PMID- 19193715
OWN - NLM
STAT- MEDLINE
DCOM- 20090723
LR  - 20131121
IS  - 1479-6805 (Electronic)
IS  - 0022-0795 (Linking)
VI  - 201
IP  - 1
DP  - 2009 Apr
TI  - Early postnatal oestradiol exposure causes insulin resistance and signs of 
      inflammation in circulation and skeletal muscle.
PG  - 49-58
LID - 10.1677/JOE-08-0534 [doi]
AB  - Early postnatal events can predispose to metabolic and endocrine disease in 
      adulthood. In this study, we evaluated the programming effects of a single early 
      postnatal oestradiol injection on insulin sensitivity in adult female rats. We 
      also assessed the expression of genes involved in inflammation and glucose 
      metabolism in skeletal muscle and adipose tissue and analysed circulating 
      inflammation markers as possible mediators of insulin resistance. Neonatal 
      oestradiol exposure reduced insulin sensitivity and increased plasma levels of 
      monocyte chemoattractant protein-1 (MCP-1) and soluble intercellular adhesion 
      molecule-1. In skeletal muscle, oestradiol increased the expression of genes 
      encoding complement component 3 (C3), Mcp-1, retinol binding protein-4 (Rbp4) and 
      transforming growth factor beta1 (Tgfbeta1). C3 and MCP-1 are both related to 
      insulin resistance, and C3, MCP-1 and TGFbeta1 are also involved in inflammation. 
      Expression of genes encoding glucose transporter-4 (Glut 4), carnitine-palmitoyl 
      transferase 1b (Cpt1b), peroxisome proliferator-activated receptor delta (Ppard) 
      and uncoupling protein 3 (Ucp3), which are connected to glucose uptake, lipid 
      oxidation, and energy uncoupling, was down regulated. Expression of several 
      inflammatory genes in skeletal muscle correlated negatively with whole-body 
      insulin sensitivity. In s.c. inguinal adipose tissue, expression of Tgfbeta1, 
      Ppard and C3 was decreased, while expression of Rbp4 and Cpt1b was increased. 
      Inguinal adipose tissue weight was increased but adipocyte size was unaltered, 
      suggesting an increased number of adipocytes. We suggest that early neonatal 
      oestrogen exposure may reduce insulin sensitivity by inducing chronic, low-grade 
      systemic and skeletal muscle inflammation and disturbances of glucose and lipid 
      metabolism in skeletal muscle in adulthood.
FAU - Alexanderson, Camilla
AU  - Alexanderson C
AD  - Department of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska 
      Academy, Goteborg University, Goteborg, Sweden.
FAU - Eriksson, Elias
AU  - Eriksson E
FAU - Stener-Victorin, Elisabet
AU  - Stener-Victorin E
FAU - Lonn, Malin
AU  - Lonn M
FAU - Holmang, Agneta
AU  - Holmang A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090204
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 4TI98Z838E (Estradiol)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adipose Tissue/drug effects/metabolism/pathology
MH  - Age Factors
MH  - Animals
MH  - Animals, Newborn
MH  - Blood Circulation/*drug effects/immunology
MH  - Body Weight/drug effects
MH  - Estradiol/*adverse effects
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Glucose/metabolism
MH  - Inflammation/*chemically induced
MH  - *Insulin Resistance
MH  - Lipid Metabolism/drug effects
MH  - Muscle, Skeletal/*drug effects/immunology/metabolism/pathology
MH  - Rats
MH  - Rats, Wistar
MH  - Vaginal Smears
EDAT- 2009/02/06 09:00
MHDA- 2009/07/25 09:00
CRDT- 2009/02/06 09:00
PHST- 2009/02/06 09:00 [entrez]
PHST- 2009/02/06 09:00 [pubmed]
PHST- 2009/07/25 09:00 [medline]
AID - JOE-08-0534 [pii]
AID - 10.1677/JOE-08-0534 [doi]
PST - ppublish
SO  - J Endocrinol. 2009 Apr;201(1):49-58. doi: 10.1677/JOE-08-0534. Epub 2009 Feb 4.