@article{MTMT:34578220,
	title = {GLP-1 Receptor Signaling Has Different Effects on the Perikarya and Axons of the Hypophysiotropic Thyrotropin-Releasing Hormone Synthesizing Neurons in Male Mice},
	url = {https://m2.mtmt.hu/api/publication/34578220},
	author = {Ruska, Yvette Magdolna and Péterfi, Zoltán Attila and Stiftné Szilvásy-Szabó, Anett and Kővári, Dóra and Hrabovszky, Erik and Dorogházi, Beáta Vanessza and Gereben, Balázs and Tóth, Blanka and Matziari, Magdalini and Wittmann, Gábor and Fekete, Csaba},
	doi = {10.1089/thy.2023.0284},
	journal-iso = {THYROID},
	journal = {THYROID},
	volume = {34},
	unique-id = {34578220},
	issn = {1050-7256},
	abstract = {Background: Glucagon-like peptide 1 (GLP-1) is involved in the regulation of energy and glucose homeostasis. As GLP-1 has similar effects on the energy homeostasis as the hypophysiotropic thyrotropin-releasing hormone (TRH) neurons that regulate the hypothalamic-pituitary-thyroid (HPT) axis, we raised the possibility that the TRH neurons are involved in the mediation of the effects of GLP-1. Therefore, the relationship and interaction of the GLP-1 system and the TRH neurons of the hypothalamic paraventricular nucleus (PVN) were studied.Methods: To examine the anatomical and functional relationship of TRH neurons and the GLP-1 system in the PVN, immunocytochemistry, in situ hybridization, in vitro patch-clamp electrophysiology, metabolic phenotyping, and explant experiments were performed.Results: Our data demonstrate that the TRH neurons of the PVN are innervated by GLP-1 producing neurons and express the GLP-1 receptor (GLP-1R). However, not only do the GLP-1-innervated TRH neurons express GLP-1R but the receptor is also present in the axons of the hypophysiotropic TRH neurons in the blood-brain barrier free median eminence (ME) suggesting that peripherally derived GLP-1 may also influence the TRH neurons. In vitro, GLP-1 increased the firing rate of TRH neurons and depolarized them. In addition, GLP-1 directly stimulated the GABAergic input of a population of TRH neurons. Furthermore, GLP-1 inhibited the release of TRH from the hypophysiotropic axons in the ME. In vivo, peripheral GLP-1R agonist administration markedly inhibited the food intake and the energy expenditure, but had no effect on the TRH expression in the PVN and resulted in lower circulating free T4 levels.Conclusions: Our results indicate that GLP-1R activation has a direct stimulatory effect on TRH neurons in the PVN, but the activation of GLP-1R may also inhibit TRH neurons by facilitating their inhibitory inputs or by inhibiting the axon terminals of these cells in the ME. The innervation of TRH neurons by GLP-1 neurons suggests that TRH neurons might be influenced by both circulating GLP-1 and by GLP-1 neurons of the nucleus tractus solitarii. The lack of GLP-1R agonist-induced regulation of TRH neurons in vivo suggests that the HPT axis does not mediate the GLP-1R agonist-induced weight loss.},
	keywords = {Release; HYPOTHALAMIC PARAVENTRICULAR NUCLEUS; median eminence; TRH; Glucagon-like peptide-1 receptor},
	year = {2024},
	eissn = {1557-9077},
	pages = {252-260},
	orcid-numbers = {Kővári, Dóra/0000-0001-5346-822X}
}

