A B S T R A C T Cell size and number of parametrial fat pads were determined in Swiss mice made obese by means of a high-fat diet (40% lard w/w) given ad lib.This diet and a control were introduced to two groups of mothers during gestation and lactation, and sucklings were given the same diets as their mothers at weaning and throughout life.2-wk old mice suckled by mothers fed a high-fat diet have fatter parametrial pads. This difference is due solely to an increase in fat cell size. After weaning, until the 18th wk, the two groups differed with a striking fat cell enlargement seen in the obese group. Later on, whereas cell numbers did not change in the control group, a constant and uninterrupted increase in number is shown in those of obese mice until the 52nd wk. Hyperplasia was observed only in adults. When the highfat diet was introduced to adult rats it also triggered an increase in fat cell number.Three sites of fat pads were compared in both sexes at 32 wk of age. All sites increased in weight in the high-fat fed group. This was due to: hyperplasia in perirenal site, hypertrophy in epididymal and subcutaneous sites, and hyperplasia plus hypertrophy in the parametrial one. So, in each sex, adipose sites in the obese mice reacted to the diet in a site-specific way. It was concluded that the level of fat in a diet is involved in both formation and maturation of new fat cells and in the regulation of fat cell lipid content. The two processes may be separated or may act together according to the adipose tissue site.

1. Male and female mice, 4 weeks old, were fed ad lib. diets containing various amounts of lard (0-300 g/kg) or various kinds of dietary fats (300 g/kg) for 13 weeks. Fat cell number and size were determined by a histological method in three different adipose sites.2. Lard at 200 g/kg diet (43% energy from lipids) was sufficient to promote fat cell hyperplasia in the parametrial fat. Hyperplasia was also observed in the subcutaneous fat in males. The relationship between fat cell hypertrophy and the level of lard in the diet was dependent on site and sex.3. Obesity was produced whatever the kind of dietary fat eaten: lard, beef tallow, sunflower oil or soya-bean oil. In the subcutaneous depot of males given lard, fat cell size and number were increased, but only cell hypertrophy was observed in those given soya-bean oil. in the female groups of mice fat cell hyperplasia or hypertrophy or both were related to the adipose site but not the kind of dietary fat.4. It is concluded that dietary fats of different origin can induce obesity in mice. The effects on adipose tissue cellularity depend on the levels and kind of fat eaten, the adipose site and sex.

Forty-four institutionalized elderly subjects with body mass indexes (BMI) of either > or = 24 or < or = 21 participated in a 16-wk crossover study designed to determine the effects of low-dose zinc supplementation [306 mumol (20 mg)/d] on food intake, anthropometry, and biochemical and immunological indexes. Initial serum zinc concentrations were low in both groups and increased by approximately 20% after zinc supplementation. Zinc supplementation allowed a partial but significant restoration of serum thymulin activity and improved nutritional status (food intake and serum albumin and transthyretin concentrations) but had no effect on anthropometric indexes or serum apolipoproteins, except apolipoprotein CII and apolipoprotein CIII. After zinc supplementation, serum copper concentration decreased but there was no change in the ratio of low-density-lipoprotein cholesterol to high-density-lipoprotein cholesterol. Low-dose zinc supplementation allows restoration, at least partially, of nutritional and thymic status without the known disadvantages of high doses of zinc.

Milk intake of mouse pups was controlled by adjusting litter size at birth to four, nine or 20 pups. Litters of nine were considered as control groups. In adult animals many differences were seen among the three groups which had received the same diet ad libitum after weaning. Differences in body lipids largely accounted for the differences in body weight in both males and females. In parametrial adipose tissue, adipose cells, compared to those of controls, were enlarged and more numerous in mice from small litters, and smaller and less numerous in mice from large litters. After an overnight fast, the insulin response to glucose loading was highest in the obese group of mice, while it was absent in the lean group, suggesting permanent impairment in the secretion of insulin. Liver slices from animals which were bred in small litters incorporated more [U14C]-glucose into triglyceride moieties and cholesterol esters. Some of the metabolic changes in adipose tissue were related to cell size. With increasing litter size, glucose was incorporated into glycogen in muscle to a greater extent. Thus early feeding patterns induced permanent morphological, metabolic and hormonal changes in adults. Animals overfed in early life became obese and underfed animals remained lean when adults.