AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM 发表关于内分泌和代谢系统生理学的原创性机械研究。将考虑对整个动物或人类进行的生理、细胞和分子研究。具体主题包括但不限于激素和生长因子作用机制；新陈代谢、炎症、微生物组和能量平衡的激素和营养调节；综合器官相声；内分泌细胞的旁分泌和自分泌控制；激素受体的功能和激活；通道、转运蛋白和膜功能的内分泌或代谢控制；激素分泌和代谢的时间分析；和代谢的数学/动力学模型。也欢迎对激素作用进行新的分子、免疫学或生物物理学研究。

The American Journal of Physiology - Endocrinology and Metabolism publishes original research on the physiology of the endocrine and metabolic systems. We welcome physiological, cellular, and molecular studies conducted on whole animals or humans. Specific topics include, but are not limited to: mechanisms of action of hormones and growth factors; hormonal and nutritional regulation of metabolism, inflammation, the microbiome, and energy balance; interactions among integrated organs; paracrine and autocrine control of endocrine cells; functions and activation of hormone receptors; endocrine or metabolic control of channels, transport proteins, and membrane functions; temporal analysis of hormone secretion and metabolism; and mathematical/dynamic modeling of metabolism. We also welcome new molecular, immunological, or biophysical studies on hormone actions.

《American Journal of Physiology - Endocrinology and Metabolism》发表关于内分泌和代谢系统生理学的原创性研究。我们欢迎对整个动物或人类进行的生理、细胞和分子研究，具体主题包括但不限于：激素和生长因子的作用机制；新陈代谢、炎症、微生物组和能量平衡的激素与营养调节；综合器官的相互作用；内分泌细胞的旁分泌和自分泌控制；激素受体的功能与激活；通道、转运蛋白和膜功能的内分泌或代谢控制；激素分泌和代谢的时间分析；以及代谢的数学和动力学模型。此外，我们也欢迎对激素作用的新分子、免疫学或生物物理学研究。

American Journal of Physiology - Endocrinology and Metabolism

Oral administration of resveratrol attenuates several symptoms associated with the metabolic syndrome, such as impaired glucose homeostasis and hypertension. Recent work has shown that resveratrol can improve glucose homeostasis in obesity via changes in the gut microbiota. Studies involving fecal microbiome transplants (FMTs) suggest that either live gut microbiota or bacterial-derived metabolites from resveratrol ingestion are responsible for producing the observed benefits in recipients. Herein, we show that obese mice receiving FMTs from healthy resveratrol-fed mice have improved glucose homeostasis within 11 days of the first transplant, and that resveratrol-FMTs is more efficacious than oral supplementation of resveratrol for the same duration. The effects of FMTs from resveratrol-fed mice are also associated with decreased inflammation in the colon of obese recipient mice. Furthermore, we show that sterile fecal filtrates from resveratrol-fed mice are sufficient to improve glucose homeostasis in obese mice, demonstrating that nonliving bacterial, metabolites, or other components within the feces of resveratrol-fed mice are sufficient to reduce intestinal inflammation. These postbiotics may be an integral mechanism by which resveratrol improves hyperglycemia in obesity. Resveratrol-FMTs also reduced the systolic blood pressure of hypertensive mice within 2 wk of the first transplant, indicating that the beneficial effects of resveratrol-FMTs may also assist with improving cardiovascular conditions associated with the metabolic syndrome.

Ty T. Kim

Nirmal Parajuli

Miranda M. Sung

Suresh C. Bairwa

Jody Levasseur

Carrie-Lynn M. Soltys

David S. Wishart

Karen Madsen

Jonathan D. Schertzer

Jason R. B. Dyck

AJP Endocrinology and Metabolism

Fecal transplant from resveratrol-fed donors improves glycaemia and cardiovascular features of the metabolic syndrome in mice

Endometriosis is a gynecologic disease common among reproductive-aged women caused by the growth of endometrial tissue outside the uterus. Altered expression of numerous genes and microRNAs has been reported in endometriosis. Steroidogenic factor 1 (SF-1), an essential transcriptional regulator of multiple genes involved in estrogen biosynthesis, is aberrantly increased and plays an important role in the pathogenesis of endometriosis. Here, we show the expression of SF-1 in endometriosis is regulated by miR-370-3p. Sera and tissue were collected from 20 women surgically diagnosed with endometriosis and 26 women without endometriosis. We found that miR-370-3p levels were decreased in the serum of patients with endometriosis while SF-1 mRNA levels were inversely upregulated in endometriotic lesions compared with respective controls. Transfection of primary endometriotic cells with miR-370-3p mimic or inhibitor resulted in the altered expression of SF-1 and SF-1 downstream target genes steroidogenic acute regulatory protein (StAR) and CYP19A1. Overexpression of miR-370-3p inhibited cell proliferation and induced apoptosis in endometriotic cells. This study reveals that miR-370-3p functions as a negative regulator of SF-1 and cell proliferation in endometriotic cells. We suggest a novel therapeutic strategy for controlling SF-1 in endometriosis.

