value 90%) and to concomitantly raised levels of TSAb and TBII at the start of treatment (predictive value 71%). Mean duration of treatment of patients with long-lasting remission was 16.8 months. When comparing various information used to predict relapse of Graves' disease, anamnestic information of familial predisposition to thyrotoxicosis carries the highest predictive value.

Adolescent↗
PubMed1985

Nuclear thyroxine receptors and cellular metabolism of thyroxine in obese subjects before and after fasting.

Nuclear binding of thyroxine (T4), cellular deiodination of T4 and nuclear accumulation of endogenous triiodothyronine (T3) were investigated in mononuclear blood cells in 5 obese persons before and after 7 days of total fast. Serum-free T4, serum-free T3 and serum thyrotropin (TSH) did not differ between lean persons and obese fed subjects, but fasting induced a significant decrease of serum-free T4 and serum-free T3 (T4 from 16.6 to 14.4 pmol/l, T3 from 5.7 to 3.2 pmol/l). The maximal specific binding capacity (MBC) for T4 was decreased in fed obese subjects (MBC = 0.6 fmol T4/100 micrograms DNA, p less than 0.05) compared to normal weight persons (MBC = 1.3 fmol T4/100 micrograms DNA), whereas the equilibrium association constant (ka) did not differ. During complete fast, the MBC increased (MBC = 1.5 fmol T4/100 micrograms DNA, p less than 0.05). Neither total deiodination of T4 nor endogenous nuclear T3 accumulation differed between the groups suggesting that cellular T4 to T3 conversion is independent of the nutritional state. We suggest that the observed increase in nuclear T4 receptor capacity may compensate the decrease in serum thyroid hormone levels.

Cell Nucleus↗
PubMed1985

Potentiometric measurements of ionized calcium in anaerobic whole blood, plasma, and serum evaluated.

The measurements of ionized calcium and pH in paired samples of anaerobic capillary whole blood, venous whole blood, venous plasma, and venous serum have been evaluated with a modified ICA 1 analyzer and compared with those of an unmodified ICA 1 analyzer. The unmodified instrument showed a significant difference between measurements in anaerobic venous whole blood, venous plasma, and venous serum, but the modified instrument did not. Statistically significant differences between the two instruments were found for whole blood (magnitude of mean difference magnitude of = 0.053 mmol/L) and for venous serum (0.016 mmol/L), but not for venous plasma. The error of residual liquid junction potential due to blood cells, previously found in the unmodified ICA 1 (salt bridge: KCl, 2.68 mol/kg) was eliminated and independent of the erythrocyte volume fraction in the modified ICA 1 (salt bridge: sodium formate, 4.56 mol/kg). From studies of procedures for measurements of ionized calcium in anaerobically handled samples, we recommend the use of anaerobic whole blood for measuring ionized calcium.

Adult↗