@article{MTMT:34729392,
	title = {A previously uncharacterized Factor Associated with Metabolism and Energy (FAME/C14orf105/CCDC198/1700011H14Rik) is related to evolutionary adaptation, energy balance, and kidney physiology},
	url = {https://m2.mtmt.hu/api/publication/34729392},
	author = {Petersen, Julian and Englmaier, Lukas and Artemov, Artem V. and Poverennaya, Irina and Mahmoud, Ruba and Bouderlique, Thibault and Tesarova, Marketa and Deviatiiarov, Ruslan and Stiftné Szilvásy-Szabó, Anett and Akkuratov, Evgeny E. and Pajuelo Reguera, David and Zeberg, Hugo and Kaucka, Marketa and Kastriti, Maria Eleni and Krivanek, Jan and Radaszkiewicz, Tomasz and Gömöryová, Kristína and Knauth, Sarah and Potesil, David and Zdrahal, Zbynek and Ganji, Ranjani Sri and Grabowski, Anna and Buhl, Miriam E. and Zikmund, Tomas and Kavkova, Michaela and Axelson, Håkan and Lindgren, David and Kramann, Rafael and Kuppe, Christoph and Erdélyi, Ferenc and Máté, Zoltán and Szabó, Gábor and Koehne, Till and Harkany, Tibor and Fried, Kaj and Kaiser, Jozef and Boor, Peter and Fekete, Csaba and Rozman, Jan and Kasparek, Petr and Prochazka, Jan and Sedlacek, Radislav and Bryja, Vitezslav and Gusev, Oleg and Adameyko, Igor},
	doi = {10.1038/s41467-023-38663-7},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {14},
	unique-id = {34729392},
	issn = {2041-1723},
	abstract = {In this study we use comparative genomics to uncover a gene with uncharacterized function ( 1700011H14Rik/C14orf105/CCDC198 ), which we hereby name FAME (Factor Associated with Metabolism and Energy). We observe that FAME shows an unusually high evolutionary divergence in birds and mammals. Through the comparison of single nucleotide polymorphisms, we identify gene flow of FAME from Neandertals into modern humans. We conduct knockout experiments on animals and observe altered body weight and decreased energy expenditure in Fame knockout animals, corresponding to genome-wide association studies linking FAME with higher body mass index in humans. Gene expression and subcellular localization analyses reveal that FAME is a membrane-bound protein enriched in the kidneys. Although the gene knockout results in structurally normal kidneys, we detect higher albumin in urine and lowered ferritin in the blood. Through experimental validation, we confirm interactions between FAME and ferritin and show co-localization in vesicular and plasma membranes.},
	year = {2023},
	eissn = {2041-1723},
	orcid-numbers = {Petersen, Julian/0000-0002-7444-0610; Englmaier, Lukas/0000-0002-0082-2616; Tesarova, Marketa/0000-0002-5200-7365; Deviatiiarov, Ruslan/0000-0003-0019-2076; Pajuelo Reguera, David/0000-0002-7715-9402; Zeberg, Hugo/0000-0001-7118-1249; Kaucka, Marketa/0000-0002-8781-9769; Krivanek, Jan/0000-0002-7590-187X; Radaszkiewicz, Tomasz/0000-0003-4850-9933; Gömöryová, Kristína/0000-0003-4407-3917; Potesil, David/0000-0003-0390-0904; Grabowski, Anna/0000-0001-7304-5697; Buhl, Miriam E./0000-0003-0627-9228; Zikmund, Tomas/0000-0003-2948-5198; Kavkova, Michaela/0000-0001-7435-9292; Kuppe, Christoph/0000-0003-4597-9833; Harkany, Tibor/0000-0002-6637-5900; Fried, Kaj/0000-0002-9997-7078; Kaiser, Jozef/0000-0002-7397-125X; Boor, Peter/0000-0001-9921-4284; Rozman, Jan/0000-0002-8035-8904; Prochazka, Jan/0000-0003-4675-8995; Sedlacek, Radislav/0000-0002-3352-392X; Bryja, Vitezslav/0000-0002-9136-5085; Adameyko, Igor/0000-0001-5471-0356}
}

@article{MTMT:34232164,
	title = {In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse},
	url = {https://m2.mtmt.hu/api/publication/34232164},
	author = {Sinkó, Richárd and Mohácsik, Petra and Fekete, Csaba and Gereben, Balázs},
	doi = {10.3791/65657},
	journal-iso = {JOVE-J VIS EXP},
	journal = {JOVE-JOURNAL OF VISUALIZED EXPERIMENTS},
	volume = {2023},
	unique-id = {34232164},
	issn = {1940-087X},
	year = {2023},
	eissn = {1940-087X}
}

