Thyroid Function and Body Weight in Psychiatric Disorders

2008 ◽  
Vol 168 (22) ◽  
pp. 2497
2019 ◽  
Vol 3 ◽  
pp. 9-14
Author(s):  
Alevtyna Kononenko ◽  
Vera Kravchenko

The present work studied the effect of aqueous extract from Feijoa leaves on thyroid function of rats with experimental hypothyroidism. Healthy albino rats weighing between 120 gand 150 gwere used. The animals were randomly allotted into four groups, each containing eight rats respectively. Three of the groups (II, III and IV), induced with hypothyroidism, were treated by 0.05 % solution of thiamazole with drinking water for 30 days. Control (vehicle) rats were given normal saline. After 13 days hypothyroid groups (III and IV) of rats were treated with aqueous extract from Feijoa leaves at a dose 1.0 ml/100 g of body weight and with Iodomarin 200 (reference drug) at a dose 12 µg/kg daily orally for 21 days. Results obtained from the study showed that the introduction of thiamazole leads to functional changes in the thyroid gland in rats, accompanied by decreasing sings of rectal temperature and level of thyroid hormones. It was found, that treatment with AEFL normalizes serum thyroid hormone levels, increases rectal temperature and reduces the thyroid mass. The investigated extract can be attributed to the regulators of the thyroid hypofunction and is promising for further study of its effectiveness as a thyroid-stimulating agent.


1973 ◽  
Vol 58 (3) ◽  
pp. 535-546 ◽  
Author(s):  
P. W. NATHANIELSZ ◽  
R. S. COMLINE ◽  
MARIAN SILVER ◽  
A. L. THOMAS

SUMMARY Foetal plasma thyroxine levels as well as thyroxine turnover and placental permeability to this hormone were investigated in the conscious pregnant ewe with foetal and maternal intravascular catheters. Foetal plasma thyroxine levels ranged from 4·6 to 6·2 μg/100 ml between 103 days of gestation and the day of birth. Maternal plasma thyroxine levels varied between 2·3 and 4·1 μg/100 ml over the same period. The maternal: foetal ratio across the placenta for thyroxine varied from 0·52 to 0·65. Distribution of radioactive thyroxine injected into the foetal or maternal circulation demonstrated the impermeability of the placenta to thyroxine. Maternal to foetal ratios for labelled thyroxine were 6·2 to 11·9 when injected into the maternal circulation and 0·013 to 0·003 when injected into the foetal circulation. The sheep placenta appears to be capable of actively transporting iodide to maintain a foetal to maternal iodide ratio of up to 8:1. Foetal thyroxine utilization was of the same order at 111 days of gestation as immediately before parturition when expressed per unit body weight. Utilization of thyroxine per kg by the foetus was about five times that of the mother. Various factors which influence thyroid function are discussed and the activity of the foetal pituitary—thyroid system is compared with other foetal endocrine systems.


2018 ◽  
Vol 27 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Mathilde M. Husky ◽  
Carolyn M. Mazure ◽  
Alexis Ruffault ◽  
Cécile Flahault ◽  
Viviane Kovess-Masfety

1971 ◽  
Vol 49 (12) ◽  
pp. 1557-1561 ◽  
Author(s):  
Dixie Chua ◽  
J. G. Eales

Both TSH and thyroid powder significantly increased skin guanine and hypoxanthine levels over a 5-week period at 15 °C. TSH was more effective than thyroid powder.Injected thyroxine as low as 0.05 μg/g body weight per 2 days and ambient thiourea as low as 0.0001% inhibited thyroid function over 3 weeks at 10 °C. This thyroxine treatment did not significantly increase skin purine levels, but thiourea as low as 0.01% significantly decreased skin hypoxanthine and total purinelevels.


1968 ◽  
Vol 46 (4) ◽  
pp. 697-700 ◽  
Author(s):  
K. Brown-Grant

The changes observed in the metabolism of radioiodide and radiophosphorus by the thyroid gland of intact adult male rats following a single injection of estradiol benzoate (4 μg/100 g body weight) are consistent with the suggestion (F. Labrie, G. Pelletier, and C. Fortier. Federation Proc. 26, 484 (1967). Abstr.) that at this dose level estrogen causes a hypersecretion of TSH in such animals.


