Reviews in Endocrine & Metabolic Disorders最新文献

The prostate gland is an endocrine-sensitive organ responding to multiple stimuli. Its development and function are regulated by multiple hormones (i.e. steroids such as androgens, estrogens and glucocorticoids) but also by other key hormonal systems such as those comprised by insulin-like growth factor 1 and insulin, which are sourced by different tissues [e.g. testicles/adrenal-gland/adipose-tissue/liver/pancreas, etc.). Particularly important for the endocrine control of prostatic pathophysiology and anatomy are hormones produced and/or secreted by different cell types of the pituitary gland [growth-hormone, luteinizing-hormone, follicle-stimulating hormone, and prolactin, oxytocin, arginine-vasopressin and melanocyte-stimulating hormone], which affect prostate gland function either directly or indirectly under physiological and pathophysiological conditions [e.g. metabolic dysregulation (e.g. obesity), and prostate transformations (e.g. prostate cancer)]. This review summarizes the impact of all pituitary hormone types on prostate gland under these diverse conditions including in vivo and in vitro studies.

Gestational diabetes mellitus (GDM) is a common complication of pregnancy that has short- and long-term adverse effects. Therefore, further exploration of the pathophysiology of GDM and related biomarkers is important. In this study, we performed a systematic review and meta-analysis to investigate the associations between metabolites in blood detected via metabolomics techniques and the risk of GDM and to identify possible biomarkers for predicting the occurrence of GDM. We retrieved case‒control and cohort studies of metabolomics and GDM published in PubMed, Embase, and Web of Science through March 29, 2024; extracted metabolite concentrations, odds ratios (ORs), or relative risks (RRs); and evaluated the integrated results with metabolites per-SD risk estimates and 95% CIs for GDM. We estimated the results via the random effects model and the inverse variance method. Our study is registered in PROSPERO (CRD42024539435). We included a total of 28 case‒control and cohort studies, including 17,370 subjects (4,372 GDM patients and 12,998 non-GDM subjects), and meta-analyzed 67 metabolites. Twenty-five of these metabolites were associated with GDM risk. Some amino acids (isoleucine, leucine, valine, alanine, aspartate, etc.), lipids (C16:0, C18:1n-9, C18:1n-7, lysophosphatidylcholine (LPC) (16:0), LPC (18:0), and palmitoylcarnitine), and carbohydrates and energy metabolites (glucose, pyruvate, lactate, 2-hydroxybutyrate, 3-hydroxybutyrate) were discovered to be associated with increased GDM risk (hazard ratio 1.06-2.77). Glutamine, histidine, C14:0, and sphingomyelin (SM) (34:1) were associated with lower GDM risk (hazard ratio 0.75-0.84). These findings suggest that these metabolites may play essential roles in GDM progression, and serve as biomarkers, contributing to the early diagnosis and prediction of GDM.

Distinguishing benign from malignant adrenocortical tumors (ACT) is not always easy, particularly for tumors with unclear malignant potential based on the histopathological features comprised of the Weiss score. Previous studies reported the potential utility of immunohistochemistry (IHC) markers to recognize malignancy, in particular the Insulin-like growth factor 2 (IGF2) and the proliferation marker, Ki-67. However, this information was not compiled before. Therefore, this review aimed to collect the evidence on the potential diagnosis utility of IGF2 and Ki-67 IHC staining. Additionally, a meta-analysis was performed to assess the Ki-67 accuracy to identify adrenocortical carcinoma. The systematic review and meta-analysis were conducted according to the PRISMA guidelines. From the 26 articles included in the systematic review, 21 articles provided individual data for IGF2 (n = 2) or for Ki-67 (n = 19), while 5 studies assessed both markers. IGF2 staining was positive in most carcinomas, in contrast to adenomas. However, the different immunostaining evaluation methods adopted among the studies impeded to perform a meta-analysis to assess IGF2 diagnostic accuracy. In contrast, for the most commonly used cut-off value of 5% stained cells, Ki-67 showed pooled specificity, sensitivity and log diagnostic odds ratio of 0.98 (95% CI 0.95 to 0.99), 0.82 (95% CI 0.65 to 0.92) and 4.26 (95% CI 3.40 to 5.12), respectively. At the 5% cut-off, Ki-67 demonstrated an excellent specificity to recognize malignant ACT. However. the moderate sensitivity observed indicates the need for further studies exploring alternative threshold values. Additionally, more studies using similar approaches are needed to assess the diagnostic accuracy of IGF2.Registration code in PROSPERO: CRD42022370389.

