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Predictive factors for pituitary response to pulsatile GnRH therapy in patients with congenital hypogonadotropic hypogonadism

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Asian Journal of Andrology 2018年第4期20卷 319-323页

作者： Jiang-Feng Mao Xi Wang Jun-Jie Zheng Zhao-Xiang Liu Hong-Li Xu Bing-Kun Huang Min Nie Xue-Yan Wu Department of endocrinology Peking Union Medical College Hospital Key Laboratory of Endocrinology Ministry of Health Beijing 100730 China

Pulsatile gonadotropin-releasing hormone （GnRH） may induce spermatogenesis in most patients with congenital hypogonadotropic hypogonadism （CHH） by stimulating gonadotropin production, while the predictors for a pituitary response to pulsatile GnRH therapy were rarely investigated. Therefore, the aim of our study is to investigate predictors of the pituitary response to pulsatile GnRH therapy. This retrospective cohort study included 82 CHH patients who received subcutaneous pulsatile GnRH therapy for at least 1 month. Patients were categorized into poor or normal luteinizing hormone （LH） response subgroups according to their LH level （LH 〈2 IU 1-1 or LH P_2 IU 1-1） 1 month into pulsatile GnRH therapy. Gonadotropin and testosterone levels, testicular size, and sperm count were compared between the two subgroups before and after GnRH therapy. Among all patients, LH increased from 0.4±0.5 IUI^-1 to 7.5±4.4 IUI^-1 and follicle-stimulating hormone （FSH） increased from 1.1±0.9 IUI^-1 to 8.8±5.3 IU 1-1. A Cox regression analysis showed that basal testosterone level （6 = 0.252, P = 0.029） and triptorelin-stimulated FSH60min（13 = 0.518, P = 0.01） were two favorable predictors for pituitary response to GnRH therapy. Nine patients （9/82, 11.0%） with low LH response to GnRH therapy were classified into the poor LH response subgroup. After pulsatile GnRH therapy, total serum testosterone level was 39± 28 ng dl^-1 versus 248±158 ng d1^-1 （P=0.001）, and testicular size was 4.0±3.1 ml versus 7.9±4.5 ml （P= 0.005） in the poor and normal LH response subgroups, respectively. It is concluded that higher levels of triptorelin-stimulated FSH60min. and basal total serum testosterone are favorable predictors of pituitary LH response to GnRH therapy.

关键词： congenital hypogonadotropic hypogonadism pulsatile GnRH therapy treatment

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Data Resource Profile:A Protocol of China National Diabetic Chronic Complications Study

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Biomedical and Environmental Sciences 2022年第7期35卷 633-640页

作者： HOU Xu Hong WANG Li Min CHEN Si Yu LIANG Ye Bei ZHANG Mei HUANG Zheng Jing CHEN Hong Li WU Jing Zhu WU Jing JIA Wei Ping Department of endocrinology and Metabolism Shanghai Jiao Tong University Affiliated Sixth People's HospitalShanghai Diabetes InstituteShanghai Key Laboratory of Diabetes MellitusShanghai Clinical Center for DiabetesShanghai Key Clinical Center for Metabolic DiseaseShanghai 200233China National Center for Chronic and Noncommunicable Disease Control and Prevention Chinese Center for Disease Control and PreventionBeijing 102206China Department of endocrinology and Metabolism Suzhou Dushu Lake Hospital(Dushu Lake Hospital Affiliated to Soochow University)Suzhou 215000JiangsuChina Department of endocrinology and Metabolism Shanghai General HospitalShanghai 200080China

Diabetes affects approximately 10.5%of adults worldwide,and its chronic complications lead to severely disabling sequelae and premature death,thus placing a heavy healthcare burden on both patients affected and society[1].China has experienced a dramatic increase in diabetes prevalence from 0.67%in 1980[2]to 12.8%in 2018[3]and has approximately one-quarter of people with diabetes worldwide[1].It is therefore essential to understand the epidemiologic characteristics of the chronic complications and co-morbidities of diabetes,and the current status of diabetes management to guide planning for appropriate diabetes care and intervention for these complications and co-morbidities at the national level[4-7].

