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Am J Physiol Endocrinol Metab (April 23, 2002). doi:10.1152/ajpendo.00439.2001
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Articles in PresS, published online ahead of print April 23, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00439.2001
Submitted on October 1, 2001
Accepted on April 12, 2002

Monosodium-glutamate lesions decrease body mass of suckling-age rats by attenuating the circadian decreases of energy expenditure

Corinna Schoelch1*, Thomas Hubschle1, Ingrid Schmidt1, and Barbara Nuesslein-Hildesheim1

1 Abt. Schmidt, Max-Planck-Institut fur Physiologsche und Klinische Forschung, Bad Nauheim, Hessen, Germany

* To whom correspondence should be addressed. E-mail: corinna.schoelch{at}aventis.com.

Suckling-age rats display endogenous circadian rhythmicity of metabolic rate (MR) with energy-saving, torpor-like decreases which are sympathetically controlled and suppressed by leptin treatment. We investigated whether neonatal monosodium glutamate (MSG) treatment, known to cause arcuate nucleus (ARC) damage and adult-age obesity, alters energy balance in the first two postnatal weeks. Continuously recorded MR and core temperatures (Tc) show that MSG treatment disinhibits the periodic, sympathetically controlled, energy-saving drops of Tc and MR. Increased energy expenditure, thus, explains reduced body fat at normal lean body mass found in MSG-treated pups artificially nourished identically to controls. In MSG-treated mother-reared pups, lean body mass is additionally reduced, suggesting that MSG also reduces suckling. Plasma leptin levels are similar in controls and MSG-treated pups but higher per unit fat mass in the latter. We conclude that the post-weaning development of MSG-obesity and depressed thermogenesis are preceded by an early phase of increased energy expenditure with decreased fat deposition during suckling-age, and hypothesize cell damage in the ARC to be involved in both.




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