@article{MTMT:34038280,
	title = {Author Correction: A previously uncharacterized Factor Associated with Metabolism and Energy (FAME/C14orf105/CCDC198/1700011H14Rik) is related to evolutionary adaptation, energy balance, and kidney physiology},
	url = {https://m2.mtmt.hu/api/publication/34038280},
	author = {Petersen, Julian and Englmaier, Lukas and Artemov, Artem V. and Poverennaya, Irina and Mahmoud, Ruba and Bouderlique, Thibault and Tesarova, Marketa and Deviatiiarov, Ruslan and Stiftné Szilvásy-Szabó, Anett and Akkuratov, Evgeny E. and Pajuelo Reguera, David and Zeberg, Hugo and Kaucka, Marketa and Kastriti, Maria Eleni and Krivanek, Jan and Radaszkiewicz, Tomasz and Gömöryová, Kristína and Knauth, Sarah and Potesil, David and Zdrahal, Zbynek and Ganji, Ranjani Sri and Grabowski, Anna and Buhl, Miriam E. and Zikmund, Tomas and Kavkova, Michaela and Axelson, Håkan and Lindgren, David and Kramann, Rafael and Kuppe, Christoph and Erdélyi, Ferenc and Máté, Zoltán and Szabó, Gábor and Koehne, Till and Harkany, Tibor and Fried, Kaj and Kaiser, Jozef and Boor, Peter and Fekete, Csaba and Rozman, Jan and Kasparek, Petr and Prochazka, Jan and Sedlacek, Radislav and Bryja, Vitezslav and Gusev, Oleg and Adameyko, Igor},
	doi = {10.1038/s41467-023-39373-w},
	journal-iso = {NAT COMMUN},
	journal = {NATURE COMMUNICATIONS},
	volume = {14},
	unique-id = {34038280},
	issn = {2041-1723},
	year = {2023},
	eissn = {2041-1723},
	orcid-numbers = {Englmaier, Lukas/0000-0002-0082-2616; Tesarova, Marketa/0000-0002-5200-7365; Deviatiiarov, Ruslan/0000-0003-0019-2076; Pajuelo Reguera, David/0000-0002-7715-9402; Zeberg, Hugo/0000-0001-7118-1249; Kaucka, Marketa/0000-0002-8781-9769; Krivanek, Jan/0000-0002-7590-187X; Radaszkiewicz, Tomasz/0000-0003-4850-9933; Gömöryová, Kristína/0000-0003-4407-3917; Potesil, David/0000-0003-0390-0904; Grabowski, Anna/0000-0001-7304-5697; Buhl, Miriam E./0000-0003-0627-9228; Zikmund, Tomas/0000-0003-2948-5198; Kavkova, Michaela/0000-0001-7435-9292; Kuppe, Christoph/0000-0003-4597-9833; Harkany, Tibor/0000-0002-6637-5900; Fried, Kaj/0000-0002-9997-7078; Kaiser, Jozef/0000-0002-7397-125X; Boor, Peter/0000-0001-9921-4284; Rozman, Jan/0000-0002-8035-8904; Prochazka, Jan/0000-0003-4675-8995; Sedlacek, Radislav/0000-0002-3352-392X; Bryja, Vitezslav/0000-0002-9136-5085}
}

