Metabolic syndrome (MS) is a significant cause of morbidity and mortality worldwide, often remaining asymptomatic until complications arise. The prevalence of MS in apparently healthy populations in western Mexico is unknown. This study aimed to determine the prevalence of MS and its components in apparently healthy individuals from western Mexico. A cross-sectional study involving 947 individuals self-appointed as healthy during a screening program of MS was conducted. All participants underwent anthropometric measurements, blood pressure assessment, and laboratory tests to determine glucose, high-density lipoprotein cholesterol (HDL-C), and triglycerides levels. The diagnosis of MS was established based on the criteria outlined by the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATPIII). Participants were categorized into three groups: healthy individuals (HS) (no components of HS), those bordering (with one or two components of MS), and those with metabolic syndrome (≥ 3 components of MS). Group comparisons were performed using ANOVA. The chi-squared test was used to assess associations between categorical variables. Student's t-test was used to compare means between the HS and MS groups. A statistical difference was considered significant when p < 0.05. The assessment identified 124 (13%) healthy individuals, 520 (55%) individuals bordering on MS, and 303 (32%) individuals with MS. The prevalence of MS was higher as age increased; women had a higher prevalence of hypoalphalipoproteinemia and elevated waist circumference, whereas men had a higher prevalence of hypertriglyceridemia. In general, men had a more impaired glycometabolic and lipidic profile. The prevalence of MS is high among self-appointed healthy individuals from Western Mexico, underscoring the need for personalized interventions focused on prevention, early detection, and treatment of MS.

Steroid metabolomics in neonatal populations is challenged by considerable physiological heterogeneity and technical variability, which complicate the interpretation and comparability of metabolite profiles. Effective normalization strategies are essential to ensure accurate data analysis in this context. We analyzed 24-hour urinary steroid profiles in a cohort of 50 neonates (including very preterm, late preterm, and full-term infants) using gas chromatography-mass spectrometry. Two normalization techniques were compared: probabilistic quotient normalization (PQN) and peer group normalization (PGN). Normalization performance was assessed via distribution metrics, correlation with anthropometric variables, and principal component analysis (PCA). PGN achieved superior distributional normalization, with 27 of 30 metabolites conforming to normality assumptions, compared to 21 using PQN. PGN also eliminated all significant correlations between steroid levels and anthropometric parameters, indicating effective reduction of physiological confounding. In contrast, PQN partially mitigated such associations but was less robust in handling high-abundance metabolites. PCA confirmed improved sample dispersion and group separation after normalization, with method-dependent differences in Scores Plot. Peer group normalization is a sophisticated approach to reducing physiological variability in neonatal steroid profiling. These observations lend further credence to PGN as a promising strategy for standardizing steroid metabolomics in the field of neonatology. Nevertheless, further validation is necessary to substantiate these findings.

Adrenocortical carcinoma (ACC) is a rare malignant neoplasm. Hypercortisolism and inhibition of gonadotropin secretion usually result in menstrual disorders and secondary amenorrhea. The coincidence of ACC and pregnancy is therefore extremely rare. The signs of hypercortisolism are commonly seen in otherwise healthy pregnancies, which decreases the doctor's vigilance. We present the diagnostic challenges and current treatment recommendations according to European guidelines from the European Society of Endocrinology (ESE) and European Network for the Study of Adrenal Tumors (ENS@T) 2018 and Polish guidelines 2024. We conducted an extensive search via MEDLINE using the phrases "Adrenocortical carcinoma", "ACC", and "Pregnancy" without temporal or language restrictions. Only cases with ACC diagnosed during pregnancy were taken into consideration. Ten papers were found, with 12 described cases. We analyzed the management and outcome both for the mother and the child. We also included a case of a woman treated in our department. A 29-year-old woman in the 20th/21st gestation week (GW) presented to us with Cushing's syndrome symptoms and androgenization. Laboratory tests showed low plasma adrenocorticotropic hormone (ACTH), high cortisol, testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), androstenedione, 24-hour urinary free cortisol (UFC), and hypokalemia. In the abdominal magnetic resonance imaging (MRI) there was a mass in the left adrenal gland. An open surgery was performed in the 21st GW with no perioperative complications. The pathology report established the diagnosis of ACC. The tumor board along with the patient decided to defer the adjuvant therapy until the 32nd GW to increase the odds for the fetus to survive. In the 31st GW an urgent caesarian section was performed due to risk of fetal hypoxia. Computed tomography (CT) scan after the delivery showed local recurrence in the tumor bed. The patient was qualified to mitotane therapy and underwent tumor bed radiotherapy followed by chemotherapy, but the treatment did not stop the progression of the disease. She passed away 14 months after the diagnosis. It is critical to remember about the possibility of ACC occurrence during pregnancy, as well as to know about the differences in hormonal tests in pregnant women such as higher free plasma cortisol, ACTH, UFC, and high rate of false-positive results of low-dose dexamethasone suppression test (LDDST) in comparison to non-pregnant women. Therapeutical options are scarce and pose an ethical dilemma.

