International Journal of Endocrinology最新文献

Purpose: To screen for the prevalence and severity of nonalcoholic fatty liver disease (NAFLD) and degree of liver fibrosis in patients with prediabetes and Type 2 diabetes. Additionally, we sought to compare the results obtained from different screening systems. Methods: We screened 254 patients for NAFLD using three systems: Fatty Liver Index (FLI), Fibrosis 4 (FIB-4) Index, and NAFLD Fibrosis Score (NFS). About two-thirds were females (63%). The mean age was 59.15 ± 10.09 years, and mean BMI was 34.14 ± 6.60 kg/m². Among participants, 85.5% had Type 2 diabetes and 14.5% had prediabetes. Additionally, 81.1% were on metformin, and 39.6% were on insulin. Results: Probable steatosis (NAFLD) prevalence was 77.0% (FLI score) in our cohort. Moderate to advanced liver fibrosis was 12.6% (NFS score) and 20.7% (FIB-4 score). Significant discrepancies were noted: FIB-4 identified 21.6% of patients with moderate to severe fibrosis, which FLI did not recognize as NAFLD. FIB-4 also identified 26 patients with moderate to severe fibrosis that NFS missed. The FIB-4 and FLI score discrepancy was more common in females (10.2% vs. 1.7%, p = 0.046) and in patients with diabetes compared to prediabetes (21.7% vs. 4.5%, p = 0.003). The FIB-4 and NFS score discrepancy was more common in patients with higher BMI (38.38 ± 7.78 vs. 33.59 ± 6.82, p < 0.001) and in those with prediabetes compared to diabetes (34.8% vs. 12.8%, p = 0.008). Conclusion: The study found a high prevalence (77%) of NAFLD in individuals with prediabetes and diabetes. About 20% had moderate to advanced liver fibrosis. NAFLD prevalence and severity varied significantly across three scoring systems. Key factors for refining screening strategies include patient sex, BMI, and the level of insulin resistance.

Background: Primary hyperparathyroidism (pHPT) caused by parathyroid neoplasm is a common endocrine disorder. Nuclear staining loss of parafibromin, encoded by the CDC73 gene, has been shown to be closely related to parathyroid malignancy and poor prognosis. Although previous studies have found that parafibromin staining loss is not always consistent with CDC73 mutation, the reasons are still unknown. Methods: Published studies from the PubMed database were searched using the terms "parafibromin," "CDC73," "HRPT2," and "parathyroid" to identify eligible studies. Among the included studies, CDC73 mutation and parafibromin immunohistochemical (IHC) results for patients with parathyroid neoplasms were reviewed, and possible reasons for the inconsistency between the parafibromin staining loss and CDC73 mutation were explored. This systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 analysis protocol. Results: A total of 299 patients from 32 studies were included in the present review. Inconsistency and consistency between parafibromin staining and CDC73status was observed in 19.40% and 80.60% of patients. Patients in the inconsistency group showed higher level of serum calcium (p = 0.026). Significant difference in the inconsistency rate was found between PC (25.15%) and non-PC group (12.50%) (p < 0.001), and NGS (8.51%) and non-NGS group (21.43%) (p = 0.006) in multivariate analysis. Conclusion: The main reasons for the inconsistency were attributed to the pathological type and sequencing method. More inconsistent results were detected in the PC group and the non-NGS group.

Astaxanthin is a carotenoid compound that has several beneficial qualities, including antioxidant, anti-inflammatory, antiapoptotic, and antidiabetic effects. This study examined the effects of astaxanthin supplementation on inflammation-related microRNAs, lysophosphatidylcholine, and α-hydroxybutyrate in individuals with Type 2 diabetes. Fifty people with Type 2 diabetes volunteered in a placebo-controlled, randomized, double-blind clinical trial. Subjects were randomly determined to consume either 10 mg of astaxanthin (n = 25) or a placebo (n = 25) for 12 weeks. Quantitative real-time PCR was employed to assess the expression of inflammation-related microRNAs in peripheral blood mononuclear cells both before and after the intervention, and we employed ELISA to ascertain the serum levels of lysophosphatidylcholine and α-hydroxybutyrate. After 12 weeks of supplementation, in comparison with placebo, astaxanthin supplementation resulted in a noteworthy decrease (p < 0.05) in hsa-miR-21, hsa-miR-34a, and hsa-miR-155 expression. In addition, astaxanthin supplementation substantially decreased (p < 0.05) the levels of lysophosphatidylcholine and α-hydroxybutyrate compared with the placebo. These changes suggest that astaxanthin may contribute to the modulation of inflammatory processes and the enhancement of metabolic homeostasis. Moreover, relative to the placebo, astaxanthin supplementation considerably diminished serum plasma glucose, HbA1c, lipid profile, and albumin-to-creatinine ratio levels. In conclusion, the current investigation indicates that astaxanthin supplementation at a dosage of 10 mg per day might be a useful strategy for ameliorating inflammation-related diabetic complications and insulin resistance in Type 2 diabetes patients. Considering the potential role of microRNAs in regulating inflammation and metabolic dysfunction in Type 2 diabetes, these findings suggest that astaxanthin supplementation may modulate inflammation-related microRNAs and metabolic markers, potentially contributing to the management of inflammatory processes and metabolic dysregulation in Type 2 diabetes. Trial Registration: Iranian Registry of Clinical Trials (IRCT): IRCT20190305042939N1.