Zhuoying Hu

Ramanaiah Mamillapalli

Hugh S. Taylor

American Journal of Physiology-Endocrinology and Metabolism

Increased circulating miR-370-3p regulates steroidogenic factor 1 in endometriosis

循环中增加的miR-370-3p调控子宫内膜异位症中的类固醇生成因子1

The obesity pandemic can be viewed as a result of an imbalanced reaction to changing environmental factors. Recent research has linked circadian arrhythmicity to obesity and related diseases; however, the underlying mechanisms are still unclear. In this study, we found that high-fat diet (HFD) feeding strikingly promoted daytime rather than nighttime caloric intake in mice, leading to feeding circadian arrhythmicity. Using scheduled feeding with a defined amount of daily HFD intake, we found that an increase in the ratio of daytime to nighttime feeding promoted weight gain, whereas a decrease of this ratio rebalanced energy expenditure to counteract obesity. In identifying the underlying mechanism, we found that hypothalamic release of anorexigenic neuropeptide oxytocin displayed a diurnal rhythm of daytime rise and nighttime decline, which negatively correlated with the diurnal feeding activities of normal chow-fed mice. In contrast, chronic HFD feeding abrogated oxytocin diurnal rhythmicity, primarily by suppressing daytime oxytocin rise. Using pharmacological experiments with hypothalamic injection of oxytocin or oxytocin antagonist, we showed that daytime manipulation of oxytocin can change feeding circadian patterns to reprogram energy expenditure, leading to attenuation or induction of obesity independently of 24-h caloric intake. Also importantly, we found that peripheral injection of oxytocin activated hypothalamic oxytocin neurons to release oxytocin, and exerted metabolic effects similar to central oxytocin injection, thus offering a practical clinical avenue to use oxytocin in obesity control. In conclusion, resting-stage oxytocin release and feeding activity represent a critical circadian mechanism and therapeutic target for obesity.

Guo Zhang

Dongsheng Cai

Circadian intervention of obesity development via resting-stage feeding manipulation or oxytocin treatment

通过休息期饲喂调控或催产素治疗干预肥胖发展的昼夜节律

The NR4A orphan nuclear receptors function as early response genes to numerous stimuli. Our laboratory has previously demonstrated that overexpression of NR4A3 (NOR-1, MINOR) in 3T3-L1 adipocytes enhances insulin-stimulated glucose uptake. To assess the in vivo effect of NR4A3 on adipocytes, we generated transgenic mice with NR4A3 overexpression driven by the adipocyte fatty acid-binding protein (AP2) promoter (AP2-NR4A3 mice). We hypothesized that AP2-NR4A3 mice would display enhanced glucose tolerance and insulin sensitivity. However, AP2-NR4A3 mice exhibit metabolic impairment, including increased fasting glucose and insulin, impaired glucose tolerance, insulin resistance, decreased serum free fatty acids, and increased low-density lipoprotein-cholesterol. AP2-NR4A3 mice also display a significant reduction in serum epinephrine due to increased expression of catecholamine-catabolizing enzymes in adipose tissue, including monoamine oxidase-A. Furthermore, enhanced expression of monoamine oxidase-A is due to direct transcriptional activation by NR4A3. Finally, AP2-NR4A3 mice display cardiac and behavioral alterations consistent with chronically low circulating epinephrine levels. In conclusion, overexpression of NR4A3 in adipocytes produces a complex phenotype characterized by impaired glucose metabolism and low serum catecholamines due to enhanced degradation by adipose tissue.

R. Grace Walton

Xiaolin Zhu

Ling Tian

Elizabeth B. Heywood

Jian Liu

Helliner S. Hill

Jiarong Liu

Dennis Bruemmer

Qinglin Yang

Yuchang Fu

W. Timothy Garvey

AP2-NR4A3 transgenic mice display reduced serum epinephrine because of increased catecholamine catabolism in adipose tissue

