PMID- 30778335
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200225
IS  - 1664-2392 (Print)
IS  - 1664-2392 (Electronic)
IS  - 1664-2392 (Linking)
VI  - 10
DP  - 2019
TI  - Age-Characteristic Changes of Glucose Metabolism, Pancreatic Morphology and 
      Function in Male Offspring Rats Induced by Prenatal Ethanol Exposure.
PG  - 34
LID - 10.3389/fendo.2019.00034 [doi]
LID - 34
AB  - Intrauterine growth restricted offspring suffer from abnormal glucose homeostasis 
      and beta cell dysfunction. In this study, we observed the dynamic changes of glucose 
      metabolic phenotype, pancreatic morphology, and insulin synthesis in prenatal 
      ethanol exposure (PEE) male offspring rats, and to explore the potential 
      intrauterine programming mechanism of the glucocorticoid-insulin-like growth 
      factor 1 (GC-IGF1) axis. Ethanol (4 g/kg.d) was administered through oral gavage 
      during gestational day (GD) 9-20. Serum glucose and insulin levels, pancreatic beta 
      cell mass, and expression of glucocorticoid receptor (GR), IGF1 and insulin were 
      determined on GD20, postnatal week (PW) 6, PW12 with/without chronic stress (CS), 
      and PW24, respectively. Both intraperitoneal glucose and insulin tolerance tests 
      were conducted at PW12 and PW24. Results showed that the serum glucose and 
      insulin levels as well as pancreatic beta cell mass were reduced on GD20 in PEE 
      males compared with the controls, while pancreatic GR expression was enhanced but 
      IGF1 and INS1/2 expression were suppressed. After birth, compared with the 
      controls, beta cell mass in the PEE males was initially decreased at PW6 and 
      gradually recovered from PW12 to PW24, which was accompanied by increased serum 
      glucose/insulin levels and insulin resistance index (IRI) at PW6 and decreased 
      serum glucose contents at PW12, as well as unchanged serum glucose/insulin 
      concentrations at PW24. In addition, both improved glucose tolerance and impaired 
      insulin sensitivity of the PEE males at PW12 were inversed at PW24. Moreover, at 
      PW6 and PW12, pancreatic GR expression in the PEE group was decreased, while IGF1 
      expression was reversely increased, resulting in a compensatory increase of 
      insulin expression. Moreover, CS induced pancreatic GR activation and inhibited 
      IGF1 expression, resulting in impaired insulin biosynthesis. Conclusively, the 
      above changes were associated with age and the intrauterine programming 
      alteration of GC-IGF1 axis may be involved in prenatal and postnatal pancreatic 
      dysplasia and impaired insulin biosynthesis in PEE male offspring.
FAU - Xiao, Di
AU  - Xiao D
AD  - Department of Pharmacology, School of Basic Medical Sciences of Wuhan University, 
      Wuhan, China.
FAU - Kou, Hao
AU  - Kou H
AD  - Department of Pharmacy, Zhongnan Hospital, Wuhan University, Wuhan, China.
AD  - Hubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan, 
      China.
FAU - Gui, Shuxia
AU  - Gui S
AD  - Department of Pharmacology, School of Basic Medical Sciences of Wuhan University, 
      Wuhan, China.
FAU - Ji, Zhenyu
AU  - Ji Z
AD  - Department of Pharmacology, School of Basic Medical Sciences of Wuhan University, 
      Wuhan, China.
FAU - Guo, Yu
AU  - Guo Y
AD  - Department of Pharmacology, School of Basic Medical Sciences of Wuhan University, 
      Wuhan, China.
AD  - Hubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan, 
      China.
FAU - Wu, Yin
AU  - Wu Y
AD  - Department of Pharmacology, School of Basic Medical Sciences of Wuhan University, 
      Wuhan, China.
AD  - Hubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan, 
      China.
FAU - Wang, Hui
AU  - Wang H
AD  - Department of Pharmacology, School of Basic Medical Sciences of Wuhan University, 
      Wuhan, China.
AD  - Hubei Provincial Key Laboratory of Developmentally Originated Diseases, Wuhan, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20190204
PL  - Switzerland
TA  - Front Endocrinol (Lausanne)
JT  - Frontiers in endocrinology
JID - 101555782
PMC - PMC6369175
OTO - NOTNLM
OT  - glucocorticoids-insulin-like growth factor 1 axis
OT  - insulin expression
OT  - intrauterine growth restriction
OT  - pancreatic beta cell development
OT  - prenatal ethanol exposure
EDAT- 2019/02/20 06:00
MHDA- 2019/02/20 06:01
PMCR- 2019/01/01
CRDT- 2019/02/20 06:00
PHST- 2018/08/09 00:00 [received]
PHST- 2019/01/16 00:00 [accepted]
PHST- 2019/02/20 06:00 [entrez]
PHST- 2019/02/20 06:00 [pubmed]
PHST- 2019/02/20 06:01 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fendo.2019.00034 [doi]
PST - epublish
SO  - Front Endocrinol (Lausanne). 2019 Feb 4;10:34. doi: 10.3389/fendo.2019.00034. 
      eCollection 2019.