Abstract

Appetite control, pubarchal timing, and catch-up growth all seem to depend, to some extent, on body mass. Information regarding this variable may be supplied to the central nervous system (“ponderostat”) by a humoral radar system employing an insulin-like molecule or dependent substrate as a signal. The intensity of this signal would vary as a function of the organism's total adipose cell surface area, which, in turn, is a product of cell size and number. The geometry of a sphere (adipose cell) is such that surface area change per unit volume change increases as the radius of the sphere is reduced. Signal shifts then are maximal when cell volume is minimal. Divergence of the adipose signal from an age-appropriate norm could influence “ponderostat” activity and, in turn, brain centers mediating appetitive and various endocrine systems. Total caloric intake and the timing of this intake with respect to somatic maturity appear to affect adipose cell volume and number respectively. If shifts in adipose surface area provide a signal source regarding organismic mass, and if this surface area reflects the quantity and chronology of antecedent nutritional events, there are obvious implications for the role of nutrition during “critical periods” in the subsequent operation of the complex systems subserving appetite, somatic growth and sexual maturation.

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