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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of a low-calorie diet (200 kcal) composed of about 50 per cent glucose and 50 per cent protein on body weight, thyroid hormone levels and pituitary thyrotrophin response was studied in 18 grossly obese subjects (relative weight 131-205 per cent) for 28 d; during the last 14 d eight subjects (Gp B) served as controls, while in the other ten subjects (Gp A) the low T3-high rT3 state was treated by T3 supplementation (150 micrograms daily). During the first 14 d (period 1) weight loss (corrected for the sodium diuresis) appeared to be constant and to be equal for both groups. The thyroid hormone concentration and the basal and TRH stimulated TSH concentrations were similar to the results from previous total starvation studies. Despite marked changes in serum T3 levels a normal pituitary TSH response was maintained and no delayed response of TSH to TRH occurred. During T3 supplementation the serum T3 levels increased to high values, the rT3 concentration declined to below initial values, the T4 and TSH concentrations were depressed and the response of the TSH concentration to TRH disappeared; apparently these 'high normal' levels of serum T3 must be considered inappropriate for this condition of severe calorie restriction. In the controls the serum T3 levels remained constant after the end of the first period; the serum rT3 concentration declined from day 14 to day 28, but remained above the initial values. The serum T4 concentration remained almost constant during the whole study; basal and TRH stimulated TSH concentrations did not change during the whole study. During period 2 weight loss diminished in the control group, but remained constant in Gp A (T3 supplemented); the correlation between the weight loss and the increase of the serum T3 concentration during triiodothyronine supplementation was significantly negative (r = -0.64; P less than 0.05). The well-being of the subjects did not change during T3 administration and no signs of hyperthyroidism developed. One could speculate this reflects a decrease in number or sensitivity of intracellular receptor sites. It is concluded that at the peripheral level no complete resistance develops against T3 administration; in the low T3 state the hypothalamic-pituitary axis reacts as if euthyroidism exists.
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PMID:The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity. 640 16

The rhythmic pattern of TSH secretion is now well-established and is characterized by a circadian (24 h) periodicity with a pre-sleep acrophase which is modulated by endogenous oscillators and environmental synchronisers. Among external synchronisers, the sleep-waking cycle has been extensively studied and sleep onset appears to have a negative influence on the nycthemeral TSH peak. Nutritional status may affect the TSH rhythmicity since a short term starvation induces a shift in the acrophase time. Major neurotransmitter involved in the TSH rhythms are serotonine which could be responsible for the TSH nadir. By contrast dopamine is not directly implicated in the circadian pattern of TSH secretion. TRH, the main neuropeptide controlling the thyrotrope cell, certainly has a major role in the mediation of the TSH rhythmicity. The involvement of somatostatine is less clear but as assumed for dopamine, its negative influence on TSH secretion would be stronger at the time of TSH peak than at the time of nadir. The major inhibitory effect of thyroid hormones on TSH secretion and release is evident on mean serum TSH levels but does not seem responsible for serum circadian variations. Likewise, the TSH rhythm is present in both sex and influence of estrogens and androgens would only be to modulate the mean serum TSH level. Finally the physiological influence of glucocorticoids on TSH secretion has not been clearly demonstrated.
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PMID:[Biological rhythms of thyrotropin secretion]. 641 Sep 56

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.
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PMID:Interrelationships between energy metabolism and thyroid hormone metabolism during starvation in the rat. 644 70

Nutrition influences thyroid function at the level of TSH secretion, at the level of monodeiodination, and possibly elsewhere. In order to study the effect of starvation on TSH secretion, 8 healthy male volunteers fasted for 30 h and were then refed with 800 kcal. Refeeding was performed at 19.00 h and blood was sampled at 20 min intervals until midnight. Control experiments were performed in the same subjects both when they were normally fed and when the starvation period was prolonged a further 5 h until midnight. Starvation decreased serum TSH levels to below 1 mU/1, and without refeeding the nocturnal peak of the TSH nycthemeral rhythm was abolished. With refeeding serum TSH tended to increase towards midnight and was significantly higher than during starvation. However, the serum TSH levels remained significantly below those at the same time of the day in the absence of a preceding starvation period. Serum T3 levels were significantly lower than in the fed state. The mean values were 1.84 +/- 0.03 vs 2.30 +/- 0.06 nmol/l (120 +/- 2 vs 150 +/- 4 ng/100 ml, mean +/- SEM P less than 0.01). Refeeding did not result in a measurable change in serum T3 concentration (1.80 +/- 0.05 nmol/l; 120 +/- 3 ng/100 ml, mean +/- SEM, n.s.). The contrary was true for rT3 levels which increased in starvation and tended to fall with refeeding, but this decrease was not significant. As glucocorticoids have been implicated in the control of monodeiodination and TSH secretion, serum cortisol levels were also measured. They did not differ during the 3 experimental periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rapid adaptations of serum thyrotrophin, triiodothyronine and reverse triiodothyronine levels to short-term starvation and refeeding. 669 50