1977 ◽  
Vol 86 (1) ◽  
pp. 128-139 ◽  
Author(s):  
Isabel Pericás ◽  
Trinidad Jolín

ABSTRACT Studies of pituitary and thyroid function have been carried out in normal (intact) and diabetic Wistar rats. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). The animals were fed a low iodine diet (LID), and received a daily sc injection of either KClO4 (20 mg/100 g body weight) or propylthiouracil (PTU) (1.5 mg/100 g body weight) to induce hypothyroidism. Control groups received the same LID but supplemented with 0.8 μg I/g dry weight. In intact rats goitrogen-treatment induces an increase in thyroid weight and in plasma TSH concentration. However, the plasma TSH response to goitrogen-treatment in diabetics indicates that pituitary TSH secretion increases following a reduction in plasma PBI, but the response is less marked than in controls. The difference in plasma TSH between control and diabetic rats provides an explanation for the findings that diabetes diminishes the thyroid growth response to goitrogen-treatment. Moreover, in intact rats the low pituitary TSH content is a consequence of the increase in pituitary TSH secretion, while in the diabetics the low pituitary TSH content cannot be explained by an increase in TSH secretion. The effect of diabetes on the pituitary-thyroid axis cannot be attributed specifically to poor growth, because the changes in pituitary-thyroid function which are observed in the diabetic groups are not seen in intact rats with a growth rate similar to that of insulin deficient rats. Insulin administration to goitrogen-treated diabetic rats results in 1) an increase in the ability of the thyroid tissue to respond to its trophic hormone, 2) an increase in pituitary TSH secretion in response to the lowering of plasma PBI and, 3) an increase in thyroid growth response to goitrogen-treatment. Results are discussed in relation to the assumption that the lack of adequate insulin levels, or its metabolic defects, diminishes the full response of the thyroid to TSH, and affects the pituitary TSH secretion probably as a consequence of altered hypothalamic control of the pituitary function.


1976 ◽  
Vol 83 (4) ◽  
pp. 752-762 ◽  
Author(s):  
E. Vigouroux

ABSTRACT The thyroid function in development was investigated in post-natal rats. The thyroid iodine content rapidly increased from birth (137 ± 26 ng iodine/mg thyroid) up to day 10 (338 ± 42 ng iodine/mg thyroid) then increased more slowly up to day 30 (425 ± 34 ng iodine/mg thyroid). The maximal plasma concentration of thyroxine was observed on day 16 (56.9 ± 3.5 ng T4/ml) and of iodide on day 10 (110.2 ± 12.6 ng I−/ml). The turnover rate constant of extrathyroidal thyroxine was higher at birth (8.0 ± 2.3 %/h) than at any older age studied (average 6 %/h). Thyroxine secretion by the thyroid was more intense before weaning (37 ng hormonal iodine/h/100 g body weight on days 10 and 20) than after weaning (22 ± 6 ng hormonal iodine/h/100 g body weight in 30 days old rats). The peripheral deiodination rate of thyroxine represented about 90 % thyroxine secretion rate in newborn and 10 days old rats and only 40% in adult females. In pre-weaning rats, after a single injection of both [131I]L-T4 and [125I]Na, extrathyroidal radioactivity disappeared more slowly than in 30 days old rats and adult animals. This suggests that iodide concentrations of extrathyroidal tissues are higher before than after weaning.


1993 ◽  
Vol 10 (3) ◽  
pp. 313-323 ◽  
Author(s):  
M R Thomas ◽  
J P Miell ◽  
A M Taylor ◽  
R J M Ross ◽  
J R Arnao ◽  
...  

