REVIEWS IN ENDOCRINE & METABOLIC DISORDERS内分泌与代谢疾病综述
REVIEWS IN ENDOCRINE & METABOLIC DISORDERS(英文缩写 REV ENDOCR METAB DIS),ISSN 1389-9155,eISSN 1573-2606,中文译名:内分泌与代谢疾病综述 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.306 | Q1 |
| 2022 | 8.200 | Q1 |
| 2023 | 6.900 | Q1 |
| 2024 | 8.000 | Q1 |
| 2025 | 8.700 | Q1 |
REVIEWS IN ENDOCRINE & METABOLIC DISORDERS 最新收录文献
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1. Gut dysbiosis, blood pressure regulation, and cardiometabolic risk in polyendocrine metabolic ovarian syndrome (PMOS).
PMID:日期:2026-10-03Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a common endocrine-metabolic disorder associated with increased hypertension and cardiometabolic risk. Gut dysbiosis is also frequently reported in affected women, raising the question of whether microbiome-linked pathways contribute to blood pressure elevation or vascular risk in this syndrome. To evaluate and synthesize the available evidence linking gut dysbiosis, gut microbial function, and microbiome-related mechanisms to hypertension, blood pressure regulation, and cardiovascular risk in women with PMOS, we conducted a narrative review of the literature in PubMed, Scopus, Web of Science, Google Scholar, and citation tracking. Search terms included PCOS, PMOS, gut microbiota, gut dysbiosis, hypertension, blood pressure, cardiovascular risk, microbial metabolites, bile acids, intestinal permeability, inflammation, renin-angiotensin signaling, renal sodium handling, and autonomic regulation. Human studies, animal models, interventional studies, and mechanistic investigations relevant to PMOS and hypertension were reviewed according to predefined inclusion and exclusion criteria. Eligible publications were preclinical studies, human studies, English language, adult females, and peer-reviewed original or review articles. Clarifying whether gut dysbiosis contributes to hypertension in PMOS may improve understanding of the mechanisms underlying cardiometabolic risk in affected women and inform the development of microbiome-targeted diagnostic and therapeutic strategies. Achieving this goal will require well-phenotyped clinical studies integrating PMOS, blood pressure and vascular assessments with functional microbiome analyses.
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2. Beyond metabolic control: the potential role of antidiabetic therapies in modulating male reproductive function and spermatogenesis.
2. 超越代谢控制：降糖治疗在调节男性生殖功能和精子发生中的潜在作用PMID:日期:2026-10-01In recent years, novel antidiabetic drugs, particularly sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RA), have attracted increasing interest for their effects beyond glycemic control, including potential actions on male reproductive function. This review critically summarizes current evidence regarding the impact of antidiabetic therapies on spermatogenesis, testicular metabolic homeostasis, and male gonadal function, focusing on the underlying molecular and pathophysiological mechanisms. Experimental evidence suggests that metabolic dysfunction, oxidative stress, inflammation, apoptosis, and impaired Sertoli cell metabolism play a central role in diabetes- and obesity-associated male reproductive dysfunction. In this context, SGLT2i and GLP-1 RA appear capable of modulating several of these pathways, improving sperm parameters, preserving testicular architecture, and attenuating oxidative and inflammatory damage in preclinical models. Emerging data also suggest possible direct gonadal effects mediated through intracellular signaling pathways involved in steroidogenesis, autophagy, and cellular energy regulation. However, clinical evidence remains limited and partly conflicting, and it is still unclear whether these findings translate into clinically meaningful reproductive benefits in humans. Preliminary evidence suggests that dual GIP/GLP-1 receptor agonists, such as tirzepatide, may exert beneficial effects on male reproductive health. However, direct evidence regarding their impact on spermatogenesis and fertility remains limited. Overall, well-designed prospective clinical studies incorporating reproductive and hormonal outcomes are warranted to better define the role of these therapies within an integrated andro-metabolic approach to the management of obesity- and diabetes-associated male reproductive dysfunction.
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3. Role of sex and gender in autoimmune thyroid diseases: mechanisms and knowledge gaps.