AP2-NR4A3转基因小鼠因脂肪组织中儿茶酚胺分解代谢增加而表现出血清肾上腺素减少

Endothelial progenitor cell (EPC) dysfunction is a key contributor to diabetic refractory wounds. Endothelial nitric oxide synthase (eNOS), which critically regulates the mobilization and function of EPCs, is uncoupled in diabetes due to decreased cofactor tetrahydrobiopterin (BH4). We tested whether GTP cyclohydrolase I (GTPCH I), the rate-limiting enzyme of BH4 synthesis, preserves EPC function in type 1 diabetic mice. Type 1 diabetes was induced in wild-type (WT) and GTPCH I transgenic (Tg-GCH) mice by intraperitoneal injection of streptozotocin (STZ). EPCs were isolated from the peripheral blood and bone marrow of WT, Tg-GCH, and GTPCH I-deficient hph-1 mice. The number of EPCs was significantly lower in STZ-WT mice and hph-1 mice and was rescued in STZ Tg-GCH mice. Furthermore, GTPCH I overexpression improved impaired diabetic EPC migration and tube formation. EPCs from WT, Tg-GCH, and STZ-Tg-GCH mice were administered to diabetic excisional wounds and accelerated wound healing significantly, with a concomitant augmentation of angiogenesis. Flow cytometry measurements showed that intracellular nitric oxide (NO) levels were reduced significantly in STZ-WT and hph-1 mice, paralleled by increased superoxide anion levels; both were rescued in STZ-Tg-GCH mice. Western blot analysis revealed that thrombospondin-1 (TSP-1) was significantly upregulated in the EPCs of STZ-WT mice and hph-1 mice and suppressed in STZ-treated Tg-GCH mice. Our results demonstrate that the GTPCH I/BH4 pathway is critical to preserve EPC quantity, function, and regenerative capacity during wound healing in type 1 diabetic mice at least partly through the attenuation of superoxide and TSP-1 levels and augmentation of NO level.

Lu Tie

Lu-Yuan Chen

Dan-Dan Chen

He-Hui Xie

Keith M. Channon

Alex F. Chen

GTP cyclohydrolase I prevents diabetic-impaired endothelial progenitor cells and wound healing by suppressing oxidative stress/thrombospondin-1

GTP环水解酶I通过抑制氧化应激/血小板反应蛋白-1预防糖尿病内皮祖细胞损伤及伤口愈合障碍

Maternal obesity decreases infant energy expenditure, subsequently predisposing infants to greater adiposity and weight gain. Conversely, some findings suggest that maternal exercise may increase infant energy expenditure; however, the impact of maternal exercise mode (i.e. aerobic or resistance exercise) on infant energy expenditure is not known. The purpose of this study was to investigate if supervised maternal exercise (aerobic, resistance, and combination (aerobic+resistance)) affects infant energy expenditure. When weight adjusted resting energy expenditure was determined at 1 month of age, infants exposed to resistance exercise in utero had &gt;35% higher energy expenditure compared to infants exposed to aerobic exercise or no exercise. Additionally, infant energy expenditure and lean mass were associated with maternal blood lipids independent of exercise mode. Increase in infant resting energy expenditure with the addition of any resistance exercise during gestation resulted in discrepancy between measured and estimated energy expenditure using common estimation equations. These results implicate maternal metabolic health in determining infant metabolic rate, and maternal resistance exercise during pregnancy as a lifestyle intervention to increase infant energy expenditure potentially decreasing the subsequent infant adiposity gain.

Filip Jevtovic

Alex Claiborne

James DeVente

Steven Mouro

Joseph A. Houmard

Nicholas T. Broskey

Linda E. May

Maternal resistance exercise increases infant energy expenditure

母亲抗阻运动增加婴儿能量消耗

Belinda Yau

Yousun An

Mark Germanos

Patricia Schwarzkopf

A Gabrielle van der Kraan

Mark Larance

Hayley Webster

Christian Burns

Cedric S Asensio

Melkam A Kebede

VPS41 deletion triggers progressive loss of insulin stores and downregulation of beta-cell identity

VPS41缺失引发胰岛素储存的渐进性丧失和β细胞特性的下调

The Lactate Shuttle concept has revolutionized our understanding and study of metabolism in physiology, biochemistry, metabolism, nutrition, and medicine. Seminal findings of the Mitochondrial Lactate Oxidation Complex (mLOC) elucidated the architectural structure of its components. Here, we report that the mitochondrial pyruvate carrier (mPC) is an additional member of the mLOC in mouse muscle and C2C12 myoblasts and myotubes. Immunoblots, mass spectrometry, and co-immunoprecipitation experiments of mitochondrial preparations revealed abundant amounts of mitochondrial lactate dehydrogenase (mLDH), monocarboxylate transporter (mMCT), basigin (CD147), cytochrome oxidase (COx), and pyruvate carriers 1 and 2 (mPC1 and 2). Additionally, using confocal laser scanning microscopy (CLSM) and in situ proximity ligation, we also demonstrated planar and 3D colocalization of pyruvate and lactate transporters with COx in fixed skeletal muscle sections, myotubes, and C2C12 myoblasts. This work serves as a landmark for configuring the final pathway of carbohydrate oxidation.

