Hormone Molecular Biology and Clinical Investigation最新文献

The current topic of sex reassignment is often under strong ideological influence and requires an impartial scientific approach. Considering the importance of corticosteroid status during male-to-female transition for numerous health aspects, here we focus on the 'transitional' functional histology of the hypothalamic-pituitary-adrenal (HPA) axis and corticosteroid output, from the perspective of our experimental experience and the available literature, both experimentally and clinically oriented. In a model of orchidectomized, estradiol-treated adult male rats we observed an increase in aldosterone secretion, as well as in corticosterone synthesis and secretion, but also a decrease in DHEA secretion, all of which were accompanied by expansive changes in adrenal tissue. Available experimental and clinical literature data support our findings. It is known that glucocorticoid excess increases the risk of metabolic complications, elevated blood aldosterone levels may underlie systemic hypertension, while reduced DHEA secretion is associated with various physical and mental issues. These health risks should be kept in mind before possibly starting the male-to-female transition through orchidectomy and estradiol administration.

Objectives: To evaluate the association of NOX1 gene expression with reproductive hormonal changes in hypothyroid infertile women and assess their diagnostic performance.

Methods: A case-control study was conducted among 150 infertile women with hypothyroidism and 150 healthy age-matched fertile controls. Hormonal (FSH, LH, prolactin) and molecular (NOX1 expression) parameters were measured using standardized assays including qRT-PCR. Group comparisons, Spearman's correlation analyses, scatterplot visualizations, and ROC curve evaluations were conducted to determine associations and diagnostic performance.

Results: Hypothyroid infertile women exhibited significantly elevated FSH (19.9 ± 7.5 mIU/mL), LH (20.0 ± 7.6 mIU/mL), prolactin (21.9 ± 8.4 ng/mL), and TSH (7.2 ± 1.8 µIU/mL), along with reduced T3 (0.82 ± 0.21 ng/mL) and T4 (5.1 ± 1.2 μg/dL) compared to controls (p<0.01). NOX1 expression was markedly higher in peripheral blood (1.9 ± 0.9 vs. 1.0 ± 0.2; p<0.01). Moderate positive correlations were observed between NOX1 and FSH (r=0.5638), LH (r=0.5787), and prolactin (r=0.5968), all statistically significant (p<0.01). ROC analysis showed good diagnostic accuracy for FSH (AUC 0.801), LH (AUC 0.732), and prolactin (AUC 0.748), while NOX1 demonstrated superior discriminative performance (AUC 0.835) with 100 % specificity and a positive predictive value of 100 %.

Conclusions: Hypothyroidism-associated infertility is characterized by combined endocrine imbalance and heightened oxidative stress. The strong discriminative ability and hormonal correlations of NOX1 expression suggest its potential use as a molecular biomarker to support infertility risk detection in thyroid-compromised women, providing a basis for oxidative-stress-targeted therapeutic strategies.

Introduction: The measurement of HbA1c plays an important role in managing Diabetes mellitus [DM] types 1 and 2. It gives the patient a further insight on diabetes control. In addition to the daily blood sugar tests that show the real-time glucose levels, HbA1c gives an insight on the long-term glucose control. Hence the patient realizes that the higher the blood glucose levels over time, the more HbA1c is formed. The formulas to convert HbA1c into an estimated Average Glucose [eAG] are many, complex and may not be memorized by the patients and investigators alike. They may not give comparable results as well. That may create difficulties when they are utilized in diabetes researches.

Content: Hence the authors have analysed six established formulas and were able to derive three simplified formulas, to help patients and doctors alike easily convert their HbA1c to eAG. The authors tried several mathematical calculations and attempts over the simplest formulas [but with a com- parable result] in order to reach to the desired formulas.

Summary: The authors suggested 3 formulas that showed around 5 % deviation from the standard formulas results.

Outlook: The suggested formulas could convert HbA1c into an [eAG] more easily than the standard formulas and make the sugar measurement easier for the patients, health care providers and investigators as well. The suggested formulas would address a real-life need which is patient understanding and simplification of diabetes management favourably.

Objectives: Osteoporosis is common among older adults, but the relationship between neuroendocrine factors - particularly catecholamines - and bone mineral density (BMD) is not well understood. This study examined associations between catecholamine levels and BMD in older adults.

Methods: Data from the 2017-2022 biomarkers wave of the Midlife in the United States (MIDUS 3) study were analyzed. Multiple linear regressions assessed associations between creatinine-adjusted urinary norepinephrine and epinephrine levels and BMD at the lumbar spine (L1-L4), right and left total femur, and one-third radius. Models adjusted for age, sex, body mass index (BMI), smoking history, diet, medications (thiazide diuretics, phosphate binders, beta blockers, and vitamin D analogues), and serum creatinine.

Results: Among 324 participants (41 % male; mean age 64.3±9.3 years), higher epinephrine levels were significantly associated with lower lumbar spine BMD (Beta=-0.122; 95 % CI: [-0.242 to -0.003], p=0.045), while norepinephrine showed no association (p=0.865). No significant relationships were observed at femoral or radial sites, though norepinephrine was marginally linked to lower one-third radius BMD (Beta=-0.087; 95 % CI: [-0.176 to 0.002], p=0.055). Male sex and higher BMI predicted greater BMD (p<0.05), whereas older age was linked to lower femoral and radial BMD (p<0.05).

