The effects of a TRH-T (protireline tartrate) treatment at a dose of 2 mg/day for 3 weeks on the serum levels of the pituitary-thyroid axis hormones, have been studied in a randomized group of 10 elderly euthyroid hospitalized patients with cerebrovascular disease. At the end of the treatment an 8.3% mean increase of serum T3 level and a 12.5% mean increase of serum FT3 level (p less than 0.02 in both cases) have been observed. At the same time a 34% mean decrease of the basal TSH (p less than 0.05) and a 26% mean decrease of the delta-TSH after TRH-test (p less than 0.025) have been noted. However, the hormone concentrations changes never exceeded the normal values. In a randomized group of 9 hospitalized untreated patients with cerebrovascular disease used as controls (matched for age and sex), no significant changes of studied hormones have been recorded. In the treated patients, one week after the withdrawal of therapy serum levels of thyroid hormones and TSH went back to the levels observed before treatment. TRH-T seems to cause these modest hormone changes by decreasing the number of TRH receptors and the activity of TSH secreting cells. Nevertheless, the presence of the normal feedback in the pituitary-thyroid axis, allows a good tolerance to such a treatment.
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Vitam Horm
January 2025
Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR, United States. Electronic address:
The balance between food intake and energy expenditure is precisely regulated to maintain adipose stores. Leptin, which is produced in and released from adipose in direct proportion to its size, is a major contributor to this control and initiates its homeostatic responses largely via binding to leptin receptors (LepR) in the hypothalamus. Decreases in hypothalamic LepR binding signals starvation, leading to hunger and reduced energy expenditure, whereas increases in hypothalamic LepR binding can suppress food intake and increase energy expenditure.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg 194223, Russia.
The approaches to correct thyroid deficiency include replacement therapy with thyroid hormones (THs), but such therapy causes a number of side effects. A possible alternative is thyroid-stimulating hormone (TSH) receptor activators, including allosteric agonists. The aim of this work was to study the effect of ethyl-2-(4-(4-(5-amino-6-(-butylcarbamoyl)-2-(methylthio)thieno[2,3-d]pyrimidin-4-yl)phenyl)--1,2,3-triazol-1-yl) acetate (TPY3m), a TSH receptor allosteric agonist developed by us, on basal and thyroliberin (TRH)-stimulated TH levels and the hypothalamic-pituitary-thyroid (HPT) axis in male rats with high-fat diet/low-dose streptozotocin-induced type 2 diabetes mellitus (T2DM).
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
Fisheries College, Huazhong Agricultural University, Wuhan 430070, China; Hubei Engineering Technology Research Center for Aquatic Animal Disease Control and Prevention, Wuhan 430070, China. Electronic address:
The toxicity of tris (2-butoxyethyl) phosphate (TBOEP) has been extensively investigated because of its prevalence in the environment. Nevertheless, the risk factors associated with maternal transmission are poorly understood. In this study, sexually mature female zebrafish were treated with TBOEP (0, 20, 100, and 500 μg/L) for 30 days and were mated with unexposed males.
View Article and Find Full Text PDFJ Community Hosp Intern Med Perspect
November 2024
UCI Medical Center, USA.
Most cases of Myxedema Coma are associated with primary hypothyroidism characterized by significantly elevated thyroid stimulating hormone (TSH) levels. However, this case presents an atypical manifestation of myxedema coma with low TSH levels despite severe hypothyroidism. The rarity of this presentation lies in the absence of central lesions typically responsible for such TSH suppression.
View Article and Find Full Text PDFSevere sepsis is cognate with life threatening multi-organ dysfunction. There is a disturbance in endocrine functions with alterations in several hormonal pathways. It has frequently been linked with dysfunction in the hypothalamic pituitary-adrenal axis (HPA).
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