Thyroid status and effects of 3,5,3' triiodothyroacetic acid and Fenproporex in genetically lean and obese female rats

Autissier, N; Dumas, Paul; Loireau, Annie; Michel, R

doi:10.1016/0006-2952(80)90621-8

Cited by 12 publications

(7 citation statements)

References 21 publications

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“…TA 3 also effectively induces the expression of T 3 -responsive genes in the liver, including Dio1, to a similar extent as T 3 (Juge-Aubry et al 1995, Liang et al 1997, Alvarez et al 2004, MedinaGomez et al 2008. No changes in serum cholesterol and lipid levels or biliary excretion were observed after treatment of euthyroid rats for 4 weeks with 200 µg TA 3 / kg/day (Van Zyl 1957, Autissier et al 1980. When given at equivalent TSH-suppressive doses to euthyroid or hypothyroid patients, TA 3 induced similar increases in serum sex hormone binding globulin (SHBG) and ferritin levels as LT 4 (Bracco et al 1993, Sherman et al 1997.…”

Section: Livermentioning

confidence: 77%

Triiodothyroacetic acid in health and disease

Groeneweg

Peeters

Visser

et al. 2017

Journal of Endocrinology

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Thyroid hormone (TH) is crucial for development and metabolism of many tissues. The physiological relevance and therapeutic potential of TH analogs have gained attention in the field for many years. In particular, the relevance and use of 3,3′,5-triiodothyroacetic acid (Triac, TA 3 ) has been explored over the last decades. Although TA 3 closely resembles the bioactive hormone T 3 , differences in transmembrane transport and receptor isoformspecific transcriptional activation potency exist. For these reasons, the application of TA 3 as a treatment for resistance to TH (RTH) syndromes, especially MCT8 deficiency, is topic of ongoing research. This review is a summary of all currently available literature about the formation, metabolism, action and therapeutic applications of TA 3 .

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Section: Livermentioning

confidence: 77%

Triiodothyroacetic acid in health and disease

Groeneweg

Peeters

Visser

et al. 2017

Journal of Endocrinology

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“…Moreover, the presence of a glucocorticoid-responsive element in the promoter region of the pro-TRH gene (19) and the occurrence of glucocorticoid receptors in TRH-synthesizing cells in the paraventricular part of the PVH (7) argued strongly for a TRH expression regulation by glucocorticoids. Therefore, the hypercorticosteronemia of obese Zucker rats may be responsible, at least in part, for the reported functional hypothyroidism in these animals (1,23,42). A mechanism for TRH decrease in obesity and food deprivation is the apparent inhibition of the TRH neurons by neuropeptide Y (NPY) (14).…”

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

“…Depressed energy expenditure in obese animals results mainly from the low thermogenic activity at the level of the brown adipose tissue (BAT) (48). Low thermogenesis in fa/fa rats is a consequence of a decreased sympathetic outflow to BAT and also probably of a mild functional hypothyroidism (1,5,23,24,42,61).The fa/fa rat is characterized by very high circulating levels of corticosterone due to the hyperactivity of the hypothalamicpituitary-adrenal (HPA) axis (13). High levels of adrenocorticotropic hormone (ACTH) have been reported in the fa/fa rat, which also exhibits an increase in the clearance of corticosterone (59).…”

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confidence: 99%

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Corticosterone-dependent metabolic and neuroendocrine abnormalities in obese Zucker rats in relation to feeding

Duclos

Timofeeva²,

Michel³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

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The obese Zucker (fa/fa) rat is characterized by hyperphagia, hyperinsulinemia, an increase in fat deposition, and a hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis in fa/fa rats is hypersensitive to stressful experimental conditions. Food deprivation even leads to a stress reaction in obese fa/fa rats. The present study was conducted to investigate the role of corticosterone in obese rats on the basal, fasting, and postprandial metabolic rate as well as on the central expression of the thyrotropin-releasing hormone (TRH) in these conditions. In addition, the study was aimed at clarifying whether the high levels of corticosterone in obese rats are responsible for the induction of the stress reaction to food deprivation in these animals. The present results demonstrate that whole body fat oxidation and postprandial metabolic responses in obese Zucker rats were improved by adrenalectomy (ADX). At the level of the central nervous system, ADX reversed a decrease in TRH mRNA expression in the paraventricular hypothalamus (PVH) detected in fasting animals. Considering all feeding conditions, the obese rats demonstrated lower TRH mRNA levels compared with lean animals. ADX resulted in an enhanced postprandial activation of the parvocellular PVH. In contrast, the magnocellular part of the PVH was less responsive to refeeding in ADX animals. Finally, ADX failed to prevent the stress response of obese rats to food deprivation. The present results provide evidence that the removal of adrenals resolve some of the metabolic defects encountered in obese Zucker rats. They also demonstrate that not all the abnormalities of the obese Zucker rats are attributable to the hyperactivity of the HPA axis.

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“…It has been suggested that obese Zucker rats may have a low energy expenditure, which might account for susceptibility to cold and obesity (see, for example, Kaplan, 1981), but the measurements made by Armitage et al (1984) showed that the obese rats have higher 'per rat' energy expenditures than non-obese rats, and both show exactly the same curvilinear relationship between environmental temperature and expenditure. Thyroid hormones may control the rate of metabolism in the cold, and obese rats have been reported to be hypothyroid (see, for example, Autissier, Dumas, Loireau & Michel, 1980). Thus impaired thyroid function might account for susceptibility to cold in congenitally obese rats.…”

Section: Introductionmentioning

confidence: 99%

Thyroid Function in Male Zucker Rats Exposed to Cold

Whitaker¹,

Robinson²,

Rayfield³

et al. 1988

Exp Physiol

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SUMMARYNon-obese and obese Zucker rats were exposed to 6 OC for 20 days. At the end of the experiment thyroid stimulating hormone (TSH), circulating thyroid hormones, and the weights of the thyroid gland and a brown adipose tissue pad were measured. TSH and 3,5,3'-triiodothyronine concentrations and brown adipose tissue weights increased in response to cold in both phenotypes but by larger amounts in obese rats. Free thyroxine was lower in obese rats. There appears to be no defect in thyroid function in congenitally obese rats exposed to cold, or in their ability to develop brown adipose tissue.

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Thyroid status and effects of 3,5,3' triiodothyroacetic acid and Fenproporex in genetically lean and obese female rats

Cited by 12 publications

References 21 publications

Triiodothyroacetic acid in health and disease

Triiodothyroacetic acid in health and disease

Corticosterone-dependent metabolic and neuroendocrine abnormalities in obese Zucker rats in relation to feeding

Thyroid Function in Male Zucker Rats Exposed to Cold

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