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Estrogenic endocrine disruptors (e-EDCs) are synthetic or natural compounds present in the environment with the capacity of modulate molecular pathways regulated by estrogen hormones. Scientific evidence suggests a link between e-EDCs exposure and the development of various types of cancers in organs as prostate, breast, cervix, uterus, colon, lung, liver, and others. Interestingly, synthetic and natural e-EDCs role on cancer development include both preventive and promotive mechanisms, that depend on their concentration and exposure period. The molecular action mechanisms of e-EDCs include diverse signaling pathways such as hormone-dependent gene expression, agonism or antagonism of hormone action, among others. This article reviews the studied molecular signaling pathways that underlie the natural and synthetic e-EDCs effects on the development of various types of cancer.

The relationship between changes in metabolic score for insulin resistance (METS-IR) and diabetes mellitus (DM) remains to be elucidated. The present study sought to explore whether changes in METS-IR were associated with incident DM. This study included 4031 individuals aged over 45 years from the China Health and Retirement Longitudinal Study. Utilizing the K-Means clustering method, participants were divided into four groups. Cumulative METS-IR was employed as a quantitative indicator reflecting changes in METS-IR. Multivariable logistic regression models and restricted cubic splines (RCS) were employed to assess the relationship between changes in METS-IR and DM. During the five-year follow-up, 338 (8.4%) incident DM cases were identified. After adjusting for potential confounders, compared to class 1, the incident DM was significantly higher in class 4 [odds ratio (OR): 2.731, 95% confidence interval (CI): 1.411-5.527, p = 0.003]. When cumulative METS-IR (per SD increase) was introduced as a continuous variable into the multivariate regression model, the association remained significant in Model 3 (OR: 1.393, 95% CI: 1.125-1.715, p = 0.003). Additionally, when cumulative METS-IR was categorized into quartiles, compared to the first quartile, the incident DM was significantly higher in the fourth quartile (OR: 2.022, 95% CI: 1.171-3.501, p = 0.011). In addition, cumulative METS-IR exhibited a nonlinear association with DM (poverall = 0.001, pnon linear = 0.038). Substantial changes in METS-IR were independently associated with the risk of DM in middle-aged and elderly Chinese people. Long-term METS-IR monitoring is significant for early identification and prevention of DM, with significant implications for clinical practice.

Non-alcoholic fatty liver disease (NAFLD) is a globally prevalent chronic liver condition, primarily characterized by excessive accumulation of fat within the liver. A pivotal factor in the progression of NAFLD is cholesterol deposition, which significantly exacerbates liver cell damage through the induction of endoplasmic reticulum (ER) stress. At the heart of this process is sterol regulatory element-binding protein 2 (SREBP2), a crucial transcription factor in cholesterol synthesis. The expression levels of SREBP2 are closely associated with the severity of NAFLD, marking it as a potential therapeutic target. In mouse liver, FOXO3a, a member of the forkhead box protein family, inhibits the expression of SREBP2. This regulation is further influenced by its phosphorylation by mammalian STE20-related kinase 1 (MST1). Our research has uncovered a novel pathway in a NAFLD model where MST1-induced phosphorylation facilitates the nuclear translocation of FOXO3a, leading to a subsequent inhibition of SREBP2 expression. This critical modulation not only curtails cholesterol synthesis but also mitigates cholesterol deposition, alleviates ER stress, and repairs liver cell damage. These findings highlight the MST1-FOXO3a-SREBP2 axis as a promising new target for NAFLD treatment strategies, offering potential pathways to ameliorate a disease that affects millions worldwide.

Diabetic angiopathy is one of the common complications of diabetes and one of the main causes of death in diabetic patients. Basic fibroblast growth factor (bFGF) has various physiological functions. This study applies it to the treatment of vascular injuries in diabetes, aiming to find new treatment methods for diabetic angiopathy. Human umbilical vein endothelial (HUVEC) cells were cultivated, and a high glucose and inflammatory environment was induced. Cell-counting kit 8 (CCK8) assay was employed to observe the stimulation concentrations of bFGF and interferon-gamma (IFN-γ) and their impacts on the activity of HUVEC cells. Scratch assay and transwell assay were utilized to detect the migratory ability of HUVEC cells. Western blot (WB) assay was carried out to detect the expression levels of apoptosis, proliferation, endoplasmic reticulum stress (ERS), and vascular function proteins. Immunofluorescence (IF) assay was used to detect the fluorescence intensity of apoptosis and vascular function proteins. Tube formation assay was performed to detect the tube-forming ability of HUVEC cells. Polymerase chain reaction (PCR) was used to detect the expression levels of ERS genes. Under high-glucose and inflammatory environments, CCK8 assay found that bFGF enhanced the activity of HUVEC cells. The scratch and transwell assays confirmed that bFGF could enhance the migratory ability of HUVEC cells. The WB and IF assays revealed that bFGF could reduce the expression levels of apoptotic proteins and increase the expression levels of proliferative and vascular function proteins. Meanwhile, both the WB and PCR assays verified that bFGF could downregulate the expression levels of ERS proteins and genes. In high-glucose and inflammatory environments, bFGF can improve HUCEV cell function by downregulating ERS.

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