The influence of growth hormone and thyroxine on iodothyronine deiodinase activity in the liver, kidney and brown adipose tissue in hypophysectomized rats

1991 ◽  
Vol 125 (2) ◽  
pp. 219-226 ◽  
Author(s):  
Liv S. Bjørn-Hansen Gøtzsche ◽  
Allan Flyvbjerg ◽  
Sally Marshall ◽  
Karin D. Jørgensen ◽  
Jørgen Weeke
Keyword(s):  
Enzyme Activity ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Iodothyronine Deiodinase ◽  
Deiodinase Activity ◽  
Brown Adipose ◽  
Significant Difference ◽  
Liver And Kidney ◽  
Hypophysectomized Rats

Abstract. The effects of GH and T4 substitution on peripheral iodothyronine deiodinase activity in the liver, kidney and brown adipose tissue of hypophysectomized rats were investigated. Animals were treated with GH (140 μg hGH/day), T4 (3 μg/day), GH plus T4 (same doses), or saline. Rats were killed 0, 4, 7 or 11 days after treatment was started. Non-hypophysectomized, age matched rats were killed after 0 and 11 days and served as controls. GH plus T4 restored body weight gain to normal, whereas GH alone and T4 alone did not. Tissue deiodinase activity and T3 concentrations were severely depressed in the hypophysectomized rats compared with non-hypophysectomized controls (to less than 10%). GH substitution in hypophysectomized rats led to a slight but significant elevation in tissue iodothyronine deiodinase activity in the liver and kidney, without concomitant increases in T3. Deiodinase activity in brown adipose tissue did not differ from that in saline-treated controls. T4 administration normalized deiodinase activity and tissue T3 content in all the evaluated tissues. GH plus T4 resulted in a lesser increase in deiodinase activity than T4 alone in the liver and kidney (p<0.01 at day 11), whereas no significant difference was observed in brown adipose tissue. In conclusion, GH stimulates iodothyronine deiodinase activity of the liver and kidney in hypophysectomized rats. Moreover, when GH is administered together with T4, the T4-stimulated enzyme activity in the liver and kidney is downregulated, suggesting that GH attenuates (or modulates) the T4 effect on this specific enzyme activity.

scholarly journals Brown adipose tissue activity is modulated in olanzapine-treated young rats by simvastatin

2020 ◽  
Author(s):  
Xuemei Liu ◽  
Xiyu Feng ◽  
Chao Deng ◽  
Lu Liu ◽  
Yanping Zeng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
Olanzapine Treatment ◽  
Brown Adipose

Abstract BackgroundPrescription of second-generation antipsychotic drugs (SGAs) to childhood/adolescent has exponentially increased in recent years, which was associated with the greater risk of significant sedation, weight gain, and dyslipidemia. Statin is considered a potential preventive and treatment approach for reducing SGA-induced weight gain and dyslipidemia in schizophrenia patients. However, the effect of statin treatment in children and adolescents with SGA-induced dyslipidemia is not clearly demonstrated.MethodsTo investigate the efficacy of interventions of statin aimed at reversing SGA-induced dyslipidemia, young Sprague Dawley (SD) rats were treated orally with either olanzapine (1.0 mg/kg, t.i.d.), simvastatin (3.0 mg/kg, t.i.d.), olanzapine plus simvastatin (O+S), or vehicle (control) for 5 weeks.ResultsOlanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O+S co-treatment significantly reversed body weight gain but had no significant effect on food intake. Moreover, olanzapine treatment induced a slight but significant reduction in body temperature, with a decrease in locomotor activity. Fasting plasma glucose, triglycerides (TG), and total cholesterol (TC) levels were markedly elevated in the olanzapine-only group, whereas O+S co-treatment significantly ameliorated these changes. A down-regulating of uncoupling protein-1 (UCP1) and peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α) expression was observed in brown adipose tissue (BAT) in the olanzapine-only group, following a significant decrease in the ratio of phosphorylated PKA (p-PKA)/PKA. Interestingly, these protein changes could be reversed by co-treatment with O+B. Our results demonstrated simvastatin to be effective in ameliorating TC and TG elevated by olanzapine.ConclusionsModulation of BAT activity could be a partial mechanism in reducing metabolic side effects caused by SGAs in child and adolescent patients.

scholarly journals Brown adipose tissue activity is modulated in olanzapine-treated young rats by simvastatin

2020 ◽  
Author(s):  
Xuemei Liu ◽  
Xiyu Feng ◽  
Chao Deng ◽  
Lu Liu ◽  
Yanping Zeng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
Olanzapine Treatment ◽  
Brown Adipose

