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Abstract
The hypothesis that adipocyte size and number influence feeding behavior, via as yet
unidentified signals to the CNS, is reviewed. The proposal is made that, due to several
metabolic alterations which favor lipid deposition, the genetically obese Zucker rat
(fafa) may be an appropriate model in which to study feeding-adipose tissue relationships.
Data from several studies are presented demonstrating that the developing male Zucker
fatty rat displays hyperphagia during the growth period which reaches a peak, or "break
point," and then declines such that intake of fatty and lean rats becomes comparable
at approximately 20 weeks of age. Beyond week 20, cycles of hyperphagia of several
weeks' duration can be detected in fatty rats. The above feeding changes are related
to data showing that on a laboratory chow-type diet, adipocytes approach maximal size
at 15-16 weeks in the fatty rat, while accelerated proliferation of adipocytes takes
place following week 20. During growth, responding for food in an operant task by
fatty rats varies in accord with the pattern of hyperphagia. Further studies in the
fatty rat show that the duration and magnitude of developmental hyperphagia can be
altered by manipulating the caloric density and macronutrient content of the diet,
with fat containing diets leading to the earliest break point of developmental hyperphagia.
Some theoretical problems with the notion of adipose tissue feedback control of feeding
behavior are discussed.