Direct Evidence of Short-Term Cold-Induced TRH Release in the Median Eminence of Unanesthetized Rats

Arancibia, Sandor; Tapia‐Arancibia, Lucía; Assenmacher, I; Astier, H

doi:10.1159/000123547

Cited by 102 publications

(47 citation statements)

References 15 publications

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“…Although it would seem surprising that a presumptive endocrine factor is strongly expressed in an exocrine gland, there have been numerous reports of other growth factors being expressed in salivary glands (15)(16)(17)(18)(19), and it has been shown that endocrine factors expressed after introduction of DNA into these glands are readily secreted into the bloodstream (20,21). Indeed, a body of opinion contends that salivary glands have a mixed exocrine and endocrine function (22)(23)(24). Similarly, we also saw expression in the lacrimal glands of newborn mice.…”

Section: Resultsmentioning

confidence: 99%

Resistance to diet-induced obesity in mice globally overexpressing OGH/GPB5

Macdonald

Wortley

Gowen

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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We identified a glycoprotein hormone ␤-subunit (OGH, also called GPB5) that, as a heterodimer with the ␣-subunit GPA2, serves as a second ligand for the thyroid-stimulating hormone receptor. Mice in which the OGH gene is deleted (OGH ؊/؊ ) are indistinguishable from WT littermates in body weight, response to high-fat diet, metabolic parameters, body composition, and insulin tolerance. Mice engineered to transgenically globally overexpress OGH (OGH-TG) develop Ϸ2-fold elevations in their basal thyroid levels and weigh slightly less than WT littermates despite increased food intake because of an increase in their metabolic rates. Moreover, when OGH-TG mice are challenged with a high-fat diet, they gain significantly less weight and body fat than their WT littermates. The OGH-TG mice also have reduced blood glucose, insulin, cholesterol, and triglycerides. In contrast to other approaches in which the thyroid axis is activated, OGH-TG mice exhibit only minor changes in heart rate and blood pressure. Our findings suggest that constitutive low-level activation of the thyroid axis (via OGH or other means) may provide a beneficial therapeutic approach for combating diet-induced obesity.cholesterol ͉ metabolic rate ͉ thyroid T hyroid-stimulating hormone (TSH) and the TSH receptor (TSHR) are key proteins in the control of thyroid function. TSH synthesis and release is stimulated by hypothalamic TSHreleasing hormone (TRH) and is down-regulated (inhibited) by thyroid hormone in a classic endocrine negative-feedback loop. The specificity inherent in TSH resides in its unique ␤-subunit that heterodimerizes with a common ␣-subunit, which it shares with the other glycoprotein hormones [i.e., follicle-stimulating hormone (FSH), luteinizing hormone, and chorionic gonadotropin]. The primary physiological actions of TSH on the thyroid are stimulation of the synthesis and release of 3,5,3Ј,5Ј-tetraiodo-L-thyronine (T4) and 3,5,3Ј-triiodo-L-thyronine (T3) (together termed thyroid hormone) and promotion of thyroid growth; for example, it has been shown that thyroid development is arrested in mice with targeted disruption of the common ␣-subunit (1).Clinically, thyroid hormone is used primarily as a replacement therapy for the patients with hypothyroidism, and it has been considered as a possible therapy for weight reduction (because of its ability to increase metabolism and energy expenditures), for lowering cholesterol, and even to build bone (in osteoporosis). One of the major hurdles in this approach has been the cardiovascular toxicity observed after administration of the endogenous ligands T4 and T3 or nonselective thyroid hormone agonists. The two major subtypes of the thyroid hormone receptors that mediate these responses, TR␣ and TR␤, are the products of different genes and are also differentially processed to each yield two isoforms. It has been argued that modulation of heart rate and rhythm is mediated predominantly by activation of TR␣ 1 (2-4), and as a result, recent pharmaceutical research efforts have focused on develop...

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Section: Resultsmentioning

confidence: 99%

Resistance to diet-induced obesity in mice globally overexpressing OGH/GPB5

Macdonald

Wortley

Gowen

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…TRH gene expression in the PVN is strictly controlled by the feedback action of thyroid hormones (Koller et al 1987, Segerson et al 1987b, Rondel et al 1988, Hollenberg et al 1995, Satoh et al 1999 and is regulated in multiple physiological conditions including: circadian and estrous cycles (Covarrubias et al 1988, Uribe et al 1991, suckling and weaning (Uribe et al 1993, 1995b, Sánchez et al 2001, cold stress (Zoeller et al 1990, Uribe et al 1993, Sánchez et al 2001 and fasting (Blake et al 1991, Legradi et al 1997a, Fekete et al 2002. In addition, a fast and transient increase in proTRH mRNA levels in the PVN (maximal at 30-60 min) is produced by cold exposure or suckling (Uribe et al 1993, Sánchez et al 2001, conditions that activate TRH release from the median eminence (Arancibia et al 1983, de Greef et al 1987, Rondel et al 1988.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone represses cAMP rapid upregulation of TRH gene transcription: identification of a composite glucocorticoid response element and a cAMP response element in TRH promoter