关键词： diabetes Chronic death

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De novo serine synthesis regulates chondrocyte proliferation during bone development and repair

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Bone Research 2022年第2期10卷 274-285页

作者： Steve Stegen Shauni Loopmans Ingrid Stockmans Karen Moermans Peter Carmeliet Geert Carmeliet laboratory of Clinical and Experimental endocrinology Department of Chronic Diseases and MetabolismKU Leuven3000 LeuvenBelgium laboratory of Angiogenesis and Vascular Metabolism VIB Center for Cancer Biology3000 LeuvenBelgium laboratory of Angiogenesis and Vascular Metabolism Department of Oncology and Leuven Cancer InstituteKU Leuven3000 LeuvenBelgium State key laboratory of Ophthalmology Zhongshan Ophthalmic CenterSun Yat-Sen UniversityGuangzhou 510080China

The majority of the mammalian skeleton is formed through endochondral ossification starting from a cartilaginous template.Cartilage cells, or chondrocytes, survive, proliferate and synthesize extracellular matrix in an avascular environment, but the metabolic requirements for these anabolic processes are not fully understood. Here, using metabolomics analysis and genetic in vivo models, we show that maintaining intracellular serine homeostasis is essential for chondrocyte function. De novo serine synthesis through phosphoglycerate dehydrogenase(PHGDH)-mediated glucose metabolism generates nucleotides that are necessary for chondrocyte proliferation and long bone growth. On the other hand, dietary serine is less crucial during endochondral bone formation, as serine-starved chondrocytes compensate by inducing PHGDH-mediated serine synthesis.Mechanistically, this metabolic flexibility requires ATF4, a transcriptional regulator of amino acid metabolism and stress responses.We demonstrate that both serine deprivation and PHGDH inactivation enhance ATF4 signaling to stimulate de novo serine synthesis and serine uptake, respectively, and thereby prevent intracellular serine depletion and chondrocyte dysfunction. A similar metabolic adaptability between serine uptake and de novo synthesis is observed in the cartilage callus during fracture repair.Together, the results of this study reveal a critical role for PHGDH-dependent serine synthesis in maintaining intracellular serine levels under physiological and serine-limited conditions, as adequate serine levels are necessary to support chondrocyte proliferation during endochondral ossification.

关键词： synthesis starting thereby

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Intrauterine hyperglycemia impairs endometrial receptivity via up-regulating SGK1 in diabetes

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Science China(Life Sciences) 2022年第8期65卷 1578-1589页

作者： Haiyan Xu Jingyi Li Luyang Jin Dan Zhang Bin Chen Xinmei Liu Xianhua Lin Yiting Huang Zhanghong Ke Juan Liu Lin Gao Jianzhong Sheng Hefeng Huang Reproductive Medicine Center Ningbo First HospitalNingbo 315100China key laboratory of Reproductive Genetics Ministry of Education(Zhejiang University)Hangzhou 310058China Department of Reproductive endocrinology Women’s HospitalZhejiang University School of MedicineHangzhou 310006China Department of Pathology&Pathophysiology Zhejiang University School of MedicineHangzhou 310058China Shanghai key laboratory of Embryo Original Diseases Shanghai 200030China

Diabetes is a complex metabolic disorder which can adversely affect reproductive function. SGK1 is found to be up-regulated in multiple tissues of diabetic patients. However, the effects of diabetes on endometrial SGK1 expression and endometrial receptivity remain unknown. In this study, we established a streptozotocin-induced diabetic mouse model and observed reduced implantation sites, retarded development of pinopodes, increased SGK1, and aberrant expression of LIF and MUC1 in the endometrial epithelium. We injected the uterine lumen of normal mice with high-glucose solution and cultured endometrial cells in high-glucose medium to mimic intrauterine hyperglycemia. Both studies provided compelling evidence that hyperglycemia could lead to diminished embryo implantation and dysregulated SGK1, LIF and MUC1. Additionally, through over-expression of SGK1 in vivo and in vitro, we found that enhanced SGK1 also decreased LIF expression, increased MUC1 expression, and attenuated embryo implantation rate. We further identified that hyperglycemia-activated SMAD2/3 might be responsible for the enhancement of SGK1 and verified directly the interaction between SMAD3 and corresponding SMAD binding elements within SGK1 promoter. Taken together, our study confirmed the association between diabetes-related hyperglycemia and endometrial receptivity defects. Hyperglycemia-induced SGK1 has a tremendous role in this pathological process, rendering it as an attractive therapeutic target for diabetes-related reproductive disorders.

