METABOLISM-CLINICAL AND EXPERIMENTAL代谢：临床与实验
METABOLISM-CLINICAL AND EXPERIMENTAL(英文缩写 METABOLISM),ISSN 0026-0495,eISSN 1532-8600,中文译名:代谢：临床与实验 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：2025-11-01 至 2026-10-31，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 | 13.934 | Q1 |
| 2022 | 9.800 | Q1 |
| 2023 | 10.800 | Q1 |
| 2024 | 11.900 | Q1 |
| 2025 | 16.700 | Q1 |
METABOLISM-CLINICAL AND EXPERIMENTAL 最新收录文献
-
1. P7C3: A novel multi-target therapeutic strategy to combat disuse-related bone loss in space and on earth.
1. P7C3：一种用于对抗太空和地球上废用性骨丢失的新型多靶点治疗策略PMID:日期:2026-10-03Extended periods of skeletal unloading cause rapid and severe bone loss, structural weakening, and increased fragility. Unlike postmenopausal osteoporosis, disuse bone atrophy is only partially responsive to pharmacological treatments, making it a critical and unresolved medical challenge in both space- and Earth-based medicine. Here, we investigate and assess the dose-response to P7C3 during the transition of bone-derived mesenchymal stem cells to osteoblasts and adipocytes, and its effect during human preosteoclast differentiation into mature osteoclasts in vitro. We further evaluate the in vivo protective properties of P7C3 against pathological bone atrophy induced by mechanical disuse. Data demonstrates that multifunctional P7C3 selectively promoted osteogenesis while inhibiting osteoclast maturation and activity. Proteomic analyses indicate osteogenic augmentation via ↑FSTL-1 and ↓IL-10Rβ, adipogenic inhibition via ↓ADIPOQ and ↑NAMPT, and osteoclastic inhibition via ↓OPN, ↑BMP-7 and ↑OPG. Enrichment analyses suggest the positive regulation of MAPK, JAK/STAT, and Wnt signaling pathways. Transcriptomic data reveal P7C3-induced cell-selective alterations in transcriptional programs within mitochondrial DNA, potentially promoting ATP generation through NADH activity, and regulating cellular energy metabolism. Hindlimb suspension (HLS) induced rapid pathologic bone loss in vivo, with an overarching drive towards adipogenesis (↑C4.A4, ↑FABP3, ↑ADIPOQ, and ↓Dcn) over osteogenesis (↑activin R2A, ↑LIFR and ↓STAT3) and augmented osteoclastic activity and cellular senescence, potentially via MAPK, JAK/STAT, and Wnt signaling. Despite HLS, P7C3 attenuated oxidative stress, RANKL, osteoclastic activity, bone marrow adiposity, cellular senescence, and pathological bone loss. P7C3 presents as an undiscovered and promising multi-target therapeutic strategy against disuse-induced bone atrophy for both space- and Earth-based applications.
-
2. Astrocyte-derived extracellular vesicles regulate proopiomelanocortin neurons and modify food intake and glucose metabolism.
PMID:日期:2026-10-03Astrocytes actively regulate hypothalamic circuits involved in energy balance, yet the mechanisms are not completely understood. Here we analyzed whether extracellular vesicles (EVs) released by hypothalamic astrocytes carry nutritionally sensitive signals that modulate metabolism, focusing on the potential role of proopiomelanocortin (POMC) neurons in this response and whether miRNAs carried in these EVs are involved. EVs were isolated from primary hypothalamic astrocyte cultures exposed to palmitic acid (PA), oleic acid, or vehicle and their effects assessed in vitro on proopiomelanocortin (POMC) neurons and in vivo. Changes in miRNA content in these EVs in response to PA were determined by miRNAseq and the effects of selected miRNAs on POMC neurons were tested. EVs were internalized by POMC neurons in vitro and increased Pomc expression. When infused into the lateral ventricle or directly into the arcuate nucleus, astrocytic EVs were internalized by POMC neurons, as well as other cells, and altered mitochondrial density and mitochondria-endoplasmic reticulum interactions in POMC neurons, food intake, eating patterns and glucose metabolism in male mice. All in vivo and in vitro responses varied depending on the previous fatty acid (FA) environment of the EV-releasing astrocytes. Indeed, the miRNA content of astrocytic EVs was modified by exposure to PA, and this response differed between EVs released from astrocytes from male or female mice. These findings indicate that astrocyte-derived EVs act as metabolic messengers by transmitting nutrient-specific information to hypothalamic neurons, influencing energy homeostasis through structural and functional remodeling.
-
3. Association of severe liver disease and diabetic retinopathy, retinal imaging phenotypes, and plasma metabolic signatures: A UK biobank study.