Conclusions: Elevated epinephrine levels are associated with reduced lumbar spine BMD in older adults, and elevated norepinephrine levels are associated with reduced distal radius BMD, suggesting catecholamines may influence bone metabolism in a site-specific manner relevant to osteoporosis pathophysiology.

Objectives: To report a rare case of ovotesticular disorder of sex development (OT-DSD) in a phenotypically male adolescent who presented with bilateral gynecomastia.

Case presentation: A 15-year-old phenotypically male child presented with progressive enlargement of bilateral breasts for the past 2 years. Clinical examination revealed Tanner stage 4 breast and pubic hair development, unilateral undescended testis, and normal external genitalia. Hormonal evaluation showed low testosterone and raised gonadotropins. Imaging revealed a hypoplastic uterus, fluid-filled vagina, and left-sided ovotestis. Karyotyping confirmed a 46, XX genotype. Clinical, hormonal, and imaging evaluations confirmed the diagnosis of OT-DSD. Because of the established male gender role in his community, he preserved his gender. The patient had liposuction and glandular removal of bilateral breast tissue, as well as left orchidopexy, before being discharged on testosterone replacement treatment.

Conclusions: Ovotesticular DSD is uncommon and may manifest in late adolescence with gynecomastia rather than ambiguous genitalia. Clinicians should consider OT-DSD in adolescents who presented with bilateral gynecomastia. Early diagnosis, karyotyping, and multidisciplinary management are crucial to optimize long-term outcomes.

Introduction: As a pivotal molecule in tissue development and homeostasis, WNT5A regulates various aspects of ovarian physiology, including folliculogenesis, oocyte maturation, and hormonal responses.

Content: This review summarizes current knowledge on the molecular mechanisms of WNT5A signaling, its role in ovarian health, and its pathological involvement in disorders such as polycystic ovary syndrome (PCOS) and ovarian cancer. We discuss how WNT5A may be a double-edged sword in ovarian diseases and explore its therapeutic potential.

Summary: In PCOS, WNT5A exacerbates the inflammatory environment and insulin resistance, disrupting normal folliculogenesis and leading to impaired ovarian function. Moreover, in ovarian cancer, WNT5A presents challenges for therapeutic targeting, as it can either inhibit or facilitate tumor progression depending on the context.

Outlook: Continued research into the peripheral and central regulatory mechanisms of WNT5A, along with its interactions with other signaling pathways, will be instrumental in unlocking its full therapeutic potential.

Objectives: The prevalence of metabolic diseases is increasing worldwide. The identification of novel biomarkers and peptides is one approach to diagnosing and treating such disorders. Spexin is a relatively new peptide hormone that plays a pivotal role in energy metabolism. The prominent role of spexin in obesity, non-alcoholic fatty liver disease, diabetes, and insulin resistance has been established. This mini-review summarizes recent findings on the physiological and potential therapeutic roles of spexin in metabolic disorders.

Methods: A targeted literature review of scientific sources was conducted using PubMed, Scopus, and Web of Science databases. The search focused on published experimental and clinical studies on the metabolic effects of spexin in the liver, adipose tissue, skeletal muscle, and pancreas.

Results: This peptide regulates energy homeostasis by affecting the metabolism of specific tissues. Spexin reduces hepatic fat accumulation by modulating lipogenesis and β-oxidation. In adipose tissue, spexin modulates adipocyte differentiation by enhancing lipolysis and inhibiting lipogenesis. In skeletal muscle, it is effective in increasing glucose uptake by upregulating glucose transporter 4. Spexin also affects insulin secretion and regulates β-cell function in the pancreas.

Conclusions: Although studies on the physiological and therapeutic effects of spexin are ongoing, current evidence highlights its involvement in metabolic regulation. Further research is required to clarify the mechanisms and therapeutic potential of this pathway in metabolic diseases.

Introduction: The aim of this review was to review and summarize the current evidence regarding the expression and role of leptin and its receptor (LEPR) in colorectal cancer (CRC). This includes discussing their involvement in carcinogenesis, progression, and prognosis, as well as assessing their potential as biomarkers and therapeutic targets.

Content: We conducted a scoping literature review using several databases. We included studies in English or French that analyzed the expression of leptin and LEPR in the serum or tissue of CRC patients. Additionally, the GEPIA2 platform was employed to investigate the association between leptin and LEPR expression levels and overall survival, as well as their expression across pathological stages and microsatellite subtypes in CRC.

Summary: A total of 76 eligible studies published between 1994 and 2024 were included. Analyses through immunohistochemical methods, transcriptomics, and serum measurements indicated elevated expression of leptin and LEPR in CRC. However, findings regarding their prognostic value varied: some studies reported a link between high leptin and LEPR levels and poor prognosis, while others found no correlation or even suggested favorable outcomes. This variability in results can be attributed to differences in methodology, patient diversity, and genetic polymorphisms.

Outlook: The leptin-LEPR system seems to play a significant role in the development and progression of CRC, but its exact prognostic impact remains uncertain due to inconsistent findings. Further standardized and large-scale studies are necessary to clarify its clinical relevance. The leptin-LEPR axis shows promise as a biomarker and potential therapeutic target, particularly in the context of obesity-related CRC.