关键词： diabetes endometrial receptivity hyperglycemia serum/glucocorticoid-regulated kinase

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Neuronal nitric oxide synthase/reactive oxygen species pathway is involved in apoptosis and pyroptosis in epilepsy

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Neural Regeneration Research 2023年第6期18卷 1277-1285页

作者： Xiao-Xue Xu Rui-Xue Shi Yu Fu Jia-Lu Wang Xin Tong Shi-Qi Zhang Na Wang Mei-Xuan Li Yu Tong Wei Wang Miao He Bing-Yang Liu Gui-Lan Chen Feng Guo Department of Pharmaceutical Toxicology School of Pharmaceutical ScienceChina Medical UniversityShenyangLiaoning ProvinceChina Department of Neurology the First Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina key laboratory of Medical Electrophysiology Ministry of Education&Medical Electrophysiological Key Laboratory of Sichuan ProvinceInstitute of Cardiovascular ResearchSouthwest Medical UniversityLuzhouSichuan ProvinceChina Department of endocrinology and Metabolism the Fourth Affiliated Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of endocrinology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Dysfunction of neuronal nitric oxide synthase contributes to neurotoxicity,which triggers cell death in various neuropathological diseases,including epilepsy.Studies have shown that inhibition of neuronal nitric oxide synthase activity increases the epilepsy threshold,that is,has an anticonvulsant effect.However,the exact role and potential mechanism of neuronal nitric oxide synthase in seizures are still unclear.In this study,we performed RNA sequencing,functional enrichment analysis,and weighted gene coexpression network analysis of the hippocampus of tremor rats,a rat model of genetic epilepsy.We found damaged hippocampal mitochondria and abnormal succinate dehydrogenase level and Na+-K+-ATPase activity.In addition,we used a pilocarpine-induced N2a cell model to mimic epileptic injury.After application of neuronal nitric oxide synthase inhibitor 7-nitroindazole,changes in malondialdehyde,lactate dehydrogenase and superoxide dismutase,which are associated with oxidative stress,were reversed,and the increase in reactive oxygen species level was reversed by 7-nitroindazole or reactive oxygen species inhibitor N-acetylcysteine.Application of 7-nitroindazole or N-acetylcysteine downregulated the expression of caspase-3 and cytochrome c and reversed the apoptosis of epileptic cells.Furthermore,7-nitroindazole or N-acetylcysteine downregulated the abnormally high expression of NLRP3,gasdermin-D,interleukin-1βand interleukin-18.This indicated that 7-nitroindazole and N-acetylcysteine each reversed epileptic cell death.Taken together,our findings suggest that the neuronal nitric oxide synthase/reactive oxygen species pathway is involved in pyroptosis of epileptic cells,and inhibiting neuronal nitric oxide synthase activity or its induced oxidative stress may play a neuroprotective role in epilepsy.

关键词： apoptosis bioinformatics analysis cell death epilepsy nitric oxide synthase oxidative stress pyroptosis RNA sequencing Tremor rat weighted gene co-expression network analysis

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An adult patient of X-linked hypophosphatemia with joint manifestation mimicking spondylarthritis

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Chinese Medical Journal 2022年第10期135卷 1255-1257页

作者： Chuhan Wang Jiuliang Zha Hongbo Yang Yan Jiang Yan Zha Weibo Xia Department of Rheumatology and Clinical Immunology Chinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100730China National Clinical Research Center for Dermatologic and Immunologic Diseases(NCRC-DID) Ministry of Science and TechnologyBeijing 100730China State key laboratory of Complex Severe and Rare Diseases Peking Union Medical College Hospital(PUMCH)Beijing 100730China key laboratory of Rheumatology and Clinical Immunology Ministry of EducationBeijing 100730China Department of endocrinology and key laboratory of endocrinology National Health CommissionPeking Union Medical College Hospital(PUMCH)Peking Union Medical College and Chinese Academy of Medical SciencesBeijing 100730China

To the Editor:X-linked hypophosphatemia(XLH)is a rare hereditary metabolic disorder characterized by hypophos-phatemic rickets associated with phosphate wasting.[1]It is caused by a loss-of-function mutation in the PHEX(Phosphate regulating gene with Homology to Endopepti-dases located on the X chromosome)gene.[2]The clinical manifestations of the adult patient are usually not specific,often including bone pain,muscle weakness,and so on.