PMID:日期:2026-10-02Severe liver disease (SLD), including non-alcoholic fatty liver disease, alcoholic liver disease, viral hepatitis, and liver fibrosis/cirrhosis, is a systemic metabolic disorder that frequently coexists with diabetes. As one of the most common diabetic complications, diabetic retinopathy (DR) still has an unclear association with SLD. This study aimed to examine the relationship between hospitalization-defined SLD and subsequent hospitalization-defined DR, multimodal retinal imaging phenotypes, and shared plasma metabolic signatures that statistically accounted for part of the observed association. We analyzed UK Biobank data from 499,852 participants. Time-dependent Cox models evaluated associations of SLD and its subtypes with incident DR. Multistate models assessed observed transitions from healthy state to diabetes and then to DR. Optical coherence tomography and color fundus photography parameters were analyzed to characterize retinal structural and vascular features cross-sectionally, and plasma metabolomic profiling was used to identify potential metabolic correlates shared by SLD and subsequent DR. During follow-up, 12,632 participants developed SLD. Incident SLD was associated with higher DR risk (HR, 2.38; 95% CI, 2.08-2.73). In multistate analyses, SLD was associated with increased observed rate of transition from diabetes to DR (HR, 1.18; 95% CI, 1.03-1.35). SLD was primarily associated with lower OCT-derived macular and neuroretinal thickness in the cross-sectional imaging subset. Exploratory mediation analyses identified a shared metabolic signature, predominantly characterized by apoB-containing lipoprotein composition and triglyceride-enriched remnant-related measures, that statistically accounted for part of the association between baseline SLD and subsequent DR. Hospitalization-defined SLD and several of its subtypes were associated with a higher subsequent risk of hospitalization-defined DR and with a higher observed rate of transition from diabetes to DR. Cross-sectional retinal imaging analyses identified retinal structural and vascular imaging phenotypes associated with SLD. Circulating lipoprotein-related measures constituted a shared metabolic signature and statistically accounted for part of the observed association. These findings identify hospitalization-defined SLD as a marker of systemic disease burden associated with DR.
-
4. ATF6 contributes to cardiac macrophage polarization and metabolic reprogramming following myocardial ischemia/reperfusion injury.
PMID:日期:2026-10-01To investigate when and how activating transcription factor 6 (ATF6) contributes to macrophages (Mφ) polarization and tissue repair after myocardial ischemia/reperfusion (I/R) injury. The WT and ATF6 knockout (ATF6) mice were subjected to myocardial I/R injury. Endoplasmic reticulum stress (ERS) markers expression levels were detected by western blotting. Echocardiography, Masson staining, Sirius red staining, Evans Blue/TTC staining and immunofluorescence techniques were used to evaluate myocardial injury context and cardiac function. Flow cytometry analyzed the phenotypes and functions of cardiac Mφ (cMφ). Single-cell sequencing technology, Seahorse oxygen consumption rate/extracellular acidification rate assays and reactive oxygen species (ROS) measurements were used to analyze how ATF6 deficiency affects the profiles of cMφ. Myocardial I/R injury resulted in an increase expression of ERS markers with ATF6 hydrolyzed and entered the nucleus. The role of heart in recruiting peripheral monocyte-derived CCR2 cMφ and driving their phenotypic transformation from pro-inflammatory (CCR2Ly6CCD206 cMφ) to reparative (CCR2Ly6CCD206 cMφ) is impaired in ATF6 mice. Moreover, the myocardial injured exacerbated, cardiac function recovery delayed and adverse early remodeling occurred, which could not be salvaged by Mφ adoptive adoption. Single-cell sequencing revealed that differentially expressed genes in CCR2Ly6CCD206 cMφ of WT and ATF6 mice and were enriched in ROS and oxidative phosphorylation signaling pathways. Functional metabolic assays in CCR2Ly6CCD206 bone marrow-derived macrophage demonstrated that ATF6 deficiency was associated with impaired mitochondrial respiration (reduced basal respiration, maximal respiratory capacity, ATP production and spare respiratory capacity) with a compensatory glycolytic upregulation, and increased ROS production, which was abrogated by the mitochondria-targeted scavenger. ATF6 deficiency is associated with altered phenotype and function of monocyte-derived CCR2 cMφ during myocardial I/R injury. This association between ATF6 and improved outcomes might be linked to phenotypic polarization and metabolic fitness of CCR2Ly6CCD206 cMφ.
-
5. Comparative outcomes of GLP-1 receptor agonist and SGLT2 inhibitor users after liver transplantation: An emulated target trial.