@article{MTMT:33917113,
	title = {Axonal T3 uptake and transport can trigger thyroid hormone signaling in the brain},
	url = {https://m2.mtmt.hu/api/publication/33917113},
	author = {Salas-Lucia, Federico and Fekete, Csaba and Sinkó, Richárd and Egri, Péter and Rada, Kristóf Róbert and Ruska, Yvette Magdolna and Gereben, Balázs and Bianco, Antonio},
	doi = {10.7554/eLife.82683},
	journal-iso = {ELIFE},
	journal = {ELIFE},
	volume = {12},
	unique-id = {33917113},
	issn = {2050-084X},
	abstract = {The development of the brain, as well as mood and cognitive functions, are affected by thyroid hormone (TH) signaling. Neurons are the critical cellular target for TH action, with T3 regulating the expression of important neuronal gene sets. However, the steps involved in T3 signaling remain poorly known given that neurons express high levels of type 3 deiodinase (D3), which inactivates both T4 and T3. To investigate this mechanism, we used a compartmentalized microfluid device and identified a novel neuronal pathway of T3 transport and action that involves axonal T3 uptake into clathrin-dependent, endosomal/non-degradative lysosomes (NDLs). NDLs-containing T3 are retrogradely transported via microtubules, delivering T3 to the cell nucleus, and doubling the expression of a T3-responsive reporter gene. The NDLs also contain the monocarboxylate transporter 8 (Mct8) and D3, which transport and inactivate T3, respectively. Notwithstanding, T3 gets away from degradation because D3's active center is in the cytosol. Moreover, we used a unique mouse system to show that T3 implanted in specific brain areas can trigger selective signaling in distant locations, as far as the contralateral hemisphere. These findings provide a pathway for L-T3 to reach neurons and resolve the paradox of T3 signaling in the brain amid high D3 activity.},
	year = {2023},
	eissn = {2050-084X},
	orcid-numbers = {Salas-Lucia, Federico/0000-0003-4141-5790; Rada, Kristóf Róbert/0000-0001-7849-5312; Bianco, Antonio/0000-0001-7737-6813}
}

@CONFERENCE{MTMT:33629260,
	title = {Enhanced food intake and abnormal deiodinase mRNA expression pattern in the triple transgenic Alzheimer’s disease model mice},
	url = {https://m2.mtmt.hu/api/publication/33629260},
	author = {Szabó, Adrienn and Farkas, Szidónia and Török, Bibiána and Correia, Pedro and Kovács, T and Kádár, Andrea and Hegedűs, P and Fekete, Csaba and Zelena, Dóra},
	booktitle = {6th Hungarian Neuroscience Doctoral Conference for Undergraduate Students, Graduate Students and Junior Postdoc},
	unique-id = {33629260},
	year = {2023},
	pages = {29; 93},
	orcid-numbers = {Correia, Pedro/0000-0002-4410-9855}
}

@CONFERENCE{MTMT:33628989,
	title = {Enhanced food intake and abnormal deiodinase mRNA expression pattern in the triple transgenic Alzheimer’s disease model mice},
	url = {https://m2.mtmt.hu/api/publication/33628989},
	author = {Szabó, Adrienn and Farkas, Szidónia and Török, Bibiána and Correia, Pedro and Kovács, T and Kádár, Andrea and Hegedűs, P and Fekete, Csaba and Zelena, Dóra},
	booktitle = {Joint Neuroscience Meeting of the Hungarian Neuroscience Society (MITT) & the Austrian Neuroscience Association (ANA)},
	unique-id = {33628989},
	year = {2023},
	orcid-numbers = {Correia, Pedro/0000-0002-4410-9855}
}

