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Jenica H Kakadia Department of Biochemistry, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada
Children's Health Research Institute, London, Ontario, Canada

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Muhammad U Khalid Department of Biochemistry, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada

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Ilka U Heinemann Department of Biochemistry, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada

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Victor K Han Department of Biochemistry, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada
Children's Health Research Institute, London, Ontario, Canada
Department of Pediatrics, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada

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established, studies have implicated the insulin-like growth factor (IGF) system to play an important role ( Holmes et al. 1997 ). IGFs are critical for optimal fetal and placental growth and development, secreted by the fetal liver and placenta in pregnancy

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-23-0137
Volume/Issue:
Volume 72: Issue 3
Open access
Philip A Gruppuso Division of Pediatric Endocrinology, Rhode Island Hospital and Brown University, Providence, RI, USA
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA

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Jennifer A Sanders Division of Pediatric Endocrinology, Rhode Island Hospital and Brown University, Providence, RI, USA
Department of Pathology and Laboratory Medicine, Brown University, Providence, RI, USA

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factors including HNF1A, HNF4, HNF1B, and FOXA2 ( Kyrmizi et al. 2006 ). The fetal liver is the major site for hematopoiesis during embryonic development, with hematopoietic progenitors colonizing the liver bud soon after the cells invade the surrounding

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-15-0313
Volume/Issue:
Volume 56: Issue 3
Free access
Kjersti M Aagaard-Tillery
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Kevin Grove Division of Maternal-Fetal Medicine, Oregon National Primate Research Center, Division of Neonatology, Department of Obstetrics and Gynecology, University of Utah Health Sciences, Salt Lake City, 84158 Utah, USA

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Jacalyn Bishop Division of Maternal-Fetal Medicine, Oregon National Primate Research Center, Division of Neonatology, Department of Obstetrics and Gynecology, University of Utah Health Sciences, Salt Lake City, 84158 Utah, USA

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Xingrao Ke Division of Maternal-Fetal Medicine, Oregon National Primate Research Center, Division of Neonatology, Department of Obstetrics and Gynecology, University of Utah Health Sciences, Salt Lake City, 84158 Utah, USA

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Qi Fu Division of Maternal-Fetal Medicine, Oregon National Primate Research Center, Division of Neonatology, Department of Obstetrics and Gynecology, University of Utah Health Sciences, Salt Lake City, 84158 Utah, USA

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Robert McKnight Division of Maternal-Fetal Medicine, Oregon National Primate Research Center, Division of Neonatology, Department of Obstetrics and Gynecology, University of Utah Health Sciences, Salt Lake City, 84158 Utah, USA

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Robert H Lane Division of Maternal-Fetal Medicine, Oregon National Primate Research Center, Division of Neonatology, Department of Obstetrics and Gynecology, University of Utah Health Sciences, Salt Lake City, 84158 Utah, USA

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employed snap-frozen fetal liver from control diet ( n =9) or high-fat diet ( n =10)-fed dams for 1 or 2 years by the above-described criteria. For the purpose of Japanese macaque species-specific cDNA cloning, tissue from corralled (non

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-08-0025
Volume/Issue:
Volume 41: Issue 2
Free access
Liping Luo Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Wanxiang Jiang Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Hui Liu Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Jicheng Bu Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Ping Tang The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Chongyangzi Du The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Zhipeng Xu Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Hairong Luo Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Bilian Liu Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Bo Xiao Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China
The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China

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Zhiguang Zhou Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China

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Feng Liu Department of Metabolism and Endocrinology and the Metabolic Syndrome Research Center of Central South University, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China
Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA

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The growth factor receptor bound protein GRB10 is an imprinted gene product and a key negative regulator of the insulin, IGF1 and mTORC1 signaling pathways. GRB10 is highly expressed in mouse fetal liver but almost completely silenced in adult mice, suggesting a potential detrimental role of this protein in adult liver function. Here we show that the Grb10 gene could be reactivated in adult mouse liver by acute endoplasmic reticulum stress (ER stress) such as tunicamycin or a short-term high-fat diet (HFD) challenge, concurrently with increased unfolded protein response (UPR) and hepatosteatosis. Lipogenic gene expression and acute ER stress-induced hepatosteatosis were significantly suppressed in the liver of the liver-specific GRB10 knockout mice, uncovering a key role of Grb10 reactivation in acute ER stress-induced hepatic lipid dysregulation. Mechanically, acute ER stress induces Grb10 reactivation via an ATF4-mediated increase in Grb10 gene transcription. Our study demonstrates for the first time that the silenced Grb10 gene can be reactivated by acute ER stress and its reactivation plays an important role in the early development of hepatic steatosis.

