µ-Crystallin is a NADPH-regulated thyroid hormone binding protein encoded by the gene in humans. It is primarily expressed in the brain, muscle, prostate, and kidney, where it binds thyroid hormones, which regulate metabolism and thermogenesis. It also acts as a ketimine reductase in the lysine degradation pathway when it is not bound to thyroid hormone. Mutations in can result in non-syndromic deafness, while its aberrant expression, predominantly in the brain but also in other tissues, has been associated with psychiatric, neuromuscular, and inflammatory diseases. CRYM expression is highly variable in human skeletal muscle, with 15% of individuals expressing ≥13 fold more mRNA than the median level. Ablation of the gene in murine models results in the hypertrophy of fast twitch muscle fibers and an increase in fat mass of mice fed a high fat diet. Overexpression of in mice causes a shift in energy utilization away from glycolysis towards an increase in the catabolism of fat via β-oxidation, with commensurate changes of metabolically involved transcripts and proteins. The history, attributes, functions, and diseases associated with , an important modulator of metabolism, are reviewed.
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http://dx.doi.org/10.2478/enr-2021-0011 | DOI Listing |
Eur J Pediatr
January 2025
Pediatric Endocrinology and Diabetes Unit, Department of Pediatrics, Mansoura Faculty of Medicine, Mansoura University Children's Hospital, Mansoura University, Gomhoria Street, Mansoura, 35516, Dakhlia, Egypt.
Unlabelled: This study aims to determine the incidence, clinical course, and risk factors of hypothyroidism following cardiac catheter (CC) in infants with congenital heart diseases (CHD). This prospective study involved 115 patients with CHD, all aged 3 years or younger, who underwent CC, as well as 100 healthy age- and sex-matched controls. Baseline thyroid function tests (TFTs) were conducted for both the patients and controls.
View Article and Find Full Text PDFEur Thyroid J
January 2025
H Heuer, Department of Endocrinology, Diabetes and Metabolism, University of Duisburg-Essen, Essen, Germany.
Objective: Mutations in the thyroid hormone (TH) transporter monocarboxylate transporter 8 (MCT8) cause Allan-Herndon-Dudley syndrome (AHDS), a severe form of psychomotor retardation with muscle hypoplasia and spastic paraplegia as key symptoms. These abnormalities have been attributed to an impaired TH transport across brain barriers and into neural cells thereby affecting brain development and function. Likewise, Mct8/Oatp1c1 (organic anion transporting polypeptide 1c1) double knockout (M/Odko) mice, a well-established murine AHDS model, display a strongly reduced TH passage into the brain as well as locomotor abnormalities.
View Article and Find Full Text PDFAnn Surg
January 2025
University of Alabama at Birmingham, Birmingham, AL, United States.
Objective: To assess the impact of parathyroid gland autotransplantation on the restoration of parathyroid function in patients who are hypoparathyroid after thyroidectomy.
Background Data: Hypoparathyroidism post-thyroidectomy arises when all parathyroid glands are devascularized or injured. Autotransplantation of compromised parathyroids aims to preserve their function and prevent permanent hypoparathyroidism.
iScience
January 2025
Medical Research Institute KITANO HOSPITAL, PIIF Tazuke-kofukai, Kita-ku, Osaka 530-8480, Japan.
Activation of thyroid-stimulating hormone receptor (TSHR) fundamentally leads to hyperthyroidism. To elucidate TSHR signaling, we conducted transcriptome analyses for hyperthyroid mice that we generated by overexpressing TSH. TSH overexpression drastically changed their thyroid transcriptome.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Statistics, Bangabandhu Sheikh Mujibur Rahman Agricultural University, Gazipur, Bangladesh.
Background: Phthalates, a large group of endocrine disruptors, are ubiquitous in the environment and detrimental to human health. This scoping review aimed to summarize the effects of phthalates on laboratory animals relevant to humans, assess toxicity, and analyze mechanisms of toxicity for public health concerns.
Methods: Articles were retrieved from Google Scholar, PubMed, ScienceDirect, and Web of Science search engines.
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