@article{MTMT:33560486,
	title = {Unique, Specific CART Receptor-Independent Regulatory Mechanism of CART(55-102) Peptide in Spinal Nociceptive Transmission and Its Relation to Dipeptidyl-Peptidase 4 (DDP4)},
	url = {https://m2.mtmt.hu/api/publication/33560486},
	author = {Kozsurek, Márk and Király, Kornél P and Gyimesi, Klára and Lukácsi, Erika and Fekete, Csaba and Gereben, Balázs and Mohácsik, Petra and Helyes, Zsuzsanna and Bölcskei, Kata and Tékus, Valéria and Pap, Károly and Szűcs, Edina and Benyhe, Sándor and Imre, Timea and Szabó, Pál Tamás and Gajtkó, Andrea and Szentesiné Holló, Krisztina and Puskár, Zita},
	doi = {10.3390/ijms24020918},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {33560486},
	issn = {1661-6596},
	abstract = {Cocaine- and amphetamine-regulated transcript (CART) peptides are involved in several physiological and pathological processes, but their mechanism of action is unrevealed due to the lack of identified receptor(s). We provided evidence for the antihyperalgesic effect of CART(55-102) by inhibiting dipeptidyl-peptidase 4 (DPP4) in astrocytes and consequently reducing neuroinflammation in the rat spinal dorsal horn in a carrageenan-evoked inflammation model. Both naturally occurring CART(55-102) and CART(62-102) peptides are present in the spinal cord. CART(55-102) is not involved in acute nociception but regulates spinal pain transmission during peripheral inflammation. While the full-length peptide with a globular motif contributes to hyperalgesia, its N-terminal inhibits this process. Although the anti-hyperalgesic effects of CART(55-102), CART(55-76), and CART(62-76) are blocked by opioid receptor antagonists in our inflammatory models, but not in neuropathic Seltzer model, none of them bind to any opioid or G-protein coupled receptors. DPP4 interacts with Toll-like receptor 4 (TLR4) signalling in spinal astrocytes and enhances the TLR4-induced expression of interleukin-6 and tumour necrosis factor alpha contributing to inflammatory pain. Depending on the state of inflammation, CART(55-102) is processed in the spinal cord, resulting in the generation of biologically active isoleucine-proline-isoleucine (IPI) tripeptide, which inhibits DPP4, leading to significantly decreased glia-derived cytokine production and hyperalgesia.},
	keywords = {HYPERALGESIA; chronic pain; spinal cord; Allodynia; cocaine- and amphetamine-regulated transcript (CART) peptide; dipeptidyl-peptidase-4 (DPP4)},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Kozsurek, Márk/0000-0001-5465-2803; Király, Kornél P/0000-0002-7252-0422; Szabó, Pál Tamás/0000-0003-2260-4641}
}

@article{MTMT:33208795,
	title = {Different hypothalamic mechanisms control decreased circulating thyroid hormone levels in infection and fasting-induced Non-Thyroidal Illness Syndrome in male Thyroid Hormone Action Indicator Mice},
	url = {https://m2.mtmt.hu/api/publication/33208795},
	author = {Sinkó, Richárd and Mohácsik, Petra and Kővári, Dóra and Penksza, Veronika and Wittmann, Gábor and Borbélyné Mácsai, Lilla and Fonseca, Tatiana L and Bianco, Antonio Carlos and Fekete, Csaba and Gereben, Balázs},
	doi = {10.1089/thy.2022.0404},
	journal-iso = {THYROID},
	journal = {THYROID},
	volume = {33},
	unique-id = {33208795},
	issn = {1050-7256},
	keywords = {fasting; Non-thyroidal illness syndrome; Thyroid Hormone Action Indicator Mouse aging; hypothalamo-pituitary-thyroid axis; tissue-specific thyroid hormone action},
	year = {2023},
	eissn = {1557-9077},
	pages = {109-118},
	orcid-numbers = {Kővári, Dóra/0000-0001-5346-822X; Borbélyné Mácsai, Lilla/0000-0002-9503-6449}
}

@CONFERENCE{MTMT:33780216,
	title = {Role of nesfatin-1 neuropeptide in metabolic changes following intrauterine undernutrition},
	url = {https://m2.mtmt.hu/api/publication/33780216},
	author = {Durst, Máté and Könczöl, Katalin and Ocskay, Klementina and Sípos, Klaudia and Stiftné Szilvásy-Szabó, Anett and Fekete, Csaba and Tóth, Zsuzsanna},
	booktitle = {International Neuroscience Meeting, Budapest 2022},
	unique-id = {33780216},
	year = {2022},
	orcid-numbers = {Durst, Máté/0000-0002-6456-4740; Ocskay, Klementina/0000-0001-5848-2506; Sípos, Klaudia/0000-0003-0534-7348; Tóth, Zsuzsanna/0000-0002-0628-1320}
}