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-18-0018
Volume/Issue:
Volume 60: Issue 4
Free access
Nora Martínez Laboratory of Reproduction and Metabolism, CEFYBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, 1121ABG Buenos Aires, Argentina

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Melisa Kurtz Laboratory of Reproduction and Metabolism, CEFYBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, 1121ABG Buenos Aires, Argentina

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Evangelina Capobianco Laboratory of Reproduction and Metabolism, CEFYBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, 1121ABG Buenos Aires, Argentina

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Romina Higa Laboratory of Reproduction and Metabolism, CEFYBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, 1121ABG Buenos Aires, Argentina

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Verónica White Laboratory of Reproduction and Metabolism, CEFYBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, 1121ABG Buenos Aires, Argentina

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Alicia Jawerbaum Laboratory of Reproduction and Metabolism, CEFYBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th floor, 1121ABG Buenos Aires, Argentina

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; Martinez et al . 2008 ). Besides, we have recently shown that lipid accumulation and peroxidation in fetal livers from diabetic rats at term gestation can be regulated by PPARα activators ( Martinez et al . 2011 ). Interestingly, we have also found that

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-10-0173
Volume/Issue:
Volume 47: Issue 1
Free access
Melisa Kurtz
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Evangelina Capobianco
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Nora Martinez
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Sabrina Lorena Roberti
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Edith Arany Laboratory of Reproduction and Metabolism, Department of Pathology, CEFyBO‐CONICET, School of Medicine, University of Buenos Aires, Paraguay 2155, 17th Floor, 1121 Buenos Aires, Argentina

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Alicia Jawerbaum
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. Nevertheless, maternal diets enriched with PPAR ligands did not increase the expression of ACO and CPT1, and did not lead to a decreased content of lipid species in the fetal heart. It is known that PPAR ligands decrease lipid content in the fetal liver

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-14-0063
Volume/Issue:
Volume 53: Issue 2
Free access
Ke-feng Yang Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China
Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China
Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China
Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China

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Wei Cai Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China
Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China
Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China
Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China

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Jia-li Xu Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China

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Wen Shi Clinical Nutrition Center, Department of Nutrition, Shanghai Institute for Pediatric Research, Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xin Hua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, People's Republic of China

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whole body energy balance and metabolism, and the development of fetal liver is a key target for altered maternal nutritional conditions ( Hyatt et al . 2008 , Ghouri et al . 2010 , Savage & Semple 2010 ). Many studies have shown an effect of

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-12-0046
Volume/Issue:
Volume 49: Issue 2
Free access
M H Abel
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D Baban
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S Lee
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H M Charlton
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P J O'Shaughnessy Department of Physiology, Institute of Comparative Medicine, Anatomy and Genetics, University of Oxford, Le Gros Clarke Building, Oxford OX1 3QX, UK

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decarboxylase 5.0 H19 H19 fetal liver mRNA 3.8 Igf1 Insulin-like growth factor 1 5.0 Pdgfc Platelet-derived growth factor C 3.7 Fah Fumarylacetoacetate hydrolase 4.9 Hsd17b11 Hydroxysteroid (17β) dehydrogenase 11 3.7 Mpzl2 Myelin protein zero-like 2 4.9 Cabc1

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-08-0107
Volume/Issue:
Volume 42: Issue 4
Open access
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H Roger Lijnen Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Campus Gasthuisberg, Onderwijs & Navorsing 1, Herestraat 49, Box 911, B-3000 Leuven, Belgium

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Ilse Scroyen Department of Cardiovascular Sciences, Center for Molecular and Vascular Biology, KU Leuven, Campus Gasthuisberg, Onderwijs & Navorsing 1, Herestraat 49, Box 911, B-3000 Leuven, Belgium

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.1007/BF01680633 ). Prewett M Huber J Li Y Santiago A O'Connor W King K Overholser J Hooper A Pytowski B Witte L 1999 Antivascular endothelial growth factor receptor (fetal liver kinase 1) monoclonal antibody inhibits tumor

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-12-0244
Volume/Issue:
Volume 50: Issue 3
Free access
Inagadapa J N Padmavathi Division of Endocrinology and Metabolism, National Centre for Laboratory Animal Sciences, National Institute of Nutrition, Jamai Osmania PO, Hyderabad 500 007, India

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Kalashikam Rajender Rao Division of Endocrinology and Metabolism, National Centre for Laboratory Animal Sciences, National Institute of Nutrition, Jamai Osmania PO, Hyderabad 500 007, India

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Manchala Raghunath Division of Endocrinology and Metabolism, National Centre for Laboratory Animal Sciences, National Institute of Nutrition, Jamai Osmania PO, Hyderabad 500 007, India

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:10.1016/0014-5793(96)01067-8 . Hostetler CE Kincaid RL 2004 Maternal selenium deficiency increases hydrogen peroxide and total lipid peroxides in porcine fetal liver . Biological Trace Element Research 97 43 – 56 . doi:10.1385/BTER:97

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-11-0010
Volume/Issue:
Volume 47: Issue 3
Free access