Sensitivity of the cortex single neurons, hippocamp, thalamus medial nucleus, periventricular and arcuate hypothalamus nuclei to the thyrotropin-releasing hormone (TRH) and its structural analog (Pyr-Ser-Leu-NH2) under conditions of their microionophoretic application by means of multichannel microelectrodes was studied and compared in experiments on rats. There was no significant similarity between TRH and its analog effects in all the test brain regions with the exception of the cortex. A significant positive correlation between their influence on the single neuron activity was recorded. However, the sensitivity to the cortex cell analog was less pronounced. The largest amount of TRH irresponsive cells were seen in the thalamus medial nucleus neurons. On the contrary, their sensitivity to the TRH analog was comparatively high.
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Dokl Biochem Biophys
January 2025
I.M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia.
Graves' disease is caused by overactivation of the thyroid-stimulating hormone receptor (TSHR). One approach for its treatment may be the use of negative allosteric modulators (NAM) of TSHR, which normalize TSHR activity and do not cause thyroid hormone (TH) deficiency. The aim of the work was to study the effect of a new compound 5-amino-4-(4-bromophenyl)-2-(methylthio)thieno[2,3-d]pyrimidine-6-carboxylic acid N-tert-butylamide (TPY4) on the basal and TSH-stimulated TH production in cultured FRTL-5 thyrocytes and on basal and thyrotropin-releasing hormone (TRH)-stimulated TH levels in the blood of rats.
View Article and Find Full Text PDFZool Res
January 2025
The Key Laboratory of Mariculture, Ministry of Education, Ocean University of China, Qingdao, Shandong 266003, China. E-mail:
Feeding behavior is regulated by a complex network of endogenous neuropeptides. In chordates, this role is suggested to be under the control of diverse factors including thyrotropin-releasing hormone (TRH). However, whether this regulatory activity of TRH is functionally conserved in non-chordate metazoans, and to what extent this process is underpinned by interactions of TRH with other neuropeptides such as cholecystokinin (CCK, known as a satiety signal), remain unclear.
View Article and Find Full Text PDFJCEM Case Rep
January 2025
Section of Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College, London W12 ONN, UK.
We report a 31-year-old man with diarrhea and tachycardia. Diagnostic workup confirmed raised free thyroid hormones with unsuppressed thyroid stimulating hormone (TSH). Laboratory assay and medication interference were excluded.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Animal Physiology, The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, Instytucka 3, Jabłonna, 05-110, Poland.
Since the early discovery of QRFP43, intensive research has been primarily focused on its role in the modulation of food intake. As is widely recognised, the regulation of the body's energy status is a highly complex process involving numerous systems, hormones and neurotransmitters. Among the most important regulators of energy status, alongside the satiety and hunger centre located in the hypothalamus, is the HPT axis, which directly and indirectly affects the regulation of metabolism in all cells of the body.
View Article and Find Full Text PDFJ Endocr Soc
November 2024
Division of Endocrinology and Metabolism, Department of Internal Medicine, Soonchunhyang University Hospital, Soonchunhyang University College of Medicine, Seoul 04401, Korea.
Context: Subclinical hypothyroidism (SCH) is characterized by elevated thyroid-stimulating hormone (TSH) levels and normal free thyroxine (fT4) levels. In upper normal TSH levels, thyrotropin-releasing hormone (TRH) stimulation test proved to be useful in identifying an exaggerated TSH response.
Objective: We aimed to evaluate the incidence and predictive ability of basal TSH, anti-thyroid peroxidase antibodies (TPOAb), and anti-thyroglobulin antibodies (TgAb) for exaggerated TRH stimulation test in SCH.
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