5. GLP-1受体激动剂与SGLT2抑制剂使用者在肝移植后的比较结局：一项模拟目标试验PMID:日期:2026-09-29We emulated a target trial to compare glucagon-like peptide-1 receptor agonists (GLP-1 RAs) with sodium-glucose cotransporter-2 inhibitors (SGLT2is) regarding hepatic, cardiovascular, and mortality outcomes among liver transplant recipients with diabetes. Using the TriNetX US Collaborative Network, we identified 33,161 liver transplant recipients with diabetes between 2015 and 2024. After propensity score matching, 564 pairs of new GLP-1 RA and SGLT2i users were analyzed. Risks of infection, graft rejection, cirrhosis, cardiovascular outcomes, hospitalization, and mortality were estimated using Cox proportional hazards models. The mean age was 65.8 years (SD, 10.8), and 65.1% were male. Compared with SGLT2i use, GLP-1 RA use was associated with lower risks of cirrhosis (HR, 0.787; 95% CI, 0.619-0.999), ischemic heart disease (HR, 0.721; 95% CI, 0.582-0.892), heart failure (HR, 0.502; 95% CI, 0.388-0.650), and all-cause mortality (HR, 0.622; 95% CI, 0.433-0.894). No significant differences were observed for infection, graft rejection, liver failure, or all-cause hospitalization. Sensitivity analyses generally supported the cardiovascular and mortality findings, whereas the association with cirrhosis was less consistent across propensity score models. Among liver transplant recipients with diabetes, GLP-1 RA use was associated with lower risks of ischemic heart disease, heart failure, and all-cause mortality compared with SGLT2i use. A lower risk of cirrhosis was also observed, although this association was of borderline statistical significance and was not consistently significant across alternative models. Given the observational design, these findings do not establish causality and warrant prospective confirmation.
-
6. Letter to the editor: Short siesta habit and cardiometabolic health: A 7-year follow-up in coronary heart disease patients from the CORDIOPREV study.
6. 致编辑的信：短暂午睡习惯与心血管代谢健康：CORDIOPREV研究中冠心病患者7年随访PMID:日期:2026-09-29该文献暂无摘要。
-
7. ETS-2 deficiency impairs brown adipose tissue function through Prdm16 repression.
PMID:日期:2026-09-26Brown adipose tissue (BAT) and beige adipocytes regulate adaptive thermogenesis and systemic energy balance, whereas BAT dysfunction contributes to obesity and metabolic disease. Although ETS transcription factors participate in adipocyte biology, the role of ETS-2 in BAT remains unclear. Adipocyte-specific Ets-2 knockout mice were generated using the Adipoq-Cre system. BAT morphology, thermogenic responses, energy expenditure, and mitochondrial structure and function were assessed under basal conditions, cold exposure, β3-adrenergic stimulation, and mTOR activation. Primary adipocytes were used for gain- and loss-of-function analyses. RNA-seq, CUT&Tag, luciferase reporter assays, Seahorse respirometry, rescue experiments, and public human adipose single-nucleus RNA-seq analyses were performed. ETS-2 was enriched in BAT and dynamically regulated during adipocyte differentiation. Adipocyte-specific Ets-2 deletion induced BAT whitening, reduced UCP-1 expression, impaired cold tolerance and β3-adrenergic responsiveness, and decreased oxygen consumption and energy expenditure. ETS-2 deficiency also disrupted mitochondrial ultrastructure and reduced respiratory capacity in brown adipocytes. Mechanistically, integrated RNA-seq and CUT&Tag identified Prdm16 as a direct ETS-2 target. ETS-2 loss repressed PRDM16, suppressed the PRDM16-PGC-1α-UCP-1 thermogenic program, and attenuated IRS-1-PI3K/Akt-mTOR signaling. PRDM16 overexpression and mTOR activation partially rescued ETS-2-deficient phenotypes. Human single-nucleus data further supported conservation of this regulatory axis. ETS-2 is a critical transcriptional regulator of BAT thermogenic function. By directly activating Prdm16 and maintaining both the PRDM16-PGC-1α-UCP-1 axis and IRS-1-PI3K/Akt-mTOR signaling, ETS-2 preserves mitochondrial integrity and adaptive thermogenesis. These findings identify the ETS-2-PRDM16 axis as a potential therapeutic target for metabolic diseases associated with BAT dysfunction.
-
8. Short siestas or healthier nappers? Interpreting seven-year cardiometabolic associations in coronary heart disease: Letter to the editor.