PMID:日期:2026-09-21Autoimmune thyroid diseases (AITDs), mainly Hashimoto's thyroiditis and Graves' disease, are the most common organ-specific autoimmune disorders and display one of the strongest sex biases in autoimmunity, with a marked female predominance. This review examines how biological sex and gender-related determinants shape AITD susceptibility, expression, and clinical heterogeneity, and their relevance to personalized care. PubMed/MEDLINE and Scopus were searched from inception to June 2026, with Web of Science used for forward citation tracking. Human studies, reviews and meta-analyses, and selected experimental studies addressing sex- and gender-related mechanisms relevant to thyroid autoimmunity were considered. Sexual dimorphism in immune function provides the biological background for the higher autoimmune susceptibility of women, who generally mount stronger innate and adaptive immune responses. Sex hormones modulate immune tolerance and inflammation, while X-chromosome dosage, incomplete or skewed X-chromosome inactivation, X-linked immune genes, and emerging Y-chromosome-related mechanisms further contribute to immune regulation. Epigenetic mechanisms may amplify sex-dependent immune responses. Pregnancy, postpartum immune rebound, reproductive history, and fetal microchimerism highlight the interaction between reproductive biology and thyroid autoimmunity. Environmental exposures, smoking, psychosocial stress, occupational patterns, and healthcare-related determinants add a gender-related dimension, while sex-specific gut microbiota differences may also contribute. However, major knowledge gaps remain. Sex-stratified analyses are often lacking, and AITD-specific evidence on epigenetic profiles, microbiota, and gender-related determinants remains limited. Integrating sex and gender into AITD research and clinical practice may improve risk stratification, diagnosis, prevention, and individualized management, supporting a precision-medicine approach to thyroid autoimmunity.
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4. Comparative effects of ketogenic diets and mediterranean diets on obesity and metabolic outcomes: a systematic review and meta-analysis.
PMID:日期:2026-09-21Ketogenic diets (KD) and Mediterranean diets (MD) are among the most widely studied dietary approaches for obesity and metabolic disorders; however, their comparative efficacy remains controversial. This systematic review and meta-analysis aimed to compare the effects of KD and MD on anthropometric and metabolic outcomes in adults. A comprehensive search of original databases was conducted from inception until March 2026. Randomized controlled trials comparing KD with MD in adults were included. Weighted mean differences (WMDs) and 95% confidence intervals (CIs) were calculated using random-effects models. KD significantly reduced body weight (WMD: -3.56 kg; 95% CI: -5.62, - 1.49), body mass index (BMI) (WMD: -1.86 kg/m²; 95% CI: -2.73, - 0.98), waist circumference (WC) (WMD: -4.25 cm; 95% CI: -7.46, - 1.04), total body fat (TBF) percentage (WMD: -2.09%; 95% CI: -3.98, - 0.20), and insulin levels (WMD: -3.15 µU/ml; 95% CI: -5.02 to - 1.28) compared with MD. In contrast, no significant differences were observed between KD and MD regarding fasting blood sugar, HbA1c, LDL-C, HDL-C, triglycerides, systolic blood pressure, diastolic blood pressure, or C-reactive protein levels. However, KD significantly reduced total cholesterol (TC) compared with MD (WMD: -9.71 mg/dl; 95% CI: -17.79, - 1.62). Publication bias was detected for triglycerides and LDL-C outcomes. KD demonstrated superior effects on anthropometric outcomes compared with MD, particularly for weight loss and body composition improvement. However, both dietary approaches showed largely comparable effects on glycemic control, lipid profile, blood pressure, and inflammatory biomarkers. While KD may provide greater short-term weight reduction, MD may remain a sustainable dietary strategy for long-term cardiometabolic health.
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5. Skeletal stem and progenitor cell niche organization, regulation and repair.