Aims: Patatin-like phospholipase domain-containing protein 3 (PNPLA3) plays a crucial role in metabolic dysfunction-related steatotic liver disease. ARO-PNPLA3 is a therapeutic agent designed to target PNPLA3, but its long-term effects remain uncertain. The objective of this study was to ascertain the impact of PNPLA3 inhibition on the risk of gout through Mendelian randomization. Methods: Mendelian randomization analysis was conducted by choosing single nucleotide polymorphisms (SNPs) in proximity to the PNPLA3 gene, which were significantly associated with the percentage of hepatic fat, to represent PNPLA3 suppression. Nonalcoholic fatty liver disease and hepatic fibrosis served as positive controls, while urate and gout were the outcomes. Results: Genetically predicted PNPLA3 inhibition significantly increased the risk of gout (OR: 1.83, 95% CI: 1.49 to 2.26, p = 1.44 × 10^-8), idiopathic gout (OR: 2.42, 95% CI: 1.60 to 3.65, p = 2.81 × 10^-5) and urate (OR: 1.12, 95% CI: 1.01 to 1.23, p = 2.56 × 10^-2), but not with gout due to impairment of renal function (OR: 1.25, 95% CI: 0.37 to 4.22, p = 7.23 × 10^-1). Conclusions: This study found that PNPLA3 inhibition increased the risk of high urate level and gout. In addition, PNPLA3 inhibition also increased triglyceride (TG) levels, which partially mediate the relationship between PNPLA3 inhibition and gout. Trial Registration: ClinicalTrials.gov identifier: NCT04844450.

Background: Baihu Jia Renshen Decoction (BJRD) applied to diabetes mellitus (DM). We explored the metabolic regulatory pathways and mechanisms of BJRD in Type 1 DM (T1DM). Methods: T1DM rat model was established with STZ induction and then continuously treated with insulin and different concentrations of BJRD for 2 weeks. The therapeutic effect of BJRD was evaluated by detecting the levels of fasting blood glucose and insulin in the blood and observing the ultrastructure of pancreatic tissues by transmission electron microscopy and immunofluorescent staining. Metabolomics analysis on rat serum was performed. Results: Compared with the diabetes model (DC) group, the high-concentration BJRD treatment (BJRD-H) group reduced fasting blood glucose, increased insulin levels, and increased the quantity of β-cells in the pancreatic tissues in rats. And rat pancreatic islet β-cells in the DC group had lost their nuclear membranes, had abnormal mitochondrial morphology, and had significantly reduced secretory granules, whereas rat pancreatic islet β-cells in the BJRD-H group had moderately increased secretory granules, and the structure of the nucleus was apparently normal. Moreover, the metabolic profile expression pattern of rats in the BJRD-H group was closer to that of normal rats, suggesting that a high concentration of BJRD combined with insulin treatment was more effective. And differentially expressed metabolites were predominantly enriched in amino acid metabolism, including amino acids, glycine, serine, and threonine metabolism. Conclusion: BJRD facilitated the therapeutic effect of insulin in T1DM rats and resulted in a significant improvement in their metabolic profiles, expanding the application of traditional Chinese medicine's alternative therapies in T1DM.

[This corrects the article DOI: 10.1155/2022/2260388.].

[This corrects the article DOI: 10.1155/2023/9957194.].