ABSTRACT Thyroid hormones are essential for the normal growth and development of many tissues. In the rat, hypothyroidism is associated with growth impairment, and hyperthyroidism with the development of a hypercatabolic state and skeletal muscle wasting but, paradoxically, cardiac hypertrophy. The mechanism by which thyroid hormone produces cardiac hypertrophy and myosin isoenzyme changes remains unclear. The role of IGF-I, an anabolic hormone with both paracrine and endocrine actions, in producing cardiac hypertrophy was investigated during this study in hyperthyroid, hypothyroid and control rats. A treated hypothyroid group was also included in order to assess the effect of acute normalization of thyroid function. Body weight was significantly lower in the hyperthyroid (mean±s.e.m.; 535·5±24·9 g, P<0·05), hypothyroid (245·3±9·8 g, P<0·001) and treated hypothyroid (265·3±9·8 g, P<0·001) animals when compared with controls (618·5±28·6 g). Heart weight/body weight ratios were, however, significantly increased in the hyperthyroid (2·74 ± 0·11×10−3, P<0·01) and treated hypothyroid (2·87±0·07 ×10−3, P<0·001) animals when compared with controls (2·26±0·03 × 10−3). Serum IGF-I concentrations were similar in the control and hyperthyroid rats (0·91±0·07 vs 0·78±0·04 U/ml, P=0·26), but bioactivity was reduced by 70% in hyperthyroid serum, suggesting a circulating inhibitor of IGF. Serum IGF-I levels (0·12±0·03 U/ml, P<0·001) and bioactivity (0·12±0·04 U/ml, P<0·001) were significantly lower in the hypothyroid group. Liver IGF-I mRNA levels were not statistically different in the control and hyperthyroid animals, but were significantly reduced in the hypothyroid animals (P<0·05 vs control). Heart IGF-I mRNA levels were similar in the control and hypothyroid rats, but were significantly increased in the hyperthyroid and treated hypothyroid animals (increased by 32% in hyperthyroidism, P<0·05; increased by 57% in treated hypothyroidism, P<0·01). Cardiac IGF-I was significantly elevated in hyperthyroidism (0·16±0·01 U/mg heart tissue, P<0·01), was low in hypothyroidism (0·08±0·01 U/mg, P<0·01) and was normalized in the treated hypothyroid group (0·11 ± 0·01 U/mg vs control, 0·13±0·01 U/mg). Low body mass during both hypothyroidism and hyperthyroidism is therefore associated with reduced systemic IGF bioactivity. In hypothyroidism there is a primary defect in the endocrine function of IGF-I, while in hyperthyroidism serum IGF bioactivity is reduced in the presence of normal endocrine production of this anabolic hormone. In contrast, the paracrine actions of IGF-I are increased in the heart during hyperthyroidism, and this hormone appears to play a part in the development of hyperthyroid cardiac hypertrophy.


2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Khalid Abdul Majeed ◽  
Muhammad Shahbaz Yousaf ◽  
Muhammad Sajid Tahir ◽  
Aamir Riaz Khan ◽  
Suliman Khan ◽  
...  

Dibutyl phthalate is an endocrine disruptor used in a wide range of industrial and agriculture applications. The present study focuses on elucidating the effect of subacute exposure (4-weeks) of DBP on insulin and its sensitivity indexes, oxidative status, thyroid function, energy metabolites, serum biochemistry, and anthropometry in rats. A total of 64 rats were divided into 4 treatment groups as mg DBP/Kg body weight per day: (a) 0 mg/Kg (control), (b) 10 mg/Kg (DBP-10), (c) 50 mg/Kg (DBP-50), and (d) 100 mg/Kg (DBP-100). The rats in each treatment ( n = 16 ) were further divided into male ( n = 8 ) and female ( n = 8 ) rats for studying treatment and gender interactions. Intraperitoneal glucose tolerance test (IPGTT) was performed on the 21st day. Anthropometry, nutritional determinants, fasting plasma glucose, fasting plasma insulin, homeostatic model assessment (HOMA), thyroid hormones, energy metabolites, and oxidative status were studied during the experimental period. Two-way ANOVA was used to analyze the data ( p < 0.05 ). Tukey’s posthoc test was used for pair-wise comparisons. DBP increased body weight gain and feed efficiency in an inverted nonmonotonic U -shaped fashion. Hyperglycemia and increased blood glucose area under the curve were observed in DBP-100 at 120 minutes in IPGTT. The HOMA also showed a linear monotonic contrast. Thyroxin decreased significantly in the DBP-100 rats, whereas malondialdehyde, nonesterified fatty acids, and beta hydroxyl butyrate were increased with the DBP treatments. In conclusion, DBP could be attributed to the development of hyperglycemia and insulin resistance in rats. Further investigations into the lipid peroxidation pathways can improve our understanding of the mechanisms involved in metabolic disruption.


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