A Rathke's cleft cyst (RCC) is a remnant of the embryologic Rathke's pouch and a common pituitary lesion. A true RCC is lined with ciliated cuboidal or columnar epithelia with occasional goblet cells and squamous metaplasia. A RCC is frequently diagnosed incidentally through magnetic resonance imaging and computed tomography of the brain or pituitary gland. Presentation can range from an asymptomatic clinical picture to a rapidly progressive disease. RCC are located most often in the sellar and suprasellar regions and a careful differential diagnosis is crucial, especially to exclude craniophryngioma. Recent studies illuminate novel molecular mechanisms and markers for understanding the pathogenesis of RCC. PROP-1, a paired-like homeodomain transcription factor, controls pituitary ontogeny and its high expression induces RCCs. Both transgenic mouse models and immunohistochemical analysis of human RCCs indicate that the leukemia inhibitory factor is involved in pathogenesis. The expression of cytokeratins 8 and 2 in RCCs, but not in craniopharyngiomas, and the presence of beta-catenin mutations in many craniopharyngiomas, but not in RCCs, help with the differential diagnosis. For asymptomatic and small RCCs, observation is appropriate, with serial magnetic resonance imaging and hormonal investigation depending on the patient's clinical status. Surgical resection may be required for symptomatic RCC and recurrence rates are generally low. For patients with a recurrence, stereotactic radiosurgery is an effective approach with low risk.

Neuroendocrine neoplasms (NENs) originating in the gastroenteropancreatic (GEP) tract are rare tumors often associated with significant metabolic disturbances and nutritional challenges. This review explores the intricate relationship between nutritional status and the development, progression, and prognosis of GEP-NENs. Through an extensive literature search encompassing studies up to April 2024, we examined various factors, including obesity, malnutrition, metabolic syndrome and type 2 diabetes mellitus, and their roles in the development and progression of GEP-NENs. The review highlights the dual role of obesity, both as a risk factor and a potential prognostic indicator, drawing attention to the 'obesity paradox' observed in cancer research. Additionally, we discuss the impact of malnutrition on patient outcomes and emphasize the need for comprehensive nutritional assessments beyond BMI. This analysis highlights the importance of incorporating nutritional interventions into preventive and therapeutic strategies for GEP-NEN patients. Future research should further clarify these associations and develop personalized nutritional management protocols to improve patient prognosis and quality of life. Acronyms adopted in the text and tables: AOR: adjusted odd ratio, BIA: Bioelectrical Impedance Analysis, BMI: Body Mass Index, CI: confidence interval, CLARINET: Controlled Study of Lanreotide Antiproliferative Response in Neuroendocrine Tumor, FLI: fatty liver index, GEP: gastroenteropancreatic, GLIM: global leadership into malnutrition, HR: hazard ratio, MS: metabolic syndrome, MUST: malabsorption universal screening tool, NEC: neuroendocrine carcinoma, NENs: Neuroendocrine neoplasms, NETs: Neuroendocrine tumors, NRS: Nutritional Risk Screening, OR: odd ratio, OS: overall survival, PFS: progression-free survival, RR: risk ratio, SGA: Subjective Global Assessment, T2DM: type 2 diabetes mellitus, VAI: visceral adiposity index, WD: well-differentiated.

The prevalence of type-2 diabetes mellitus (T2DM) has increased over 10-fold in the past 40 years in China, which now has the largest T2DM population in the world. Insulin resistance and β-cell dysfunction are the typical features of T2DM. Although both factors play a role, decreased β-cell function and β-cell mass are the predominant factors for progression to T2DM. Considering the differences between Chinese T2DM patients and those of other ethnicities, it is important to characterize β-cell dysfunction in Chinese patients during T2DM progression. Herein, we reviewed the studies on the relationships between β-cell function and T2DM progression in the Chinese population and discussed the differences among individuals of varying ethnicities. Meanwhile, we summarized the risk factors and current treatments of T2DM in Chinese individuals and discussed their impacts on β-cell function with the hope of identifying a better T2DM therapy.

