PMID- 26887388
OWN - NLM
STAT- MEDLINE
DCOM- 20171026
LR  - 20181113
IS  - 1479-6813 (Electronic)
IS  - 0952-5041 (Print)
IS  - 0952-5041 (Linking)
VI  - 56
IP  - 3
DP  - 2016 Apr
TI  - Regulation of liver development: implications for liver biology across the 
      lifespan.
PG  - R115-25
LID - 10.1530/JME-15-0313 [doi]
AB  - The liver serves a spectrum of essential metabolic and synthetic functions that 
      are required for the transition from fetal to postnatal life. Processes essential 
      to the attainment of adequate liver mass and function during fetal life include 
      cell lineage specification early in development, enzymic and other functional 
      modes of differentiation throughout gestation, and ongoing cell proliferation to 
      achieve adequate liver mass. Available data in laboratory rodents indicate that 
      the signaling networks governing these processes in the fetus differ from those 
      that can sustain liver function and mass in the adult. More specifically, fetal 
      hepatocytes may develop independent of key mitogenic signaling pathways, 
      including those involving the Erk mitogen-activated protein kinases MAPK1/3 and 
      the mechanistic target of rapamycin (mTOR). In addition, the fetal liver is 
      subject to environmental influences that, through epigenetic mechanisms, can have 
      sustained effects on function and, by extension, contribute to the developmental 
      origin of adult metabolic disease. Finally, the mitogen-independent phenotype of 
      rat fetal hepatocytes in late gestation makes these cells suitable for cell-based 
      therapy of liver injury. In the aggregate, studies on the mechanisms governing 
      fetal liver development have implications not only for the perinatal metabolic 
      transition but also for the prevention and treatment of liver disorders 
      throughout the lifespan.
CI  - (c) 2016 Society for Endocrinology.
FAU - Gruppuso, Philip A
AU  - Gruppuso PA
AD  - Division of Pediatric EndocrinologyRhode Island Hospital and Brown University, 
      Providence, RI, USA Department of Molecular BiologyCell Biology and Biochemistry, 
      Brown University, Providence, RI, USA Philip_Gruppuso@brown.edu.
FAU - Sanders, Jennifer A
AU  - Sanders JA
AD  - Division of Pediatric EndocrinologyRhode Island Hospital and Brown University, 
      Providence, RI, USA Department of Pathology and Laboratory MedicineBrown 
      University, Providence, RI, USA.
LA  - eng
GR  - R01 DK100301/DK/NIDDK NIH HHS/United States
GR  - R01 HD024455/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20160217
PL  - England
TA  - J Mol Endocrinol
JT  - Journal of molecular endocrinology
JID - 8902617
RN  - 0 (Insulin)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
SB  - IM
MH  - Animals
MH  - Cell Differentiation
MH  - Cell Lineage
MH  - Cell- and Tissue-Based Therapy
MH  - Female
MH  - Gene Expression Regulation, Developmental
MH  - Hepatocytes/cytology/metabolism
MH  - Humans
MH  - Insulin/genetics/metabolism
MH  - Intercellular Signaling Peptides and Proteins/genetics/metabolism
MH  - Liver/*embryology/growth & development/*physiology
MH  - Liver Diseases/etiology/metabolism/therapy
MH  - Maternal Nutritional Physiological Phenomena
MH  - *Organogenesis
MH  - Phenotype
MH  - Primates
MH  - Rats
MH  - Signal Transduction
PMC - PMC4882189
MID - NIHMS788176
OTO - NOTNLM
OT  - development
OT  - epigenetics
OT  - growth factors
OT  - insulin action
OT  - metabolism
COIS- Declaration of Interest The authors have no conflicts of interest to report.
EDAT- 2016/02/19 06:00
MHDA- 2017/10/27 06:00
PMCR- 2017/04/01
CRDT- 2016/02/19 06:00
PHST- 2016/02/11 00:00 [received]
PHST- 2016/02/16 00:00 [accepted]
PHST- 2016/02/19 06:00 [entrez]
PHST- 2016/02/19 06:00 [pubmed]
PHST- 2017/10/27 06:00 [medline]
PHST- 2017/04/01 00:00 [pmc-release]
AID - JME-15-0313 [pii]
AID - 10.1530/JME-15-0313 [doi]
PST - ppublish
SO  - J Mol Endocrinol. 2016 Apr;56(3):R115-25. doi: 10.1530/JME-15-0313. Epub 2016 Feb 
      17.