The LH receptor (LHR) is a G protein-coupled receptor involved in the regulation of ovarian and testicular functions. In this study we demonstrate novel and unexpected patterns of receptor expression and regulation in fetal and adult rodent urogenital and adrenal tissues. Two rat LHR promoter fragments (approximately 2 and 4 kb) were shown to direct expression of the lacZ reporter in transgenic mice to gonads, adrenal glands, and kidneys, starting at 14.5 d post coitum, and to genital tubercles, starting at 11.5 d post coitum. These tissues were also found to express the full-length LHR mRNA and protein during rat fetal development, but, importantly, only immature receptors carrying unprocessed N-linked glycans were detected. After birth, the receptor gene activity ceased, except in the gonads, which started to express the mature receptor carrying fully processed N-linked glycans. Surprisingly, both LHR mRNA and mature protein levels were up-regulated substantially in pregnant female adrenal glands and kidneys at a time that coincides with differentiation of fetal urogenital tissues. Taken together, these results indicate that the LHR protein is expressed constitutively in gonadal and nongonadal urogenital tissues as well in adrenal glands, but its final functional maturation at the posttranslational level appears to be developmentally and physiologically regulated.
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http://dx.doi.org/10.1210/en.2005-0073 | DOI Listing |
Mol Syst Biol
January 2025
Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100, Israel.
Elevated cortisol in chronic stress and mood disorders causes morbidity including metabolic and cardiovascular diseases. There is therefore interest in developing drugs that lower cortisol by targeting its endocrine pathway, the hypothalamic-pituitary-adrenal (HPA) axis. However, several promising HPA-modulating drugs have failed to reduce long-term cortisol in mood disorders, despite effectiveness in other hypercortisolism conditions such as Cushing's syndrome.
View Article and Find Full Text PDFNat Rev Dis Primers
January 2025
Endocrine Division, Department of Medicine, Centre hospitalier de l'Université de Montréal (CHUM), Montreal, Québec, Canada.
Cushing syndrome (CS) is a constellation of signs and symptoms caused by excessive exposure to exogenous or endogenous glucocorticoid hormones. Endogenous CS is caused by increased cortisol production by one or both adrenal glands (adrenal CS) or by elevated adrenocorticotropic hormone (ACTH) secretion from a pituitary tumour (Cushing disease (CD)) or non-pituitary tumour (ectopic ACTH secretion), which stimulates excessive cortisol production. CS is associated with severe multisystem morbidity, including impaired cardiovascular and metabolic function, infections and neuropsychiatric disorders, which notably reduce quality of life.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: Adrenal Vein Sampling (AVS) is the gold standard for categorizing primary aldosteronism (PA). However, catheterization of the right adrenal vein (RAV) can be technically challenging. This study aimed to investigate the validity of the right renal vertebral contour as fluoroscopic landmarks to help RAV orifice localization during AVS.
View Article and Find Full Text PDFInt J Colorectal Dis
January 2025
General Surgery, Cannizzaro Hospital, Catania, Italy.
In this article, we aim to demonstrate that thyroid carcinoma can metastasize to the small bowel. This case report involves a 66-year-old woman who underwent total thyroidectomy surgery in 2019, with histopathology revealing a 3A undifferentiated thyroid cancer. She presented with symptoms of bowel obstruction, including abdominal pain, nausea, and vomiting.
View Article and Find Full Text PDFJ Community Hosp Intern Med Perspect
November 2024
Kaiser Permanente Hospital, California, USA.
Background: Nonislet cell tumor hypoglycemia (NICTH) is a rare but serious complication of malignancy. Various causes of this type of hypoglycemia include excessive tumor burden resulting in destruction of the liver or adrenal glands, production of autoantibodies against insulin and tumoral production of incompletely processed IGF-2.
Objectives: Objective of this case report is to explore pathogenic mechanisms for hypoglycemia in hepatocellular carcinoma (HCC), and evidence-based treatment options.
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