Abstract Background Prescription of second-generation antipsychotic drugs (SGAs) to childhood/adolescent has exponentially increased in recent years, which was associated with the greater risk of significant weight gain and dyslipidemia. Statin is considered a potential preventive and treatment approach for reducing SGA-induced weight gain and dyslipidemia in schizophrenia patients. However, the effect of statin treatment in children and adolescents with SGA-induced dyslipidemia is not clearly demonstrated.Methods To investigate the efficacy of statin interventions for reversing SGA-induced dyslipidemia, young Sprague Dawley rats were treated orally with either olanzapine (1.0 mg/kg, t.i.d.), simvastatin (3.0 mg/kg, t.i.d.), olanzapine plus simvastatin (O+S), or vehicle (control) for 5 weeks. Results Olanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O+S co-treatment significantly reversed body weight gain but without significant effects on food intake. Moreover, olanzapine treatment induced a slight but significant reduction in body temperature, with a decrease in locomotor activity. Fasting plasma glucose, triglycerides (TG), and total cholesterol (TC) levels were markedly elevated in the olanzapine-only group, whereas O+S co-treatment significantly ameliorated these changes. Pronounced activation of lipogenic gene expression in the liver and down-regulated expression of uncoupling protein-1 (UCP1) and peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α) in brown adipose tissue (BAT) was observed in the olanzapine-only group. Interestingly, these protein changes could be reversed by co-treatment with O+B. Conclusions Simvastatin is effective in ameliorating TC and TG elevated by olanzapine. Modulation of BAT activity by statins could be a partial mechanism in reducing metabolic side effects caused by SGAs in child and adolescent patients.

Refeeding and insulin increase lipoprotein lipase activity in rat brown adipose tissue

1989 ◽  
Vol 256 (5) ◽  
pp. E645-E650 ◽  
Author(s):  
C. M. Carneheim ◽  
S. E. Alexson
Keyword(s):  
Enzyme Activity ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Starvation Period ◽  
Lipoprotein Lipase Activity ◽  
Mrna Synthesis ◽  
Beta Adrenergic ◽  
Brown Adipose

Induction of lipoprotein lipase activity in brown adipose tissue (BAT) in response to cold stress has earlier been shown to be regulated by a beta-adrenergic mechanism and to be dependent on mRNA synthesis. In the present study, we have investigated the acute effects of refeeding after a short starvation period and the hormonal mechanism underlying the observed effects. Refeeding was found to rapidly increase tissue wet weight and lipoprotein lipase activity. The increase in enzyme activity could be blocked by the RNA synthesis inhibitor actinomycin D, indicating a gene activation. beta-Adrenergic blockade had no effect on this elevation of enzyme activity, but the increase could be mimicked by insulin injection. The results suggest that BAT contains two different pathways for regulation of lipoprotein lipase activity, both involving mRNA synthesis.

Effects of cold acclimation in dystrophic hamsters: reduction of heart necrosis

1986 ◽  
Vol 250 (2) ◽  
pp. R167-R174
Author(s):  
M. Desautels ◽  
R. A. Dulos
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Ventricular Hypertrophy ◽  
Body Weight Gain ◽  
Calcium Content ◽  
Co2 Production ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Plasma Creatine Kinase

The effects of cold acclimation on brown adipose tissue, heart, and skeletal muscles were evaluated to assess if the increase in metabolic activity associated with chronic exposure to 4 degrees C had any influence on the progression of the syndrome in dystrophic hamsters. Body weight gain was much slower in dystrophic animals kept at 22 degrees C and was unaffected by cold acclimation. Rates of O2 consumption and CO2 production were similar in normal and dystrophic hamsters kept at 22 degrees C, and both were increased in cold-acclimated normal and dystrophic animals. The amount of interscapular brown adipose tissue was about one-half of normal in dystrophic hamsters kept at 22 degrees C. In response to cold acclimation, as in normal hamsters, brown adipose tissue of dystrophic hamsters grew and increased its thermogenin content by more than fourfold. However, the concentration of thermogenin in isolated mitochondria remained unchanged. Heart ventricular hypertrophy was also observed in both normal and dystrophic hamsters after cold acclimation. The number and extent of cardiac necrotic lesions were significantly reduced in cold-acclimated dystrophic animals when compared with age-matched dystrophic hamsters kept at 22 degrees C. Heart calcium content and plasma creatine kinase levels were also reduced in dystrophic hamsters after cold acclimation. However, in soleus muscles the prevalence of centronucleated fibers, an indirect cumulative index of necrosis, as well as the extent of tissue necrosis were not significantly reduced in cold-acclimated dystrophic animals. Thus cold acclimation of dystrophic hamsters appeared to reduce necrosis predominantly in the heart.