The global prevalence of obesity and overweight is a significant concern in the field of public health. Numerous interventional studies have been conducted to assess the possible meal replacements (MRs) effect on anthropometric indicators and indices and laboratory test that reflect obesity. However, there are no comprehensive results in this field. The study aim was to understand the possible effects of MRs on body weight, body mass index (BMI), fat mass, waist circumferences (WC), and leptin levels. A systematic search was conducted in five electronic databases in order to find randomized clinical trials (RCTs) that examined the possible MRs effect on obesity. Analyses were performed in R software, version 4.2.1. The random-effects model analysis was used to provide pooled mean difference and 95% confidence intervals (95% CI). Seventy studies were included. Body weight (WMD: -3.35 kg, 95% CI: -4.28 to -2.42), BMI (WMD: -1.12 kg/m2, 95% CI: -1.51 to -0.72), fat mass (WMD: -2.77 kg, 95% CI: -3.59 to -1.6), WC (WMD: -2.82 cm, 95% CI: -3.51 to -2.12) were significantly reduced after MRs compared to control. No significant effect was observed on leptin (WMD: -3.37 ng/ml, 95% CI: -8.23 to 1.49). Subgroup analyses indicated that impact of total MRs on anthropometric factors was greater in comparison to partial MRs. Considering other lifestyle factors, MRs can lead to anthropometric indicators and indices reduction.

HOXA10 belongs to the homeobox gene family and is essential for uterine biogenesis, endometrial receptivity, embryo implantation, and stromal cell decidualization. Available evidence suggests that the expression of HOXA10 is dysregulated in different endometrial disorders like endometrial hyperplasia, endometrial cancer, adenomyosis, endometriosis, recurrent implantation failure, and unexplained infertility. The downregulation of HOXA10 occurs by genetic changes in the HOXA10 gene, methylation of the HOXA10 locus, or selected miRNAs. Endocrine disruptors and organic pollutants also cause the reduced expression of HOXA10 in these conditions. In vivo experiments in mouse models and in vitro studies in human cell lines demonstrate that downregulation of HOXA10 leads to endometrial epithelial cell proliferation, failure of stromal cell decidualization, altered expression of genes involved in cell cycle regulation, immunomodulation, and various signaling pathways. These disruptions are speculated to cause infertility associated with the disorders of the endometrium.

Pasireotide long-acting release (PAS-LAR) is a second-generation somatostatin receptor ligand (SRL) approved for acromegaly treatment. This meta-analysis aimed to evaluate the real-world effectiveness and safety of PAS-LAR in patients with acromegaly resistant to first-generation somatostatin receptor ligands (fgSRL). A systematic literature search was conducted in PubMed and Web of Science for real-world studies on PAS-LAR in acromegaly published between 2014 and 2023. Random-effects meta-analyses were performed on biochemical control rates, tumor shrinkage, and metabolic parameters. Twelve studies comprising 409 patients were included. The pooled rate of insulin-like growth factor 1 (IGF-1) control was 57.9% [95% CI: 48.4-66.8] and the percentage of patients with tumor shrinkage was 33.3% [95%CI: 19.7-50.4]. Significant reductions were observed in growth hormone standardized mean difference (SMD) 0.6 ng/mL [95% CI: 0.3 to 1.0] and IGF-1 levels SMD 0.9 ULN [95% CI: 0.4 to 1.4]. However, as expected, a worsening in glucose metabolism was noted as an increase in fasting glucose SMD - 0.8 mg/dL [95% CI: -1.0 to -0.5, p < 0.01], glycated hemoglobin SMD - 0.5% [95% CI: -0.7 to -0.2]. and type 2 diabetes mellitus prevalence SMD - 11.5% (95% CI: -17.5 to -5.5). PAS-LAR demonstrated higher effectiveness in real-world settings, with over 60% of patients achieving IGF-1 control compared to the around 30% efficacy observed in clinical trials. These findings suggest that PAS-LAR is an effective option for acromegaly patients resistant to fgSRL, but careful monitoring of glucose levels is essential. The high heterogeneity observed across studies emphasizes the need for identifying PAS-LAR response biomarkers to set-up individualized treatment approaches for optimizing patient outcomes.