Objective: The primary objective of this study was to further subclassify Bethesda III atypia of undetermined significance (AUS) cytological findings in thyroid lesions using fine-needle aspiration cytology (FNAC). The secondary objective was to propose a novel scoring system to estimate the malignancy risk within these subcategories. Methods: We conducted a retrospective analysis of patients diagnosed with Bethesda III AUS who underwent thyroidectomy at King Khalid University Hospital, Riyadh, Saudi Arabia, from January 2017 to December 2024. Clinical, radiological, and pathological data-including FNAC slides and surgical specimens-were thoroughly reviewed. Cases classified as Bethesda III were further subclassified into six subtypes: III-A (small follicular pattern, poorly cohesive cells, and minimal colloid), III-B (nuclear and/or cellular atypia), III-C (cytological and architectural atypia), III-D (predominantly Hurthle cells), III-E (indeterminate atypia), and III-F (atypical lymphoid cells suggestive of possible lymphoma). A structured malignancy risk scoring system was developed by integrating cytological subtypes, radiologic features (microcalcifications, irregular margins, and hypervascularity), clinical risk factors (family history and prior radiation), and patient age. Statistical analysis was performed using SPSS Version 22, with chi-squared and Fisher's exact tests used to assess associations between variables and malignancy. Results: A total of 338 cases were analyzed, with a mean age of 42 ± 5 years and a female predominance. The malignancy distribution by subcategory was as follows: III-A: 10.65% (n = 36), III-B: 54.73% (n = 185), III-C: 22.49% (n = 76), III-D: 5.03% (n = 17), III-E: 7.69% (n = 26), and III-F: 0.3% (n = 1). Significant associations were found between malignancy and both cytological subcategory and presence of high-risk ultrasound features (p < 0.05). The proposed scoring system stratified patients into three risk groups: low (scores 0-2), moderate (2.5-4), and high (≥ 4.5), offering a predictive framework for clinical decision-making. Conclusion: This study highlights the heterogeneity within Bethesda III AUS nodules and supports subclassification as a meaningful step toward more accurate malignancy risk assessment. The proposed scoring system may serve as a practical tool to guide individualized management decisions. Further prospective validation is warranted.

Neurotensin (NT) is a hypothalamic peptide that acts as a neurohormone and exerts a potent vascular effect. NT is also implicated in regulating the reproductive system. In the present study, we examined the role of NT in the hypothalamic-pituitary-gonadal axis using rat and cell-based models. In female rats, NT gene expression within the posterior part of the hypothalamus was increased by 1.53 ± 0.2-fold by ovariectomy (OVX), and this increase was prevented by estradiol (E2) supplementation after OVX. E2 administration to ovary-intact rats reduced NT gene expression in this part of the hypothalamus. Progesterone (P4) and dihydrotestosterone (DHT) administration also prevented the OVX-induced increase of NT gene expression, while P4 and DHT administration to ovary-intact rats reduced hypothalamic NT gene expression. As previously reported, Kiss-1 gene expression in the posterior part of the hypothalamus was increased by OVX, and this increase was repressed by sex steroid supplementation after OVX. In experiments using hypothalamic cell models, E2 slightly increased NT mRNA expression by 1.67 ± 0.19-fold in GT1-7 cells but failed to increase its expression in rHypoE-8 cells. E2 stimulation slightly increased Kiss-1 gene expression in GT1-7 and rHypoE8 hypothalamic cells by 1.45 ± 0.03-fold and 1.57 ± 0.25-fold, respectively. NT stimulation failed to increase Kiss-1 gene expression in GT1-7 cells but increased its expression significantly in rHypoE8 cells by 1.96 ± 0.22-fold. In contrast, kisspeptin significantly increased NT mRNA expression in GT1-7 (1.85 ± 0.18-fold) and rHypoE8 (4.41 ± 1.03-fold) cells. In the mHypoA-55 hypothalamic KNDy neuron cell model, kisspeptin also significantly increased NT gene expression by 2.13 ± 0.28-fold. Although E2 had some effect on NT expression in hypothalamic cells, kisspeptin significantly increased NT gene expression in three different hypothalamic cell lines. Given that the NT and Kiss-1 gene expression patterns in OVX rats and the effects of sex steroid supplementation were similar, the OVX-induced increase in NT gene expression in the hypothalamus might depend on the increase in Kiss-1/kisspeptin expression within this part of the hypothalamus.

Objective: The cardiometabolic index (CMI) serves as a comprehensive indicator of metabolic risk. Recent findings indicate a potential association between CMI and the likelihood of diabetes onset. The objective of this research is to explore the correlation between initial CMI values and the occurrence of newly diagnosed diabetes mellitus in individuals aged 45 years and above in China. Methods: In this research, data were sourced from the China Health and Retirement Longitudinal Study (CHARLS). To evaluate the association between baseline CMI and the incidence of newly diagnosed diabetes, multivariate logistic regression models were employed, with adjustments made for various potential confounding factors. Additionally, stratified analyses evaluated subgroup variations, and mediation analysis explored pathways through which CMI influences diabetes risk. Results: A cohort of 4,944 participants was followed, with 786 diagnosed with new-onset diabetes. The occurrence of diabetes escalated with increasing CMI quartiles, with Q4 showing a 141% increased risk (OR 2.41, 95% CI, 1.94-3.02) in unadjusted models. This association remained significant after adjustment. Stratified analyses found that dyslipidemia modified the CMI-diabetes association. CMI, age, BMI, HbA1c, and hypertension were identified as independent predictors of new-onset diabetes. Mediation analysis revealed that HbA1c mediated 9.70% of the CMI-diabetes relationship. Conclusion: In summary, our research establishes a connection between increased levels of CMI and the onset of diabetes, suggesting its potential as a predictive tool. The findings highlight CMI's role in assessing diabetes risk and call for targeted interventions. Future research should validate these associations and explore underlying mechanisms for better prevention strategies.