关键词： patient clinical adult

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Combination therapy with saxagliptin and vitamin D for the preservation ofβ-cell function in adult-onset type 1 diabetes:a multi-center,randomized,controlled trial

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Signal Transduction and Targeted Therapy 2023年第5期8卷 2354-2362页

作者： Xiang Yan Xia Li Bingwen Liu Jiaqi Huang Yufei Xiang Yuhang Hu Xiaohan Tang Ziwei Zhang Gan Huang Zhiguo Xie Houde Zhou Zhenqi Liu Xiangbing Wang Richard David Leslie Zhiguang Zhou National Clinical Research Center for Metabolic Diseases Key Laboratory of Diabetes Immunology(Central South University)Ministry of Educationand Department of Metabolism and EndocrinologyThe Second Xiangya Hospital of Central South UniversityChangshaHunanChina Division of endocrinology and Metabolism Department of MedicineUniversity of Virginia Health SystemCharlottesvilleVAUSA Division of endocrinology Metabolism and NutritionRutgers University-Robert Wood Johnson Medical SchoolNew BrunswickNJUSA Centre for Immunobiology Blizard InstituteQueen Mary University of LondonLondonUK

Disease modifying therapies aiming to preserveβ-cell function in patients with adult-onset autoimmune type 1 diabetes are lacking.Here,we conducted a multi-centre,randomized,controlled trial to assess theβ-cell preservation effects of saxagliptin alone and saxagliptin combined with vitamin D as adjunctive therapies in adult-onset autoimmune type 1 diabetes.In this 3-arm trial,301 participants were randomly assigned to a 24-month course of the conventional therapy(metformin with or without insulin)or adjunctive saxagliptin or adjunctive saxagliptin plus vitamin D to the conventional therapy.The primary endpoint was the change from baseline to 24 months in the fasting C-peptide.The secondary endpoints included the area under the concentration-time curve(AUC)for C-peptide level in a 2-h mixed-meal tolerance test,glycemic control,total daily insulin use and safety,respectively.The primary endpoint was not achieved in saxagliptin plus vitamin D group(P=0.18)and saxagliptin group(P=0.26).However,compared with the conventional therapy,2-h C-peptide AUC from 24 months to baseline decreased less with saxagliptin plus vitamin D(-276 pmol/L vs.-419 pmol/L;P=0.01),and not to the same degree with saxagliptin alone(-314 pmol/L;P=0.14).Notably,for participants with higher glutamic acid decarboxylase antibody(GADA)levels,the decline ofβ-cell function was much lower in saxagliptin plus vitamin D group than in the conventional therapy group(P=0.001).Insulin dose was significantly reduced in both active treatment groups than in the conventional therapy group despite all groups having similar glycemic control.In conclusion,the combination of saxagliptin and vitamin D preserves pancreaticβ-cell function in adult-onset autoimmune type 1 diabetes,an effect especially efficacious in individuals with higher GADA levels.Our results provide evidence for a novel adjunct to insulin and metformin as potential initial treatment for adult-onset type 1 diabetes.(ClinicalTrials.gov identifier:NCT02407899).

关键词： vitamin alone treatment

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Peripheral actions and direct central-local communications of melanocortin 4 receptor signaling

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Journal of Sport and Health Science 2023年第1期12卷 45-51页

作者： Lei Li Jinye Liang Cong Zhang Tiemin Liu Chao Zhang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine Shanghai East HospitalShanghai Key Laboratory of Signaling and Disease ResearchFrontier Science Center for Stem Cell ResearchSchool of Life Sciences and TechnologyTongji UniversityShanghai 200092China Department of Biology University of IowaIowa CityIA 52242USA State key laboratory of Genetic Engineering Department of Endocrinology and Metabolismand School of Life SciencesZhongshan HospitalFudan UniversityShanghai 200032China

Melanocortin 4 receptor(MC4R),the most important monogenetic cause of human metabolic disorders,has been of great interest to many researchers in the field of energy homeostasis and public health.Because MC4R is a vital pharmaceutical target for maintaining controllable appetite and body weight for professional athletes,previous studies have mainly focused on the central,rather than the peripheral,roles of MC4R.Thus,the local expression of MC4R and its behavioral regulation remain unclear.In an attempt to shed light on different directions for future studies of MC4R signaling,we review a series of recent and important studies exploring the peripheral functions of MC4R and the direct physiological interaction between peripheral organs and central MC4R neurons in this article.

