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Biomedical subjects

A G Burger

Publications and source records attributed to A G Burger.

88 records · Page 5Linked to original sources
PubMed1982

Effects of starvation on circadian variations of plasma TSH in rats.

Diurnal fluctuations of plasma TSH were investigated in ad libitum fed rats as well as after a 3 day starvation period in order to study the relationship between the circadian pattern of TSH secretion and nutritional status. Our study showed the persistence of a circadian TSH rhythm after a 3-day starvation without any change in the amplitude of plasma TSH variations. However, the 24 h average plasma TSH levels were significantly lower. A suggestive acrophase occurred at the same period of the day in starved and fed rats. Our results suggest that the control of plasma TSH concentrations and nycthemeral rhythm are not closely related and may even possibly be independent of one another.

Animals↗
PubMed1981

General comments on tissue sensitivity to thyroid hormones in starvation.

The interrelationship between thyroid hormones and catecholamines is discussed. It is known that hypothyroidism will decrease tissue sensitivity to exogenous catecholamines. There is, however, no experimental proof that the thyroid hormones changes, particularly the low serum T(3) levels encountered in systemic illness and starvation, are sufficient to change tissue sensitivity to catecholamines. Catecholamines and thyroid hormones influence thermogenesis. Recently a decreased effectiveness of thyroid hormones in the starving hypothyroid rat has been documented. It has, however, not been excluded that part of this change is due to a combined change in effectiveness of thyroid hormones and catecholamines on thermogenesis.

Catecholamines↗
PubMed1980

The metabolism of 3,3'-diiodothyronine in man.

The production rate of 3,3'-Diiodothyronine (3,3'-T2) was measured in five healthy subjects after a single injection of [125I]3,3'-T2. The [125I]3,3'-T2 was measured by immunoprecipitation. To reduce the large amount of nonspecific serum radioactivity (iodides, 3,3'-T2 metabolites, and protein-bound iodine), the sear were treated before the immunoprecipitation with an anion exchanger and polyethylene glycol (final concentration, 10%). The noncompartmental analysis of the data gave the following results: MCR, 0.52 +/- 0.07 liters/min or 926 +/- 142 liters/day (mean +/- SD); and production rate, 23.7 +/- 8.2 ng/min or 34 +/- 12 micrograms/day.

Adult↗
PubMed1980

A study of the relationship between thermogenesis and thyroid hormones.

To investigate the relationship between serum T3 levels and thermogenesis in euthyroid subjects, the conversion of T4 to T3 was partially blocked over a period of 3 weeks by weekly ingestion of 2 g iopanoic acid. Serum T3 decreased by 56 +/- 6 ng/100 ml without affecting the metabolic rate or total heat loss. Because an increase in serum T4 levels was observed (3.70 +/- 0.2 microgram/100 ml), the experiment was repeated in T4-substituted subjects. Serum T3 decreased even more in these subjects, (by 85 +/- 12 ng/100 ml), and the increase of serum T4 was also larger (4.6 +/- 0.7 microgram/100 ml). Again, the metabolic rate did not change. Experiments performed on hypothyroid patients and T3-substituted subjects demonstrated that iopanoic acid alone was without effect on the metabolic rate. Furthermore, the effect of a low energy, high protein diet (1672 kilojoules or 400 Cal) on the metabolic rate was confirmed. These results show that the decrease in magnitude of serum T3 seen with iopanoic acid is not sufficient by itself to reduce the metabolic rate.

Body Temperature Regulation↗
PubMed1980

Starvation induces a partial failure of triiodothyronie to inhibit the thyrotropin response to thyrotropin-releasing hormone.

