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Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA
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Department of Pathology and Laboratory Medicine, Brown University, Providence, RI, USA
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, including cell lineage specification; basic mechanisms regulating functional differentiation gleaned from studies in the late gestation fetal rat; signaling pathways involved in the regulation of liver mass during rodent development; nonhuman primate studies
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Mup1 in murine hepatocyte cell line Because Mup1 mRNA expression and mTOR nutrient signaling were differentially altered in the livers of female offspring that experienced manipulation of placental mTOR during fetal development, we next evaluated
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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
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The State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, Sichuan, China
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Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
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unknown. GRB10 is highly expressed at the fetal stage in mouse liver, but its hepatic expression is almost completely suppressed in adult mice ( Wang et al . 2007 , Zhang et al . 2012 ). There is some evidence suggesting that GRB10 expression could be
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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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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offspring has been well investigated, further studies are needed to unravel the molecular and epigenetic mechanisms, which may be essential for the prevention and treatment of the fetal origins of metabolic disorders. The liver plays an important role in
Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang, China
Key Laboratory of Pollution Exposure and Health Intervention of Zhejiang Province, Hangzhou, China
Department of Endocrinology and Metabolism, Shanghai Fourth People's Hospital Affiliated to Tongji University School of Medicine, Shanghai, China
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supporting mammary gland development and energy requirements for fetal growth. Furthermore, our results showed that in the periparturient period, mice exhibited obvious glucose intolerance and insulin resistance compared to non-pregnancy, and the liver and
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ABSTRACT
Insulin is important for optimal fetal and neonatal growth and development. Its continued availability is due, in part, to ongoing islet cell growth within the pancreas. IGFs and IGF-binding proteins (IGFBPs) have been implicated as paracrine regulators of islet cell growth within the developing pancreas. The purpose of this study was to determine whether the intact rat pancreas expresses mRNAs for IGF-I, IGF-II and IGFBPs, and how these might change with development. Liver was studied as a control tissue. Pancreas and liver were taken from fetal rats at 20–22 days of gestation, from postnatal rats at 1–21 days and from adult animals, and mRNAs for IGFs-I and -II and IGFBPs-1 to -6 were detected by Northern blot hybridization. The amount of IGF-II mRNA was greatest in the liver and pancreas of the fetal rat, and declined in both tissues during the neonatal period. Conversely, IGF-I mRNA levels were low but detectable in fetal life, and rose to adult levels within 2 weeks of birth. Both IGFBP-1 and IGFBP-2 mRNAs were present in fetal rat liver, increasing in amount over the first week of life, and declining in the adult. However, within the pancreas, IGFBP-1 mRNA was undetectable and IGFBP-2 mRNA was very low in the fetus and neonate. Both IGFBP-1 and IGFBP-2 mRNAs transiently appeared in the pancreas between postnatal weeks 2 and 3 and declined in the adult. IGFBP-3 and IGFBP-4 mRNAs were detected in both the liver and pancreas throughout the developmental period studied. IGFBP-3 mRNA increased in amount immediately following birth, while the quantity of IGFBP-4 mRNA increased sharply in liver from postnatal day 21, but declined in the pancreas. mRNA for IGFBP-5 or -6 was undetectable in either tissue.
The results show that both IGF-I and IGF-II are expressed by rat pancreas from at least 20 days of gestation, the latter being predominant in fetal life and the former during postnatal development. In addition, at least four IGFBP mRNAs (IGFBPs-1, -2, -3 and -4) were expressed within the pancreas with distinct developmental patterns. IGFBP-3 and -4 were predominant in the fetal and neonatal periods, while increased expression of IGFBPs-1 and -2 occurred 2–3 weeks after birth. The ontogeny of IGFBP mRNA expression in pancreas differed from that in liver. The temporal and spatially specific pattern of IGF and IGFBP gene expression within the developing pancreas supports a paracrine role for the IGF—IGFBP axis during pancreatic development in the rat.
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Although growth hormone (GH) receptor (GHR) mRNA and protein are present in fetal tissues such as the lung, there is little evidence that GH mediates growth in the fetus. We have identified functional responses to GH in fetal rat lung epithelia and suggest a possible role for GHR in the developing lung. GHR mRNA in lung extracts was high before birth at day 16 of gestation (16f), decreased to low levels at day 22f but increased again after birth. At day 20f GHR mRNA levels were higher in lung than in liver, whereas growth hormone binding protein mRNA levels were approximately equal in lung and liver. Stimulation of primary cell cultures of day 19f lung epithelia with GH caused increased tyrosine phosphorylation in specific proteins, demonstrating functional GHR. Lung fibroblasts isolated at the same time did not respond to GH. Ligand and Northern blot analysis of the epithelial cultures revealed that GH stimulation increased insulin-like growth factor binding protein-2 (IGFBP-2) activity and mRNA. These experiments demonstrate the functional activity of GHR, specifically in fetal lung epithelium. We suggest that one role for GH in vivo may be indirectly to modify insulin-like growth factor activity in the developing fetal lung by increasing IGFBP-2.
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ABSTRACT
IGF-II in the rat is an embryonic/fetal growth factor. Transcription of its gene falls abruptly in the liver at about 18–20 days postnatally. In an attempt to elucidate the mechanisms controlling this phenomenon, we used Northern analysis to investigate the effect of corticosterone and thyroid hormones (tri-iodothyronine and tetra-iodothyronine) on hepatic IGF-II mRNA levels. The administration of either corticosterone or tri-iodothyronine to 8-day-old pups resulted in a significant decrease in IGF-II mRNA when the animals were examined on day 12 of life. Adrenalectomy, thyroidectomy or adrenalectomy combined with thyroidectomy were, however, without effect. Our results indicate that glucocorticoid and thyroid hormones are not the exclusive regulators of IGF-II gene transcription in the rat liver, but participate in this process, which appears to involve multifactorial interactions.
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ABSTRACT
Insulin-like growth factor-II (IGF-II) is thought to be a major growth factor during fetal and neonatal development. Levels of IGF-II mRNA fall dramatically in the liver - the major site of endocrine production - between 18 and 20 days post-natally. No information concerning the control of gene expression post-natally has hitherto been available. Using Northern blotting and in-situ hybridization, we show here that cortisone acetate rapidly extinguishes IGF-II mRNA expression in the neonatal rat liver. The effect at putative autocrine/paracrine locations such as skeletal muscle and choroid plexus is much less marked or absent. The repression by cortisone acetate is discussed in the light of the available IGF-II gene sequence.