Robert G. Leija

Jose A. Arevalo

Dianna Xing

José Pablo Vázquez-Medina

George A. Brooks

The Mitochondrial Lactate Oxidation Complex: endpoint for carbohydrate carbon disposal

线粒体乳酸氧化复合物：碳水化合物碳处理的终点

The rising prevalence of metabolic diseases is a significant global health concern. Beyond lifestyle management, targeting key molecules involved in metabolic regulation is essential. C1q/TNF-related protein 6 (CTRP6) is notably associated with glucose and lipid metabolism, with numerous studies highlighting its regulatory functions in metabolic diseases. This review summarizes the current knowledge on CTRP6, focusing on its gene expression profiles, protein structure, gene regulation, and role in metabolic diseases. CTRP6 is widely expressed across various tissues and features four distinct domains, with the C1q domain predicted to bind to its receptor. Notably, serum levels of CTRP6 are significantly elevated in patients with obesity and type 2 diabetes. In these conditions, adipose tissue serves as a key source of CTRP6, and its involvement in adipose tissue expansion, inflammation, and nutrient sensing has been observed in several studies. CTRP6 is also implicated in type 1 diabetes, gestational diabetes mellitus, and diabetic complications, particularly diabetic nephropathy. Although some studies have suggested that CTRP6 has protective roles in atherosclerotic cell models, myocardial infarction rat models, and ischemia/reperfusion injury mouse models, methodological issues such as unreliable antibodies and unstrict controls make it difficult to draw accurate conclusions from these studies. Patients with polycystic ovary syndrome (PCOS) exhibit elevated serum levels of CTRP6, though its direct impact on PCOS phenotypes remains unclear. In conclusion, CTRP6 emerges as a promising therapeutic target for metabolic diseases. A deeper understanding of CTRP6 will empower the scientific community to develop effective interventions to address the increasing prevalence of these diseases.

Jeevotham Senthil Kumar

Muhammad Zubair Mehboob

Xia Lei

Exploring CTRP6: a biomarker and therapeutic target in metabolic diseases

探索CTRP6：代谢疾病的生物标志物和治疗靶点

Diabetic kidney disease (DKD) is a severe diabetic microvascular complication featured by chronic low-grade inflammation. Roux-en-Y gastric bypass (RYGB) surgery has gained importance as a safe and effective surgery to treat DKD. Bile acids are significantly changed after RYGB, which brings a series of metabolic benefits, but the relationship with the improvement of DKD is unclear. Therefore, this study performed RYGB surgery on db/db mice to observe the beneficial effects of the surgery on the kidneys, and performed bile acid targeted metabolomics analysis to explore bile acid changes. We found that RYGB significantly reduced albuminuria in db/db mice, improved renal function, reversed renal structural lesions, and attenuated podocyte injury, inflammation. Notably, bile acid metabolomic analysis revealed taurolithocholic acid (TLCA) as the most significantly altered bile acid after RYGB. Further in vitro and in vivo validation experiments revealed that TLCA supplementation improved renal function and reduced renal inflammatory damage in db/db mice. In addition, TLCA inhibited high glucose-induced inflammatory damage in MPC-5 cells, and its mechanism of action may be related to activating Takeda G protein-coupled receptor 5 (TGR5), inhibiting NF-κB phosphorylation, and thus inhibiting inflammatory response. In conclusion, RYGB may play a protective role in the kidneys of diabetic mice by activating the TLCA/TGR5 pathway.

Hongmei Lang

Jie Xiang

Xiaorong Chen

Dan Tong

Lijuan Wang

Aidi Mou

Daoyan Liu

Peng Gao

Zongshi Lu

Zhiming Zhu

Roux-en-Y gastric bypass alleviates kidney inflammation and improves kidney function in db/db mice by activating TLCA/TGR5 pathway

Roux-en-Y胃旁路手术通过激活TLCA/TGR5通路减轻db/db小鼠的肾脏炎症并改善肾功能

Abbreviation	Am. J. Physiol. Endocrinol. Metab.
Journal Impact	4.09
Quartiles(Global)	PHYSIOLOGY(Q1)

ISSN	0193-1849, 1522-1555
h-index	224

Publication Information	Publisher: American Physiological Society，Publishing cycle: Monthly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 1980，Proportion of original research papers: 88.54%，Self Citation Rate:2.40%， Gold OA Rate: 11.17%
Average review cycle	网友分享经验：平均1.0个月
Average recruitment ratio	网友分享经验：较难

American Journal of Physiology - Endocrinology and Metabolism

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