Thyroxine 5'-deiodinase in brown adipose tissue of myopathic hamsters

1986 ◽  
Vol 251 (1) ◽  
pp. E8-E13 ◽  
Author(s):  
J. Kopecky ◽  
L. Sigurdson ◽  
I. R. Park ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Uncoupling Protein ◽  
High Fat ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Endogenous Production ◽  
Deiodinase Activity ◽  
Brown Adipose

Myopathic Syrian hamsters (BIO 14.6) have less brown adipose tissue (BAT) than normal. The trophic response of this tissue to cold is smaller than normal and trophic responses to diet and to photoperiod are absent. The objective was to find out whether activity of thyroxine 5'-deiodinase in their BAT was increased normally in response to cold and thus whether a defect in endogenous production of 3,5,3'-triiodothyronine might underlie the attenuated trophic response. The effect of feeding a high-fat diet on activity of 5'-deiodinase was also studied. Cold acclimation increased thyroxine 5'-deiodinase activity in BAT of the myopathic hamster, but the total remained smaller than normal because of the smaller size. The cold-induced increase in concentration of mitochondrial uncoupling protein was also smaller than normal. The level of serum 3,5,3'-triiodothyronine was low in myopathic hamsters and remained lower than normal when they were cold-exposed or cold acclimated. Feeding the high-fat diet to myopathic hamsters resulted in a greater than normal suppression of thyroxine 5'-deiodinase activity than in normal hamsters; the normal increases in protein content and in concentration of mitochondrial uncoupling protein were absent. We conclude that the defective trophic response of BAT of the myopathic hamster is not secondary to defective regulation of its thyroxine 5'-deiodinase activity because this activity does not appear to be obligatorily linked to hypertrophy of BAT. The low level of serum 3,5,3'-triiodothyronine in the myopathic hamster may be secondary to reduced capacity for peripheral thyroxine deiodination in its BAT.

Inhibition of Type 1 Iodothyronine Deiodinase by Bisphenol A

2019 ◽  
Vol 51 (10) ◽  
pp. 671-677 ◽  
Author(s):  
Maurício Martins da Silva ◽  
Carlos Frederico Lima Gonçalves ◽  
Leandro Miranda-Alves ◽  
Rodrigo Soares Fortunato ◽  
Denise P. Carvalho ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Bisphenol A ◽  
Brown Adipose Tissue ◽  
Tissue Type ◽  
Deiodinase Activity ◽  
Brown Adipose

AbstractPlastics are ubiquitously present in our daily life and some components of plastics are endocrine-disrupting chemicals, such as bisphenol A and phthalates. Herein, we aimed to evaluate the effect of plastic endocrine disruptors on type 1 and type 2 deiodinase activities, enzymes responsible for the conversion of the pro-hormone T4 into the biologically active thyroid hormone T3, both in vitro and in vivo. Initially, we incubated rat liver type 1 deiodinase and brown adipose tissue type 2 deiodinase samples with 0.5 mM of the plasticizers, and the deiodinase activity was measured. Among them, only BPA was capable to inhibit both type 1 and type 2 deiodinases. Then, adult male Wistar rats were treated orally with bisphenol A (40 mg/kg b.w.) for 15 days and hepatic type 1 deiodinase and brown adipose tissue type 2 deiodinase activities and serum thyroid hormone concentrations were measured. In vivo bisphenol A treatment significantly reduced hepatic type 1 deiodinase activity but did not affect brown adipose tissue type 2 deiodinase activity. Serum T4 levels were higher in bisphenol A group, while T3 remained unchanged. T3/T4 ratio was decreased in rats treated with bisphenol A, reinforcing the idea that peripheral metabolism of thyroid hormone was affected by bisphenol A exposure. Therefore, our results suggest that bisphenol A can affect the metabolism of thyroid hormone thus disrupting thyroid signaling.

THYROXINE 5′-DEIODINASE ACTIVITY IN BROWN ADIPOSE TISSUE

Endocrinology ◽  
1983 ◽  
Vol 112 (3) ◽  
pp. 1153-1155 ◽  
Author(s):  
JACK L. LEONARD ◽  
SARAH A MELLEN ◽  
REED P. LARSEN
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Deiodinase Activity ◽  
Brown Adipose
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