PMID:日期:2026-09-17Bone has traditionally been viewed through the lens of structural support and mineral homeostasis, but it is increasingly recognized as a dynamic endocrine organ. Similarly, the concept of skeletal maintenance and repair has historically been considered through tightly coordinated regulation of specialized mature cell types. Recently, a refined understanding of skeletal stem cells (SSCs) and skeletal stem/progenitor cells (SSPCs) as key cellular drivers of skeletal development, homeostasis and regeneration has underscored their importance and broadened that framework. In this review, we examine skeletal endocrine biology through the high-resolution mapping of SSCs and SSPCs and their crosstalk with immune and matrix-associated niche components. We discuss how bone-derived endocrine factors, systemic hormones and neuroendocrine cues may act as local and systemic niche modulators that shape SSC and SSPC behavior during skeletal maintenance, physiological adaptation and repair. We further highlight how timed immune activation as well as inflammatory resolution shape successful skeletal repair, whereas aging, osteoporosis and chronic inflammation disrupt SSC competence, progenitor lineage progression and niche coordination. Together, these insights define stem cell-based skeletal actions as a niche-regulated process in which endocrine and immune cell programs are temporally and spatially coordinated. Understanding the interactive endocrine-SSPC niche may open new therapeutic avenues for restoring regenerative capacity of the aging and diseased skeleton.
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6. Time-efficient exercise strategies to reduce visceral adipose tissue in children and adolescents with overweight or obesity: evidence from a pairwise and network meta-analysis.
PMID:日期:2026-09-12High-quality meta-analyses focusing specifically on exercise-induced changes in visceral adipose tissue (VAT) in children and adolescents with overweight or obesity (CAO) remain limited. This study compared the relative effects of four common exercise modalities and identified potentially promising strategies for reducing VAT in CAO. Seven databases were searched from inception to September 2025 for studies comparing exercise interventions with controls on VAT in CAO. A multi-level and network meta-analysis were performed to estimate effect sizes and rank exercise modalities. Subgroup and meta-regression analyses explored the influence of various moderators. Risk of bias, publication bias, sensitivity, and certainty of evidence were also assessed. A two-dimensional analysis was conducted to compare efficacy, acceptability, and time efficiency across different exercise modalities. A total of 34 studies and 2060 participants were included. High-intensity interval training (HIIT) showed the most pronounced effect (g = -0.78 [-1.24 to -0.32]) on reducing VAT, followed by aerobic combined resistance training (g = -0.65 [-1.01 to -0.29]) and aerobic exercise (g = -0.42 [-0.63 to -0.21]), while resistance training showed no significant benefit. Exploratory subgroup analyses suggested greater VAT reductions in interventions conducted at least three times per week and lasting 12 weeks or longer. Meta-regression identified study-level associations of VAT reduction with baseline BMI, changes in cardiorespiratory fitness, and sex distribution. Network and two-dimensional analyses suggested that HIIT had the highest ranking probability for VAT reduction and was associated with the shortest weekly intervention time and the lowest dropout rate, although the certainty of evidence was low to very low. The effects of different exercise modalities on VAT vary, with intervention efficacy influenced by duration and individual characteristics. HIIT may be a promising and time-efficient exercise option for reducing VAT in CAO; however, this finding should be interpreted cautiously given the low to very low certainty of evidence.
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7. Hypothalamic neurovascular and extracellular matrix remodeling: Cellular niche orchestration of immune-metabolic adaptation to nutritional stress.
PMID:日期:2026-08-28Under normal physiological conditions, hypothalamic resident immune cells interact with neurons and other non-neuronal cells to maintain tissue homeostasis. Accumulated evidence from studies with rodents shows that excessive intake of saturated fatty acids triggers hypothalamic neuroinflammation, innate and adaptive immune activation, and chemotaxis of peripheral immune cells toward the hypothalamus. The functional consequences of this immune activation are not uniformly detrimental, as specific immune subsets can instead support metabolic resilience. Beyond this functional heterogeneity, the structural mechanisms underlying immune cell recruitment within the arcuate nucleus (ARC) and median eminence (ME), particularly extracellular matrix (ECM) and neurovascular remodeling, remain poorly defined. To address this gap, this review integrates established mechanisms from other central nervous system compartments with recent hypothalamic findings, proposing a framework for how structural changes, including microgliosis, tanycyte barrier breakdown, and ECM and neurovascular remodeling, orchestrate immune-metabolic adaptations within the ARC and ME under nutritional stress. We further provide an overview of the hypothalamic immune landscape and describe how microglia, perivascular macrophages, and tanycytes, are involved with this hypothalamic niche remodeling.
