Plasma Levels of Insulin-like Growth Factor-I Are Reduced at One Week of Age in Monosodium L-Glutamate-Treated Mice

Administration of monosodium L-glutamate (MSG) to neonatal mice produces a hypothalamic syndrome consisting of stunted growth and later development of obesity. We assayed plasma insulin (IRI), thyroxine (T4) and insulin-like growth factor-I (IGF-I) to investigate their roles in the growth of the mic...

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Bibliographic Details
Published in:Endocrine Journal 1993, Vol.40(4), pp.461-465
Main Authors: YAMAMOTO, TORU, MATSUO, SATOSHI, UESHIMA, YASUO, INOUE, FUMIO, KINUGASA, AKIHIKO, SAWADA, TADASHI
Format: Article
Language:English
Subjects:
Age Factors
Animals
Animals, Newborn
Biological and medical sciences
Growth Disorders - chemically induced
Hypothalamus - drug effects
IGF-I
Insulin - blood
Insulin-Like Growth Factor I - metabolism
Male
Medical sciences
Metabolic diseases
Mice
Mice, Inbred ICR
MSG-treated mice
Obesity
Obesity - chemically induced
Sodium Glutamate - administration & dosage
Sodium Glutamate - toxicity
Thyroxine - blood
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Summary:Administration of monosodium L-glutamate (MSG) to neonatal mice produces a hypothalamic syndrome consisting of stunted growth and later development of obesity. We assayed plasma insulin (IRI), thyroxine (T4) and insulin-like growth factor-I (IGF-I) to investigate their roles in the growth of the mice. Two mg/g body weight of MSG was injected into newborn male mice daily for five successive days after birth. Plasma IRI levels were increased on and after 8 weeks of age in MSG-treated mice. There was no significant difference between the plasma T4 levels in MSG-treated mice and those in controls at any age studied. In contrast to this, plasma IGF-I levels in MSG-treated mice were reduced at one week and after. These results suggest that a decreased plasma IGF-I level contributes to the retarded linear growth which develops soon after the administration of MSG, and hyperinsulinemia contributes to the later development of obesity in MSG-treated mice.
ISSN:0918-8959
1348-4540
DOI:10.1507/endocrj.40.461