During starvation the response of TSH to TRH decreases in many subjects. This could be due to an increased sensitivity to TSH secretion to circulating thyroid hormones. To study this hypothesis, 13 subjects were starved twice for 2-day periods. After both starvation periods, a standard TRH test (200 micrograms TRH, iv) was performed; during 1 starvation period 15 micrograms T3 were injected iv 24 h before the TRH test. The TRH tests were also performed while on normal nourishment, once without pretreatment and once 24 h after the iv injection of 15 micrograms T3. The spontaneous decrease of the TSH response to TRH was seen in 10 of 13 subjects. In these 10 subjects it decreased from 18.0 +/- 1.9 to 9.7 +/- 1.2 microU/ml (mean +/- SEM; P < 0.001). The additional inhibition of the TRH test with T3 was small compared with the one observed under normal conditions. In starvation, T3 decreased the maximal TSH response from 9.7 +/- 1.2 to 8.4 +/- 1 microU/ml (P = NS), while during the control period the maximal TSH response fell from 18.0 +/- 1.9 to 11.4 +/- 1.3 microU/ml (P < 0.001). These data indicate a diminished effectiveness of T3 in inhibiting TSH secretion and are consistent with the hypothesis of a more generalized resistance of target organs to T3 during starvation in man.

Adult↗
PubMed1980

Interrelationships between energy metabolism and thyroid hormone metabolism during starvation in the rat.

Thyroid hormone metabolism and plasma concentrations of TSH were studied after short-term hypocaloric refeeding of rats starved for 2-6 days. Carbohydrate and protein (10 kcal) refeeding after 4 days of starvation resulted in a rapid increase in serum T3 (P less than 0.01) and, less consistently of T4. Plasma TSH did not change. These findings were not due to changes in the metabolic clearance rates or in thyroid hormone binding proteins, as the disappearance of injected labelled T3 and T4, and the free fractions of T3 and T4, were unchanged. Increased thyroidal secretion, and for T3, increased peripheral conversion from T4 were therefore responsible for these changes. Fat refeeding had no immediate effect on plasma T4, T3 or TSH. After 6 days of starvation, refeeding of any nutrient was ineffective in altering the plasma concentrations of T3 and T4. The intraperitoneal administration of nicotinamide (100 mg/100 g body weight) to starving animals caused an increase in blood glucose and a decrease in blood beta-hydroxybutyrate similar to that which followed carbohydrate refeeding; T3, however, did not increase. In spite of producing a profile of substrates in the serum similar to that found following carbohydrate refeeding, nicotinamide administration had no effect on the blood lactate/pyruvate ratio which was increased following carbohydrate refeeding. Therefore, the cytoplasmic redox state, as reflected by the lactate/pyruvate ratio, may be closely related to the control of peripheral thyroid hormone metabolism.

Animals↗
PubMed1979

Dietary-induced alterations in thyroid hormone metabolism during overnutrition.

Diet-induced alterations in thyroid hormone concentrations have been found in studies of long-term (7 mo) overfeeding in man (the Vermont Study). In these studies of weight gain in normal weight volunteers, increased calories were required to maintain weight after gain over and above that predicted from their increased size. This was associated with increased concentrations of triiodothyronine (T3). No change in the caloric requirement to maintain weight or concentrations of T3 was found after long-term (3 mo) fat overfeeding. In studies of short-term overfeeding (3 wk) the serum concentrations of T3 and its metabolic clearance were increased, resulting in a marked increase in the production rate of T3 irrespective of the composition of the diet overfed (carbohydrate 29.6 +/- 2.1 to 54.0 +/- 3.3, fat 28.2 +/- 3.7 to 49.1 +/- 3.4, and protein 31.2 +/- 2.1 to 53.2 +/- 3.7 microgram/d per 70 kg). Thyroxine production was unaltered by overfeeding (93.7 +/- 6.5 vs. 89.2 +/- 4.9 microgram/d per 70 kg). It is still speculative whether these dietary-induced alterations in thyroid hormone metabolism are responsible for the simultaneously increased expenditure of energy in these subjects and therefore might represent an important physiological adaptation in times of caloric affluence. During the weight-maintenance phases of the long-term overfeeding studies, concentrations of T3 were increased when carbohydrate was isocalorically substituted for fat in the diet. In short-term studies the peripheral concentrations of T3 and reverse T3 found during fasting were mimicked in direction, if not in degree, with equal or hypocaloric diets restricted in carbohydrate were fed. It is apparent from these studies that the caloric content as well as the composition of the diet, specifically, the carbohydrate content, can be important factors in regulating the peripheral metabolism of thyroid hormones.

Adult↗
PubMed1979

The effects of tetraiodothyroacetic and triiodothyroacetic acids on thyroid function in euthyroid and hyperthyroid subjects.

