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  1. AU="Soledad Bárez-López"
  2. AU="Raser, K J"
  3. AU=Pons Douwe AU=Pons Douwe
  4. AU="Johnson, James W"
  5. AU="Menon, Pradeep A"
  6. AU="van Eyk, Clare L"
  7. AU="Portela, Ricardo Dias"
  8. AU="Ouyang, Wei"
  9. AU="Zwarthoff, Ellen C."
  10. AU="de Souza, G T"
  11. AU="Nagel, Sean J"
  12. AU="Patel, Devendra K"
  13. AU="Xie, B W"
  14. AU="Grandal-Platero, Marta"
  15. AU=Fetz Allison E.
  16. AU="Owens, Jeana"
  17. AU="Kohn, Samuel"
  18. AU="Saitoh, Yuji"
  19. AU="Chiarini, Elisabetta"
  20. AU="Bilodeau, Marc"
  21. AU=Arora Neelima AU=Arora Neelima
  22. AU="Eline Boghaert"
  23. AU=Hurwitz Naama
  24. AU="Trocha, Andrzej M"
  25. AU="Smits, Anthal I P M"
  26. AU=Milton Ross D.
  27. AU="Mónica Lopes-Marques"
  28. AU="Olasińska-Wiśniewska, Anna"
  29. AU="Michel, Alexander"
  30. AU="Ku, Chin-Jen"
  31. AU="Potts, Daniel"
  32. AU="Liu, Xiang"
  33. AU="Mire, Erik"
  34. AU="Ching-Yi Hu"

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  1. Artikel ; Online: Osmoadaptive GLP-1R signalling in hypothalamic neurones inhibits antidiuretic hormone synthesis and release

    Michael P. Greenwood / Mingkwan Greenwood / Soledad Bárez-López / Joe W. Hawkins / Katherine Short / Danijela Tatovic / David Murphy

    Molecular Metabolism, Vol 70, Iss , Pp 101692- (2023)

    2023  

    Abstract: Objectives: The excessive release of the antidiuretic hormone vasopressin is implicated in many diseases including cardiovascular disease, diabetes, obesity, and metabolic syndrome. Once thought to be elevated as a consequence of diseases, data now ... ...

    Abstract Objectives: The excessive release of the antidiuretic hormone vasopressin is implicated in many diseases including cardiovascular disease, diabetes, obesity, and metabolic syndrome. Once thought to be elevated as a consequence of diseases, data now supports a more causative role. We have previously identified CREB3L1 as a transcription factor that co-ordinates vasopressin synthesis and release in the hypothalamus. The objective here was to identify mechanisms orchestrated by CREB3L1 that co-ordinate vasopressin release. Methods: We mined Creb3l1 knockdown SON RNA-seq data to identify downstream target genes. We proceeded to investigate the expression of these genes and associated pathways in the supraoptic nucleus of the hypothalamus in response to physiological and pharmacological stimulation. We used viruses to selectively knockdown gene expression in the supraoptic nucleus and assessed physiological and metabolic parameters. We adopted a phosphoproteomics strategy to investigate mechanisms that facilitate hormone release by the pituitary gland. Results: We discovered glucagon like peptide 1 receptor (Glp1r) as a downstream target gene and found increased expression in stimulated vasopressin neurones. Selective knockdown of supraoptic nucleus Glp1rs resulted in decreased food intake and body weight. Treatment with GLP-1R agonist liraglutide decreased vasopressin synthesis and release. Quantitative phosphoproteomics of the pituitary neurointermediate lobe revealed that liraglutide initiates hyperphosphorylation of presynapse active zone proteins that control vasopressin exocytosis. Conclusion: In summary, we show that GLP-1R signalling inhibits the vasopressin system. Our data advises that hydration status may influence the pharmacodynamics of GLP-1R agonists so should be considered in current therapeutic strategies.
    Schlagwörter Liraglutide ; Hypothalamus ; Hydration ; Vasopressin ; Oxytocin ; Glucagon like peptide 1 ; Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-04-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Intracerebroventricular administration of the thyroid hormone analog TRIAC increases its brain content in the absence of MCT8.

    Soledad Bárez-López / Carmen Grijota-Martínez / Xiao-Hui Liao / Samuel Refetoff / Ana Guadaño-Ferraz

    PLoS ONE, Vol 14, Iss 12, p e

    2019  Band 0226017

    Abstract: Patients lacking the thyroid hormone (TH) transporter MCT8 present abnormal serum levels of TH: low thyroxine and high triiodothyronine. They also have severe neurodevelopmental defects resulting from cerebral hypothyroidism, most likely due to impaired ... ...

