Low doses of insulin-like growth factor I improve insulin resistance, lipid metabolism, and oxidative damage in aging rats.

@article{GarcaFernndez2008LowDO,
  title={Low doses of insulin-like growth factor I improve insulin resistance, lipid metabolism, and oxidative damage in aging rats.},
  author={Mar{\'i}a Inmaculada Garc{\'i}a-Fern{\'a}ndez and Gloria Delgado and Juan Enrique Puche and S. Gonz{\'a}lez-bar{\'o}n and Inma Castilla Cort{\'a}zar},
  journal={Endocrinology},
  year={2008},
  volume={149 5},
  pages={
          2433-42
        }
}
GH and IGF-I concentrations decline with age. Age-related changes appear to be linked to decreases in the anabolic hormones, GH and IGF-I. The aim of this study was to investigate the antioxidant, anabolic, and metabolic effects of the IGF-I replacement therapy, at low doses, in aging rats. Three experimental groups were included in this protocol: young healthy controls (17 wk old); untreated old (O) rats (103 wk old); and aging rats (103 wk old) treated with IGF-I during 1 month (2.25 microg… 
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Low doses of insulin-like growth factor-I induce mitochondrial protection in aging rats.
TLDR
Results show that the cytoprotective effect of IGF-I is closely related to a mitochondrial protection, leading to reduce free radical production, oxidative damage, and apoptosis, and to increased ATP production.
Liver mitochondrial dysfunction is reverted by insulin-like growth factor II (IGF-II) in aging rats
TLDR
The cytoprotective effects of IGF-II are related to mitochondrial protection leading to increased ATP production reducing free radical generation, oxidative damage and apoptosis.
Hepatoprotection and neuroprotection induced by low doses of IGF-II in aging rats
TLDR
It is demonstrated that low doses of IGF-II induce hepatoprotective, neuroprotective and metabolic effects, improving mitochondrial function, without affecting testosterone and IGF-I levels.
Insulin-Like Growth Factor I (IGF-I); cytoprotective effects, idea of replacement therapy in the healthy elderly subjects
TLDR
The general functional properties of IGF-I and implications of its possible use as a replacement to the healthy elderly subjects are discussed and its downfalls and new perceptions are emphasis.
Human conditions of insulin-like growth factor-I (IGF-I) deficiency
TLDR
The aim of this review is to summarize the increasing list of roles of IGF-I, both in physiological and pathological conditions, underlying that its potential therapeutical options seem to be limited to those proven states of local or systemic IGF- I deficiency as a replacement treatment, rather than increasing its level upper the normal range.
Partial IGF-1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy.
TLDR
IGF-1 deficiency is responsible for increased brain oxidative damage, edema, and impaired learning and memory capabilities which are rescued by IGF-1 replacement therapy, which improved all these alterations.
Altered liver expression of genes involved in lipid and glucose metabolism in mice with partial IGF-1 deficiency: an experimental approach to metabolic syndrome
TLDR
The mere partial IGF-1 deficiency is responsible for the reduction in the expression of genes involved in glucose and lipid metabolism, resulting in dyslipidemia and hyperglycemia, which may seriously contribute to the establishment of MetS.
Insulin-like growth factor-1 short-period therapy improves cardiomyopathy stimulating cardiac progenitor cells survival in obese mice.
An experimental model of partial insulin-like growth factor-1 deficiency in mice
TLDR
Evidence is provided for considering heterozygous Igf-1+/− mice as a suitable experimental model, from early stages, to get more insight into the mechanisms of the beneficial actions induced by IGF-1 replacement therapy.
Reviews of Physiology, Biochemistry and Pharmacology Vol. 170
TLDR
The purpose is to establish if IUGR could be considered as a novel condition of IGF-1 deficiency and if its treatment with low doses of IGF -1 could be a suitable therapeutic strategy.
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