Starvation is accomplished by significant changes in the hypothalamic-pituitary-thyroid axis and in peripheral thyroid hormone metabolism. Less well studied, however, are the effects on thyroid hormone economy produced by hypocaloric feeding. We explored these changes in obese patients fed 200, 400, or 600 cal/day of either carbohydrate of protein for 28 days. T4' T3' reverse T3 and the TSH response to TRH were measured at frequent intervals. Each patient demonstrated a transient rise in reverse T3 and a fall in T2 that returned to near basal levels by the end of the study period. The TSH response to TRH on the other hand, declined to approximately 50% of control values and remained at that level throughout the course of study, regardless of the type of substrate or calorie level chosen. The results indicated that hypocaloric feeding is associated with changes in thyroid hormone economy similar to those in starvation and that peripheral (changes in T3 and rT3) and central (TRH response) events are controlled by separate mechanisms.
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PMID:Thyroid hormone homeostasis in states of relative caloric deprivation. 677 21

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.
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PMID:Starvation induces a partial failure of triiodothyronie to inhibit the thyrotropin response to thyrotropin-releasing hormone. 677 98

Sixteen bull calves were fasted during two periods, 31/2 and 7 months old. Blood samples were taken every 6 h during an experimental period of 9 days: 2 control days, 5 fasting days and 2 refeeding days. During the control days with ad libitum feeding, T3, T4 and TSH increased during the day. During the fasting period, T4 decreased with a half-life of 3.5 days and T3 with a half-life of 3 days. TSH decreased in a less regularly way to a mean of 60% of control mean. Six h after refeeding, TSH had increased to 300% of control mean. T3 and T4 had a maximum 12 h after refeeding. As the T4 decreased with a rate nearly similar to the T4 disappearance rate in starving bulls, the secretion of T4 from the thyroid gland must have been almost stopped during the starvation period. The morning values were below normal for all three hormones after 2 days of refeeding.
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PMID:Suppression and stimulation of TSH and thyroid hormones in bulls during starvation and refeeding. 685 55

In several pathophysiologic states, i.e., cirrhosis of liver, protein calorie malnutrition, starvation, carbohydrate deprivation, etc., thyroid hormone metabolism is reported to be altered with a decrease in serum T3 and a reciprocal increase in TR3. Uncontrolled diabetes mellitus is a similar state in which glucose does not enter the cells causing cellular starvation and hyperglycemia ensues. Therefore, serum T4, T3, RT3, T3-resin uptake, TSH, and glucose were determined after an overnight fast in 94 male diabetics (aged 28 to 85 years) during a routine follow-up visit to the outpatient clinic and 24 healthy male adults (aged 24 to 81 years). Glycosylated hemoglobin concentrations were measured as well in normal subjects and 16 newly discovered diabetics. In normal subjects, no significant relationships between fasting plasma glucose and T3 and RRT3 levels were observed. In diabetics there was a significant positive (r = 0.611; p less than 0.001) correlation between glucose and RT3. Similarly, a significant negative relationship was observed between glucose and T3 (r = 0.491; p less than 0.001). T4, free T4, T3-resin uptake, and TSH were normal in diabetics. In 16 newly discovered diabetics, with fasting plasma glucose greater than 200 mg/dl, serum T3 rose (96 +/- 5 to 128 +/- 5 ng/dl) and RT3 declined (26.3 +/- 10.4 +/- 1.4 ng/dl) on improvement of hyperglycemia (fasting plasma glucose less than 140 mg/dl) after intensive therapy for 6 to 8 weeks. Glycosylated hemoglobin levels declined as well (14.6 +/- 0.9% to 9.3 +/- 0.7%). These data indicate: (1) thyroid hormone metabolism may be altered in diabetes mellitus with a fall in serum T3 and a reciprocal rise in RT3; and (2) T3 and RT3 concentrations may serve as indicators of metabolic control in diabetes mellitus.
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PMID:Low serum 3, 5, 3'-triiodothyronine (T3) and raised 3, 3', 5'-triidothyronine (reverse T3 or RT3) in diabetes mellitus: normalization on improvement in hyperglycemia. 714 29

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.
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PMID:Effects of starvation on circadian variations of plasma TSH in rats. 714 38

The effect of starvation on thyroid hormones was studied during a starvation period of 48 h in 10 young bulls. Mean thyroxine degradation rate decreased from K/day 0.32 during feeding to 0.23 during fasting. Mean plasma concentration of T4 decreased to 75% of normal, and it was calculated that the mean thyroxine secretion rate during the starvation period was 24% of normal. Plasma concentration of free thyroxine decreased to 54% of normal, indicating that the concentration of binding protein was not decreased. T3 and reverse T3 decreased to about 60% of normal. This indicated a parallel decrease in the secretion of all 3 hormones. We did not find evidence of an inactivating pathway for T4 as has been shown in humans during starvation. TSH decreased to 85% of normal.
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PMID:T4 degradation rate and plasma levels of TSH and thyroid hormones in ten young bulls during feeding conditions and 48 h of starvation. 738 13


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