    Abstract Patients lacking the thyroid hormone (TH) transporter MCT8 present abnormal serum levels of TH: low thyroxine and high triiodothyronine. They also have severe neurodevelopmental defects resulting from cerebral hypothyroidism, most likely due to impaired TH transport across the brain barriers. The use of TH analogs, such as triiodothyroacetic acid (TRIAC), that can potentially access the brain in the absence of MCT8 and restore at least a subset of cerebral TH actions could improve the neurological defects in these patients. We hypothesized that direct administration of TRIAC into the brain by intracerebroventricular delivery to mice lacking MCT8 could bypass the restriction at the brain barriers and mediate TH action without causing hypermetabolism. We found that intracerebroventricular administration of therapeutic doses of TRIAC does not increase further plasma triiodothyronine or further decrease plasma thyroxine levels and does not alter TH content in the cerebral cortex. Although TRIAC content increased in the brain, it did not induce TH-mediated actions on selected target genes. Our data suggest that intracerebroventricular delivery of TRIAC has the ability to target the brain in the absence of MCT8 and should be further investigated to address its potential therapeutic use in MCT8 deficiency.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2019-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Intranasal delivery of Thyroid hormones in MCT8 deficiency.

    Carmen Grijota-Martínez / Soledad Bárez-López / Eva Ausó / Samuel Refetoff / William H Frey / Ana Guadaño-Ferraz

    PLoS ONE, Vol 15, Iss 7, p e

    2020  Band 0236113

    Abstract: Loss of function mutations in the gene encoding the thyroid hormone transporter monocarboxylate transporter 8 (MCT8) lead to severe neurodevelopmental defects in humans associated with a specific thyroid hormone phenotype manifesting high serum 3,5,3'- ... ...

    Abstract Loss of function mutations in the gene encoding the thyroid hormone transporter monocarboxylate transporter 8 (MCT8) lead to severe neurodevelopmental defects in humans associated with a specific thyroid hormone phenotype manifesting high serum 3,5,3'-triiodothyronine (T3) and low thyroxine (T4) levels. Patients present a paradoxical state of peripheral hyperthyroidism and brain hypothyroidism, this last one most likely arising from impaired thyroid hormone transport across the brain barriers. The administration of thyroid hormones by delivery pathways that bypass the brain barriers, such as the intranasal delivery route, offers the possibility to improve the neurological defects of MCT8-deficient patients. In this study, the thyroid hormones T4 and T3 were administrated intranasally in different mouse models of MCT8 deficiency. We have found that, under the present formulation, intranasal administration of thyroid hormones does not increase the content of thyroid hormones in the brain and further raises the peripheral thyroid hormone levels. Our data suggests intranasal delivery of thyroid hormones is not a suitable therapeutic strategy for MCT8 deficiency, although alternative formulations could be considered in the future to improve the nose-to-brain transport.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Abnormal motor phenotype at adult stages in mice lacking type 2 deiodinase.

    Soledad Bárez-López / Daniel Bosch-García / David Gómez-Andrés / Irene Pulido-Valdeolivas / Ana Montero-Pedrazuela / Maria Jesus Obregon / Ana Guadaño-Ferraz

    PLoS ONE, Vol 9, Iss 8, p e

    2014  Band 103857

    Abstract: Background Thyroid hormones have a key role in both the developing and adult central nervous system and skeletal muscle. The thyroid gland produces mainly thyroxine (T4) but the intracellular concentrations of 3,5,3'-triiodothyronine (T3; the ... ...

    Abstract Background Thyroid hormones have a key role in both the developing and adult central nervous system and skeletal muscle. The thyroid gland produces mainly thyroxine (T4) but the intracellular concentrations of 3,5,3'-triiodothyronine (T3; the transcriptionally active hormone) in the central nervous system and skeletal muscle are modulated by the activity of type 2 deiodinase (D2). To date no neurological syndrome has been associated with mutations in the DIO2 gene and previous studies in young and juvenile D2-knockout mice (D2KO) did not find gross neurological alterations, possibly due to compensatory mechanisms. Aim This study aims to analyze the motor phenotype of 3-and-6-month-old D2KO mice to evaluate the role of D2 on the motor system at adult stages in which compensatory mechanisms could have failed. Results Motor abilities were explored by validated tests. In the footprint test, D2KO showed an altered global gait pattern (mice walked slower, with shorter strides and with a hindlimb wider base of support than wild-type mice). No differences were detected in the balance beam test. However, a reduced latency to fall was found in the rotarod, coat-hanger and four limb hanging wire tests indicating impairment on coordination and prehensile reflex and a reduction of muscle strength. In histological analyses of cerebellum and skeletal muscle, D2KO mice did not present gross structural abnormalities. Thyroid hormones levels and deiodinases activities were also determined. In D2KO mice, despite euthyroid T3 and high T4 plasma levels, T3 levels were significantly reduced in cerebral cortex (48% reduction) and skeletal muscle (33% reduction), but not in the cerebellum where other deiodinase (type 1) is expressed. Conclusions The motor alterations observed in D2KO mice indicate an important role for D2 in T3 availability to maintain motor function and muscle strength. Our results suggest a possible implication of D2 in motor disorders.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 796
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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