By G.D. Aurbach (Eds.)

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The glucose concentration in rats with EXPERIMENTAL OBESITY 19 hypothalamic obesity may be low initially (Smith and Campfield, 1986). Changes in glucose may be a signal for initiation of a meal. Campfield et al. (1985) have shown that a 15%drop in glucose followed by a rise toward baseline is the signal for a meal in more than 60% of these transitions in glucose. In rats with VMH lesions the onset of meals may be delayed, but when they occur they are larger than in control rats. Changing blood glucose levels produce reciprocal changes in the afferent vagal firing rate (Niijima, 1983a,b, 1984a,b, 1986).

1984). , 1986a1, creating questions about the suggested relationship be- EXPERIMENTAL OBESITY 37 tween this enzyme and the hyperphagia of these rats (see Section III,D,1). Adrenalectomy may not restore body composition and serum insulin concentration precisely to normal. This may indicate the irreversibility of some of the changes. This is best illustrated by consideration of serum insulin, which falls to low levels after adrenalectomy but still remains somewhat elevated compared to the lean animals.

The hypothalarnohypophysialladrenalaxis is of central importance in controlling the development of the genetic obesities, although neither the precise mechanism nor the primary hormone responsible for this control has yet been clarified. In the mouse genotypes clear evidence of the excessive secretion of corticosterone has been reported by a number of laboratories, and the progressive rise in serum corticosterone has been related to the diminishing insulin sensitivity (see Bray and York, 1979).

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Advances in Research and Applications by G.D. Aurbach (Eds.)

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