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8. FGF23 - A hormone produced by bone and has many faces.
PMID:日期:2026-08-28Fibroblast growth factor 23 (FGF23) was identified as an etiological factor for hypophosphatemic rickets/osteomalacia approximately a quarter-century ago. Since then, FGF23 has been shown to be a bone-derived hormone that regulates phosphate and vitamin D metabolism by binding to the α-KLOTHO-FGF receptor complex. Dysregulation of FGF23 activity results in hypophosphatemic and hyperphosphatemic disorders. Medical therapy targeting FGF23 is now available for hypophosphatemic diseases caused by FGF23 excess. Furthermore, elevated FGF23 levels have been associated with various adverse clinical outcomes, including left ventricular hypertrophy, cardiovascular events, vascular calcification, and increased mortality. Beyond its role in mineral metabolism, FGF23 has been reported to exert direct effects on other organs, contributing to conditions such as left ventricular hypertrophy, anemia, and cardiac and renal fibrosis. However, the exact mechanisms underlying these pleiotropic actions have not yet been fully elucidated. This review summarizes recent findings regarding FGF23, focusing on its classical role as a hormone and its broader effects as a humoral factor on other organs.
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9. The central role of the β-cell in diabetes: from monogenic forms to type 1, type 2, and gestational diabetes.
PMID:日期:2026-08-28Diabetes encompasses a heterogeneous group of metabolic disorders characterized by hyperglycemia resulting from inadequate insulin secretion and/or impaired insulin action. A central, common feature across all major forms of diabetes is the loss of functional pancreatic β-cell mass. Recent advancements have significantly highlighted the critical role of pancreatic β-cell in diabetes, primarily driven by advances in genome-wide and multi-omics approaches, the availability of isolated human islets, and the data from large clinical trials. This review synthesizes current evidence on the pathogenesis of different diabetes types including monogenic diabetes (MD), type 1 diabetes (T1D), type 2 diabetes (T2D), and gestational diabetes (GD), from the perspective of the pancreatic β-cell, emphasizing its contribution to disease heterogeneity and progression. In MD, single-gene defects directly impair β-cell function, highlighting the genetic basis of insulin secretion and offering insights into personalized treatment. In T1D, β-cells are not merely passive targets of autoimmunity but may actively participate in initiating immune responses through stress-induced changes. T2D is characterized by β-cell failure in the context of insulin resistance (IR), with genetic and functional studies underscoring the key role of β-cell decline in disease development. GD results from an inadequate β-cell compensatory response to pregnancy-related IR, revealing the intrinsic metabolic defect. Overall, a β-cell-centered framework helps elucidate the diverse mechanisms underlying different types of diabetes, provides a mechanistic foundation for improved disease subclassification.
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10. Shades of insulinoma one century after first extensive evaluation by Wilder and colleagues; a figurative review between light and dark.
PMID:日期:2026-08-26In the fall of 1926, a 40-year-old physician was admitted to Mayo Clinic with worsening bouts bouts of faintness and paraesthesias associated with missed meals and physical exertion and which could be prevented by food or sweet drinks. Given that the symptoms were similar to an insulin overdose, the patient wanted his "spontaneous hyperinsulinism" evaluated. The dedicated team of R.M. Wilder, F.N. Allan, M.H. Power and H.E. Robertson investigated of Langerhans. Upon surgical exploration by Dr. W.J.Mayo, the body and tail of the pancreas were found to have multiple tumors, and there were liver metastases. The disease was unresectable, and the patient died one month after surgery. Pathology revealed the tumor cells to be consistent with carcinoma of the Islets of Langerhans. Extracts dervied from the liver metastases lowered blood glucose in rabbits, proving the metastases were from the insulin-producing carcinoma. Thus, Wilders, et al. published the first report of an insulinoma in 1927. One century later, insulinomas remain fascinating and challenging. In commemoration of one century of insulinoma-related clinical and basic research, this narrative review describes key breakthroughs and presents, by means of seven case studies, the clinical spectrum of insulinomas and their clinical courses, from benign to fatally malignant.