Cote-Vélez

Pérez-Martı́nez²,

My³

et al. 2005

Journal of Molecular Endocrinology

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Hypothalamic proTRH mRNA levels are rapidly increased (at 1 h) in vivo by cold exposure or suckling, and in vitro by 8Br-cAMP or glucocorticoids. The aim of this work was to study whether these effects occurred at the transcriptional level. Hypothalamic cells transfected with rat TRH promoter (−776/+85) linked to the luciferase reporter showed increased transcription by protein kinase (PK) A and PKC activators, or by dexamethasone (dex), but co-incubation with dex and 8Br-cAMP decreased their stimulatory effect (as observed for proTRH mRNA levels). These effects were also observed in NIH-3T3-transfected cells supporting a characteristic of TRH promoter and not of hypothalamic cells. Transcriptional regulation by 8Br-cAMP was mimicked by noradrenaline which increased proTRH mRNA levels, but not in the presence of dex. PKA inhibition by H89 avoided 8Br-cAMP or noradrenaline stimulation. TRH promoter sequences, cAMP response element (CRE)-like (−101/−94 and −59/−52) and glucocorticoid response element (GRE) half-site (−210/−205), were analyzed by electrophoretic mobility shift assays with nuclear extracts from hypothalamic or neuroblastoma cultures. PKA stimulation increased binding to CRE (−101/−94) but not to CRE (−59/−52); dex or 12-O-tetradecanoylphorbol-13-acetate (TPA) increased binding to GRE, a composite site flanked by a perfect and an imperfect activator protein (AP-1) site in the complementary strand. Interference was observed in the binding of CRE or GRE with nuclear extracts from cells co-incubated for 3 h with 8Br-cAMP and dex; from cells incubated for 1 h, only the binding to GRE showed interference. Rapid cross-talk of glucocorticoids with PKA signaling pathways regulating TRH transcription constitutes another example of neuroendocrine integration.

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“…As CART is the only known peptide that coexists with TRH in the PVN (Fekete et al, 2000) it is feasible that under the appropriate circumstances, the genes for both peptides may become simultaneously activated. The paradigm of the lactating rat subject to either suckling or cold exposure, conditions when TRH neurons are rapidly activated in the PVN (Sánchez et al, 2001), exemplify in vivo situations where TRH is released but the secretion of TSH and prolactin diverge (Adels et al, 1986;Arancibia et al, 1983;de Greef and Visser, 1981;Sanchez et al, 2001;van Haasteren et al, 1996). Using this paradigm, we demonstrate herein a differential activation of CART neurons in the PVN, stimulated by cold exposure but not by suckling.…”

Section: Discussionmentioning

confidence: 63%

“…Included among the physiologic stimuli associated with activation of hypophysiotropic TRH neurons are suckling and cold exposure that induce TRH release (Arancibia et al, 1983;de Greef and Visser, 1981;Fink and Ben-Aroya, 1983;Hefco et al, 1975) and a rapid (30-60 min) and transient increase in proTRH mRNA levels in the PVN (Rage et al, 1994;Sanchez et al, 2001;Uribe et al, 1993;van Haasteren et al, 1996). However, the response of pituitary target cells is specific to the stimulus.…”

Section: Introductionmentioning

confidence: 99%

Cocaine- and amphetamine-regulated transcript (CART) expression is differentially regulated in the hypothalamic paraventricular nucleus of lactating rats exposed to suckling or cold stimulation

et al. 2007

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Neural stimuli, such as suckling or cold exposure, increase TRH mRNA in the paraventricular nucleus (PVN) of the rat hypothalamus, yet only suckling induces prolactin secretion. As TRH co-localizes with cocaine-and amphetamine-regulated transcript (CART) in hypophysiotropic neurons of the PVN, and CART inhibits TRH-induced prolactin release but not TRH-induced TSH release in adenohypophyseal cell cultures, we raised the possibility that differential regulation of CART gene expression in the PVN may explain the differences in prolactin secretion following each of the two stimuli. Primiparous female rats were mated and handled daily during the pre-and postpartum periods. After delivery, the litter was adjusted to 8 pups and at mid-lactation, dams were separated from their pups for 8 hours and exposed to either 1h of cold or 30 min of suckling. Long term effects of suckling were studied by separating pups from their mothers for 24h, followed by a 12h period of continuous suckling. Serum TSH levels increased in response to cold exposure, while prolactin levels were increased by suckling and diminished by cold exposure. CART mRNA levels increased in rostral and mid parts of the medial parvocellular PVN following cold exposure but not after suckling stimulation. These data demonstrate a differential regulation of CART gene expression in hypophysiotropic neurons in response to stimuli that increase TRH mRNA levels, and suggest that CART activation in the PVN may contribute to the decrease in PRL release when the thyroid axis is activated by cold exposure.Section: Regulatory systems

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Direct Evidence of Short-Term Cold-Induced TRH Release in the Median Eminence of Unanesthetized Rats

Cited by 102 publications

References 15 publications

Resistance to diet-induced obesity in mice globally overexpressing OGH/GPB5

Resistance to diet-induced obesity in mice globally overexpressing OGH/GPB5

Dexamethasone represses cAMP rapid upregulation of TRH gene transcription: identification of a composite glucocorticoid response element and a cAMP response element in TRH promoter

Cocaine- and amphetamine-regulated transcript (CART) expression is differentially regulated in the hypothalamic paraventricular nucleus of lactating rats exposed to suckling or cold stimulation

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