The effects of tetraiodothyroacetic (Tetrac) and triiodothyroacetic acids (Triac) on thyroid function have been investigated in euthyroid and hyperthyroid subjects. 50, 100, 200, 400 or 800 micrograms of Triac were administered to 8 euthyroid volunteers three times (tds) over a 24 hour period. 3 X 800 micrograms Triac/24 h was sufficient to cause a significant reduction in serum T3. Tetrac, given as an iv bolus of 3600 microgram, produced a sustained reduction in serum T3 for up to 4 days after the injection. Intermediate doses of Tetrac (1200 micrograms) or Triac (400 micrograms tds) significantly reduced the TSH response to TRH (66% and 43% respectively). Seven hyperthyroid patients received Triac 200 micrograms tds for 2 days, and in 2, a rapid decrease in serum T3 was seen. Similar changes in serum T3 were also produced with iodide administration. The results suggest that 1) in euthyroidism, Tetrac and Triac act directly at the pituitary level to inhibit the TSH response to TRH; 2) in some cases of hyperthyroidism, Triac produces a block in T3 secretion by virtue of the iodide produced by its metabolism.

Administration, Oral↗
PubMed1978

Nutritionally-induced alterations in thyroid hormone metabolism and thermogenesis.

Serum 3,5,3'-triiodothyronine (T3) is increased by overnutrition and decreased by starvation. The production rate of T3 was increased by overfeeding (82%), but T4 production did not change. Feeding a weight maintenance diet with high CHO mimiced serum T3 and rT3 changes of overfeeding, substitution of CHO by FAT those of starvation. VO2 increased during overfeeding and in T4 equilibrated volunteers supplemented with 40 microgram T3 daily for 2 weeks. No weight change occurred in the latter subjects. Yet no decrease in VO2 was found when serum T3 was reduced by the administration of iopanoic acid. VO2 decreased during starvation in normal and hypothyroid rats, and in hypothyroid animals replaced with T4 or T3.

Animals↗
PubMedDate not supplied

Lack of loss of heterozygosity at the c-erbA beta locus in gastrointestinal tumors.

The cellular homologues of the viral oncogene c-erbA encode for the nuclear thyroid hormone receptor c-erbA (TR). The gene for the human TR beta subtype is located on chromosome 3p24, and a loss of heterozygosity around this region has been reported in breast and small cell lung cancers, suggesting that TR beta might act as a tumor suppressor gene. In the present study, we used PCR-based restriction fragment length polymorphisms to examine the 3p24 region of 19 patients with gastrointestinal tumors for loss of heterozygosity (LOH). Interestingly, only 1 of the patients had an LOH at this locus, while 4 patients had a microdeletion of both alleles in the 3p24 region. These results suggest that, in contrast to previous reports on lung and breast cancers, a loss of heterozygosity of the TR locus at 3p24 is a rare event. A critical review of the literature, however, suggests, that some of the earlier studies have used markers whose location is only imprecisely mapped and may hence point to a tumor suppressor gene candidate other than TR beta. However, a selective microdeletion of both alleles was detected in the tumors of 4 of the 19 patients, indicating that this region on chromosome 3p may be genetically unstable in gastrointestinal tumors.

Aged↗
PubMedDate not supplied

[Interference in the conversion of T4 to T3 and rT3 by medications in man].

Several drugs are known to interfere in thyroid hormone metabolism: 1) They can affect directly and specifically T4 to T3 conversion. This can be observed in vivo and in vitro. In vivo serum T3 concentrations will decrease and rT3 concentrations increase. Amiodarone, other iodinated compounds (cholecystographic agents: ipodate and iopanoic acid), propylthiouracil and propranolol are known to act in this way. 2) Other drugs which induce the hepatic capacity to catabolize drugs will also affect thyroid hormone metabolism, e.g. diphenylhydantoine. Clinically, inhibitors of conversion will increase serum total and free T4, however this finding per se does not proof hyperthyroidism as in some cases serum TSH will increase after i.v. injection of 400 micrograms TRH. Furthermore the increase in serum T4 can be explained in part by a low metabolic clearance rate, T4 production being barely increased.

Amiodarone↗