8. 短时午睡还是更健康的午睡者？解读冠心病中七年心血管代谢关联：致编辑的信PMID:日期:2026-09-26该文献暂无摘要。
-
9. Deletion of glucocorticoid receptors in Lepr-expressing neurons attenuates the effects of negative energy balance on female reproduction.
PMID:日期:2026-09-25Negative energy balance increases glucocorticoids (GC) and inhibits reproduction; however, the neurocircuitry mediating these effects remains poorly understood. We hypothesized that GC signaling in leptin receptor (Lepr)-expressing neurons mediates reproductive disruption caused by metabolic stress. We generated a mouse model with selective deletion of glucocorticoid receptor (GR) in Lepr-expressing cells (Lepr). We characterized pubertal development, reproductive phenotype, ovarian folliculogenesis, and hypothalamic gene expression in female Lepr mice and in GR controls under both physiologic conditions and negative energy balance. In addition, we assessed the activation status of Agrp- and Pomc-expressing neurons by quantifying c-Fos co-expression in female Lepr mice and GR controls subjected to negative energy balance. Lepr female mice had normal body weight, puberty, and reproduction in physiologic conditions. Following caloric restriction (CR), prepubertal Lepr females were resistant to delayed puberty onset, compared to controls. Peri-pubertal CR was associated with reduced Pomc mRNA levels in the posterior hypothalamic region (PH) and a greater decrease in Kiss1 expression in the preoptic area (POA) of control females, compared with Lepr mice. Adult Lepr females were more resistant to disruption of estrous cyclicity by CR than controls. Under ad libitum feeding, Lepr females had higher LH pulse frequency, amplitude, mean concentration, basal LH levels, and a normal preovulatory LH surge, compared to controls. However, both one (CR-1) and four (CR-4) days of CR were sufficient to suppress LH secretion and the preovulatory LH surge in both Lepr and control females. Serum LH levels declined in controls, but not in Lepr females, within 24 h of fasting. After CR-1, Pomc and Kiss1 mRNA levels were higher in the PH and POA, respectively, while Agrp expression was lower in the PH of Lepr females, compared to controls. Consistent with the mRNA data, the number of Agrp- and Pomc-expressing neurons were lower and higher, respectively, in the ARC of Lepr females compared with controls, and the percentage of Agrp neurons expressing c-Fos was also reduced in Lepr females. After fasting for 24 h, Kiss1 mRNA levels were higher in both PH and POA, while Pdyn, Agrp, and Pomc expression were lower in the PH of Lepr females, compared to controls. In addition, the number of Agrp-expressing neurons and the percentage of Agrp neurons expressing c-Fos were lower in the ARC of Lepr females compared to controls. The number of Pomc-expressing neurons and the percentage of Pomc neurons expressing c-Fos did not differ between Lepr and GR females. Our data suggest that absence of GC signaling in Lepr-expressing cells attenuates effects of metabolic stress on disruption of reproductive function through direct regulation of Kiss1 and/or indirectly through regulation of Pomc and Agrp expression and AgRP neuronal activation.
-
10. Identification of lipid-defined profiles and their associations with glucose metabolism.
PMID:日期:2026-09-24Current evidence suggests that certain lipids are associated with specific parameters of glucose metabolism. However, a comprehensive understanding of these associations - especially regarding detailed lipid signatures - is still lacking. Therefore, the aim of this study was to identify lipid-defined profiles based on NMR-derived lipidomics data and to investigate their cluster-specific associations with glucose metabolism. In this cross-sectional study, a total of 34 lipids measured in serum samples of 586 participants from the MEIA study were subjected to a preprocessing step involving principal component analysis followed by K-means clustering. Based on the resulting profiles, associations with the glucose-related parameters fasting glucose, 2-h post-load glucose from an oral glucose tolerance test, and HbA1c were investigated using a doubly robust estimation approach. Potential confounders were selected using a directed acyclic graph. Following lipid-defined profiles were identified: (1) severe atherogenic, (2) hyperlipidemic, (3) phospholipid-enriched HDL-dominant, and (4) optimal. Considering the first profile as the reference, the fourth profile was associated with lower fasting glucose levels (β=-0.05; 95% CI [-0.08; -0.02]; P=0.013) as well as lower HbA1c values (β=-0.07; 95% CI [-0.11; -0.03]; P=0.005) on the log-scale. Additionally, the third profile was associated with 2-h glucose levels (β=-0.12; 95% CI [-0.21; -0.04]; P=0.040). Sensitivity analyses confirmed these results. Depending on the specific lipid-defined profile, differences in glucose metabolism were found. These findings suggest that lipid-defined patterns might capture clinically relevant variation in glucose metabolism beyond individual lipid parameters and may improve risk assessment for glucose metabolism disorders.