ArticleiScience2019
Loss of Adipose Growth Hormone Receptor in Mice Enhances Local Fatty Acid Trapping and Impairs Brown Adipose Tissue Thermogenesis.
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Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16citing papers in PubMed
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16 citing papers in PubMed, 26 citations in OpenAlex.
- Hepatocyte Growth Hormone Receptor Ablation Is Associated With Aging Phenotypes and Hepatic Mitochondrial Dysfunction.Aging cell · 2026Article
- Deletion of hepatic growth hormone receptor contributes to the pathogenesis of lean MAFLD by elevating CD36.Life metabolism · 2026Article
- Adipose-Specific GHR Deletion Attenuates Brain Aging and Cognitive Decline in Aged Mice.Aging cell · 2026Article
- Integrating whole-genome resequencing data reveals adaptive selection signatures in sheep populations under extreme environments.BMC genomics · 2025Article
- Sexual dimorphism in the effects of maternal adipose tissue growth hormone receptor deficiency on offspring metabolic health.Biology of sex differences · 2024Article
- An Overview of Cardiovascular Risk in Pituitary Disorders.Medicina (Kaunas, Lithuania) · 2024Review
- Growth hormone receptor gene disruption.Vitamins and hormones · 2023Article
- Damaging missense variants inCell genomics · 2022Article
- Growth Hormone Improves Adipose Tissue Browning and Muscle Wasting in Mice with Chronic Kidney Disease-Associated Cachexia.International journal of molecular sciences · 2022Article
- Empagliflozin Treatment Attenuates Hepatic Steatosis by Promoting White Adipose Expansion in Obese TallyHo Mice.International journal of molecular sciences · 2022Article
- The Impact of Curcumin on Growth Performance, Growth-Related Gene Expression, Oxidative Stress, and Immunological Biomarkers in Broiler Chickens at Different Stocking Densities.Animals : an open access journal from MDPI · 2022Article
- Growth hormone receptor disrupts glucose homeostasis via promoting and stabilizing retinol binding protein 4.Theranostics · 2021Article
- Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish.Scientific reports · 2020Article
- Integrative Analyses of mRNA Expression Profile RevealFrontiers in genetics · 2020Article
- Tissue-Specific GHR Knockout Mice: An Updated Review.Frontiers in endocrinology · 2020Review
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Authors and funding
21 authors at 5 institutions in 2 countries.
Liyuan RanInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Xiaoshuang WangInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Ai MiInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Yanshuang LiuInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China.
Jin WuInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Haoan WangInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Meihua GuoInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Jie SunInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China; College of Integrative Medicine, Dalian Medical University, Dalian 116044, China.
Bo LiuInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Youwei LiInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Dan WangInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Rujiao JiangInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Ning WangInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Wenting GaoInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China.
Li ZengInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China.
Lin HuangDepartment of Pathophysiology, Dalian Medical University, Dalian 116044, China.
Xiaoli ChenDepartment of Food Science and Nutrition, University of Minnesota, Twin Cities, MN, USA.
Derek LeRoithDivision of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn Mount Sinai School of Medicine, New York 10029, USA.
Bin LiangKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Center for Excellence in Animal Evolution and Genetics, Chinese Academy of Sciences, Kunming 650223, China. Electronic address: liangb@mail.kiz.ac.cn.
Xin LiDepartment of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York 10010, USA; Department of Urology, New York University Langone Medical Center, New York 10016, USA; Perlmutter Cancer Institute, New York University Langone Medical Center, New York 10016, USA. Electronic address: xl15@nyu.edu.
Yingjie WuInstitute for Genome Engineered Animal Models of Human Diseases, Dalian Medical University, Dalian 116044, China; National Center of Genetically Engineered Animal Models for International Research, Dalian Medical University, Dalian 116044, China; Liaoning Provence Key Lab of Genome Engineered Animal Models, Dalian Medical University, Dalian 116044, China; College of Integrative Medicine, Dalian Medical University, Dalian 116044, China; Division of Endocrinology, Diabetes and Bone Disease, Department of Medicine, Icahn Mount Sinai School of Medicine, New York 10029, USA; Department of Basic Science and Craniofacial Biology, New York University College of Dentistry, New York 10010, USA. Electronic address: yingjiewu@dmu.edu.cn.
Dalian Medical University · CNNew York University · USChinese Academy of Sciences · CNIcahn School of Medicine at Mount Sinai · USUniversity of Minnesota · US
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth hormone (GH) binds to its receptor (growth hormone receptor [GHR]) to exert its pleiotropic effects on growth and metabolism. Disrupted GH/GHR actions not only fail growth but also are involved in many metabolic disorders, as shown in murine models with global or tissue-specific Ghr deficiency and clinical observations. Here we constructed an adipose-specific Ghr knockout mouse model Ad-GHRKO and studied the metabolic adaptability of the mice when stressed by high-fat diet (HFD) or cold. We found that disruption of adipose Ghr accelerated dietary obesity but protected the liver from ectopic adiposity through free fatty acid trapping. The heat-producing brown adipose tissue burning and white adipose tissue browning induced by cold were slowed in the absence of adipose Ghr but were recovered after prolonged cold acclimation. We conclude that at the expense of excessive subcutaneous fat accumulation and lower emergent cold tolerance, down-tuning adipose GHR signaling emulates a healthy obesity situation which has metabolic advantages against HFD.
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Cellular PhysiologyDiabetologyEndocrinologyPhysiology
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