Early postnatal oestradiol exposure causes insulin resistance and signs of inflammation in circulation and skeletal muscle.

@article{Alexanderson2009EarlyPO,
  title={Early postnatal oestradiol exposure causes insulin resistance and signs of inflammation in circulation and skeletal muscle.},
  author={Camilla Alexanderson and Elias Eriksson and Elisabet Stener-Victorin and Malin L{\"o}nn and Agneta B. Holm{\"a}ng},
  journal={The Journal of endocrinology},
  year={2009},
  volume={201 1},
  pages={
          49-58
        }
}
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… 
View on PubMed
joe.bioscientifica.com
19 Citations
Highly Influential Citations
1
Background Citations
10

19 Citations

Citation Type

Citation Type

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner.
TLDR
During postnatal life male and female Control rats have similar patterns of expression for genes involved in mitochondrial biogenesis and glucose transport, however, following uteroplacental insufficiency these gene expression patterns diverge in males and females during early postnatalLife, with MnSOD gene expression reduced in later postnatallife.
Metabolic and ovarian consequences of perinatal sex steroid programming
TLDR
The authors' observations of dyslipidemia and increased BMI and body weight in opposite-sex female twins are consistent with the results of animal experiments, indicating that the programming effects of early androgen exposure are of relevance also for humans.
Early Life Factors and Type 2 Diabetes Mellitus
TLDR
It might be possible to prevent or delay the risk for type 2 diabetes mellitus by improving pre- and/or postnatal factors, and the potential mechanisms that may underlie the developmental programming of T2DM are addressed.
Increase in endogenous estradiol in the progeny of obese rats is associated with precocious puberty and altered follicular development in adulthood
TLDR
It is demonstrated that maternal obesity in rats alters follicular development and induces follicular cysts generation in the adult offspring and a programmed failure in hepatic metabolism of estradiol is probably the cause of its increase.
The effect of testosterone on factors associated with diabetes, atherosclerosis and obesity.
TLDR
Although testosterone therapy showed a positive effect on some risk factors of obesity and its associated conditions, negative effects were also seen and further studies are needed to fully elucidate the above finding.
Differences in neonatal exposure to estradiol or testosterone on ovarian function and hormonal levels.
A single early postnatal estradiol injection affects morphology and gene expression of the ovary and parametrial adipose tissue in adult female rats
Neonatal exposure to estradiol valerate reprograms the rat ovary androgen receptor and anti-Müllerian hormone to a polycystic ovary phenotype.
Insulin Resistance, Type 1 and Type 2 Diabetes, and Related Complications: Current Status and Future Perspective
TLDR
Research and review papers that address a broad range of mechanisms associated with insulin resistance, type 1 diabetes, type 2 diabetes, and related cardiometabolic complications are discussed and show that nutritional, environmental, and physiological factors at prenatal age are correlated to the manifestation of insulin resistance and type 2 Diabetes in later stages of adult life.
Prenatal androgen treatment alters body composition and glucose homeostasis in male rats.
TLDR
It is concluded that transient exposure to androgen excess in utero increases body fat in adult male rats and only T males exhibit increased circulating glucose levels and subcutaneous fat suggesting that these changes may be mediated by aromatization of androgen to estrogen rather than by direct androgenic actions.
...
1
2
...

References

SHOWING 1-10 OF 102 REFERENCES
Increased maternal nutrition increases leptin expression in perirenal and subcutaneous adipose tissue in the postnatal lamb.
TLDR
It is demonstrated that exposure to increased prenatal nutrition increases leptin expression at 1 month of age in both PAT and SCAT, providing evidence that the nutritional environment before and immediately after birth can influence the development of adipose tissue in early postnatal life.
Retinol binding protein 4 expression in humans: relationship to insulin resistance, inflammation, and response to pioglitazone.
TLDR
RBP4 gene expression in humans is associated with inflammatory markers, but not with insulin resistance, suggesting a complex regulation of this novel adipokine.
Inflammatory status and insulin resistance
  • R. Grimble
  • Biology, Medicine
    Current opinion in clinical nutrition and metabolic care
  • 2002
TLDR
Evidence at present favours chronic inflammation as a trigger for chronic insulin insensitivity, rather than the reverse situation.
Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes
TLDR
It is shown that expression of retinol binding protein-4 (RBP4) is elevated in adipose tissue of adipose-Glut4-/- mice and RBP4 is an adipocyte-derived ‘signal’ that may contribute to the pathogenesis of type 2 diabetes.
Monocyte chemotactic protein-1 is a potential player in the negative cross-talk between adipose tissue and skeletal muscle.
TLDR
The data show that adipocytes secrete various adipokines that may be involved in the negative cross-talk between adipose tissue and skeletal muscle assigning a completely novel important role to MCP-1 besides inflammation.
Acylation-stimulating protein precursor proteins in adipose tissue in human obesity.
Retinol-Binding Protein 4 in Human Obesity
TLDR
The findings point to profound differences between rodents and humans in the regulation of adipose or circulating RBP4 and challenge the notion that glucose uptake by adipocytes has a dominant role in theregulation ofRBP4.
Skeletal muscle insulin resistance: role of inflammatory cytokines and reactive oxygen species.
TLDR
Accumulating evidence indicates that low-grade chronic inflammation and oxidative stress play fundamental roles in the development of insulin resistance, and inflammatory cytokines likely contribute to the link between inflammation, oxidative stress, and skeletal muscle insulin resistance.
Postnatal Programming of Glucocorticoid Metabolism in Rats Modulates High-Fat Diet–Induced Regulation of Visceral Adipose Tissue Glucocorticoid Exposure and Sensitivity and Adiponectin and Proinflammatory Adipokines Gene Expression in Adulthood
TLDR
The data show for the first time that postnatal manipulation programs high-fat diet–induced upregulation of MAT glucocorticoid exposure, sensitivity, and inflammatory status and therefore reveal the pivotal role of the environment during the perinatal period on the development of diet-induced adipose tissue dysregulation in adulthood.
Neonatal hypothalamic androgenization in the female rat induces changes in peripheral insulin sensitivity and adiposity function at adulthood.
TLDR
This study strongly supports the hypothesis that development of insulin resistance seems to be dependent on early hyperandrogenicity.
...
1
2
3
4
5
...