关键词： Body weight Energy homeostasis GPCR Melanocortin-4 receptor

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Clinical and genetic findings in a Chinese family with VDR-associated hereditary vitamin D-resistant rickets

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Bone Research 2016年第1期4卷 48-54页

作者： Qianqian Pang Xuan Qi Yan Jiang Ou Wang Mei Li Xiaoping Xing Jin Dong Weibo Xia Department of endocrinology Key Laboratory of EndocrinologyThe Ministry of HealthPeking Union Medical College HospitalChinese Academy of Medical Sciences Department of endocrinology The First Affiliated Hospital of Shanxi Medical University

Hereditary vitamin D-resistant rickets （HVDRR） is a rare autosomal recessive disorder characterized by severe rickets, hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and elevated alkaline phosphatase. This disorder is caused by homogeneous or heterogeneous mutations affecting the function of the vitamin D receptor （VDR）, which lead to complete or partial target organ resistance to the action of 1,25- dihydroxy vitamin D~ A non-consanguineous family of Chinese Han origin with one affected individual demonstrating HVDRR was recruited, with the proband evaluated clinically, biochemically and radiographically. To identify the presence of mutations in the VDR gene, all the exons and exon-intron junctions of the VDR gene from all family members were amplified using PCR and sequenced. The proband showed rickets, progressive alopecia, hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and elevated alkaline phosphatase. She also suffered from epilepsy, which is rarely seen in patients with HVDRR. Direct sequencing analysis revealed a homozygous missense mutation c.122G 〉 A （p.C41Y） in the VDR gene of the proband, which is located in the first zinc finger of the DNA-binding domain. Both parents had a normal phenotype and were found to be heterozygous for this mutation. We report a Chinese Han family with one individual affected with HVDRR. A homozygous missense mutation c.122G 〉 A （p.C41Y） in the VDR gene was found to be responsible for the patient＇s syndrome. In contrast to the results of treatment of HVDRR in other patients, our patient responded well to a supplement of oral calcium and a low dose of calcitriol.

关键词： VDR Clinical and genetic findings in a Chinese family with VDR-associated hereditary vitamin D-resistant rickets

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FGF23 and Phosphate Wasting Disorders

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Bone Research 2013年第2期1卷 120-132页

作者： Xianglan Huang Yan Jiang Weibo Xia Department of endocrinology Key Laboratory of EndocrinologyMinistry of HealthPeking Union Medical College HospitalChinese Academy of Medical Sciences

A decade ago, only two hormones, parathyroid hormone and 1,25（OH）2D, were widely recognized to direct-ly affect phosphate homeostasis. Since the discovery of fibroblast growth factor 23 （FGF23） in 2000 （1）, our understanding of the mechanisms of phosphate homeostasis and of bone mineralization has grown exponentially. FGF23 is the link between intestine, bone, and kidney together in phosphate regulation. However, we still do not know the complex mechanism of phosphate homeostasis and bone mineralization. The physiological role of FGF23 is to regulate serum phosphate. Secreted mainly by osteocytes and osteo- blasts in the skeleton （2-3）, it modulates kidney handling of phosphate reabsorption and calcitriol produc-tion. Genetic and acquired abnormalities in FGF23 structure and metabolism cause conditions of either hyper-FGF23 or hypo-FGF23. Hyper-FGF23 is related to hypophosphatemia, while hypo-FGF23 is related to hyperphosphatemia. Both hyper-FGF23 and hypo-FGF23 are detrimentalto humans. In this review, we will discuss the vathovhvsiology of FGF23 and hvver-FGF23 related renal vhosvhate wasting disorders （4）.

关键词： FGF23 Klotho hypophosphatemic rickets XLH ADHR ARHR ENS OGD NF McCune Albrightsyndrome DMP-1 PHEX

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