The normal course of fat accretion in male rats from birth to 3 years is described. The relative amount of fat and relative size of fat pads increased steadily throughout life (except for a brief cessation in fat accretion at weaning), in a manner closely related to body weight and independent of age. Several new rat strains with extremes of growth or fat accretion, fed the same diet, were used to define and illustrate courses of fat accretion: very large and very small non-obese strains and a hereditarily obese rat. Rats of different known strains fed a variety of more refined diets show a course of fat growth different from that obtained with stock diets. Several types of obesity are discussed: insulin obesity, nutritional obesity, and hereditary obesity. Hereditary size and growth of the rat were readily (in a few generations) altered up or down, by consistently using the largest or the smallest 25% of the population for breeders. It is probable that the large increase in size of some laboratory rats over the past 40 years has been accomplished not only by improvement in stock diets and colony conditions, but also by selection for increased hereditary size.This report deals with the body fat of the rat both under conditions that would be called "normal" and conditions that justify classification as obesity. Relatively few data on "normal' fat accretion are available. We wiII reproduce some of these for comparison with our data.On the subject of obesity in laboratory animals the following should be considered. In mice Fenton (1,2) found that some strains become obese when fed high fat diets, while others do not. Mickelsen et al. (3) studied such nutritional obesity in rats and more recently found 2 indications that in this species also a genetic predisposition is a factor. Extreme obesity can be produced in rats, mice, monkeys and dogs by surgical interference with the intactness of the hypothalamus (4). In mice hypothalamic lesions with resulting obesity also foIIow injection of goldthioglucose (5,6). Continued injection of protamine insulin in rats and mice causes increased lipogenesis and fat accretion (7). In some species (mouse and man, but not rat) corticosteroids can lead to hyperinsulinism with resultant obesity (8). In every case it appears that obesity is made possible by an ZuckerTF, Zucker LM. Fat accretionand growthin the rat. J Nutr. 1963;80:6-19 increased caloric intake.Besides the above instances which depend on conditions imposed by the experimenter, there are also obesities related to a cause entirely within the animal. Four mutations in mice are known which lead to obesity. Two of these are due to single recessive genes -the gene ob, caIIed obese (9), and the gene ad, called adipose, which is at a different locus fromob (10). The yeIIow obese mouse depends on the dominant gene AY which is an allele of agouti (11). These 3 types of obesities with genetically different mechanisms presumably Received for publication December 17, 1962. 1This investigation was supported in part by researc...
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