Different levels of food restriction have opposite effects on adipocyte cellularity and lipoprotein-lipase activity in obese rats.

The effects of several levels of chronic energy restriction on epididymal and perirenal adipose tissue cellularity and lipoprotein lipase activity, serum glucose and insulin and hepatic enzyme activities were studied in lean Fa/- and genetically obese fafa rats. The restricted rats were compared to rats fed ad libitum 24/24h or 8/24h. Restricting time of feeding was associated with increases in fat cell number in the lean, increases in perirenal adipose tissue fat cell size and serum insulin in the obese and increases in lipoprotein lipase activity in both phenotypes. Mild food restriction (-25%) had similar effects in the obese: perirenal adipose tissue fat cell size and serum insulin levels were even higher but fat cell hyperplasia was reduced. Restriction by 50% normalized lipoprotein lipase activity and markedly reduced fat cell size in the lean; in the obese, lipoprotein lipase activity and insulin levels were similar to or lower than those of the corresponding ad libitum 24/24h group but fat cell hypertrophy was not particularly affected. Restriction by 75% in the obese prevented adipocyte hyperplasia. Furthermore, lipoprotein lipase activity in adipose tissue was normalized, serum insulin and lipids being within normal limits. However, these animals had large adipocytes and were still fat.

Serum lipoprotein and apolipoprotein profiles of the genetically obese ob/ob mouse.

The lipid transport system of 3-month-old male C57BL/6J obese (ob/ob) mice was investigated. Serum lipoproteins were separated by density gradient ultracentrifugation and characterized by their chemical and electrophoretic properties as well as their relative apolipoprotein contents, defined according to molecular weight and charge. Obese, ob/ob mice exhibited a marked hyperlipoproteinemia resulting from large increases in low-density lipoproteins (LDL, d 1.021-1.058 g/ml) and high-density lipoproteins (HDL, d 1.058-1.137 g/ml), particularly, the HDL2 subclass (d 1.058-1.109 g/ml). This increase in lipoproteins was entirely responsible for their hypercholesterolemia and hyperphospholipidemia. By contrast, these obese mice had a net decrease in very-low-density lipoproteins (VLDL, d less than 1.016 g/ml) and intermediate-density lipoproteins (IDL, d 1.016-1.021 g/ml), which accounted for their moderate hypotriglyceridemia. The chemical composition of heterogeneous light LDL (d 1.021-1.040 g/ml and dense LDL (d 1.040-1.058 g/ml) overlapped by HDL-like particles was highly modified. These modifications consisted of increases in the percentages of cholesteryl ester and phospholipid and decreases in that of triacylglycerol. There were also marked changes in the relative values of the apolipoproteins of VLDL, but principally, IDL and LDL. IDL and light LDL were poorer in apolipoproteins BH (Mr 340,000-320,000) and eventually in apolipoprotein BL (Mr 220,000-200,000) and enriched in apolipoproteins E (Mr 37,000-35,000) and C-A-II (Mr approximately equal to 12,000). A similar and very significant change occurred in VLDL for both the apolipoproteins BL and C-A-II. Dense LDL, mainly poorer in apolipoprotein BH and enriched in apolipoprotein A-I (Mr 28,000-27,000), closely resembled HDL2 in all the groups, and were enriched in apolipoproteins C-A-II in only the obese mice. We suggest that ob/ob mice are probably protected against atheromata because of the low VLDL and IDL levels, and the increase in HDL2.

Dietary-induced obesity: effect of dietary fats on adipose tissue cellularity in mice.

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.

Effect of early postnatal under- and overnutrition on the development of IgA plasma cells in mouse gut.

Development of gut IgA plasma cells was studied in early postnatal under- and overnutrition. Female mice were allowed to suckle in litters of 4, 9 or 20 pups to produce a state of obesity (litter of 4) or protein-energy malnutrition (litters of 20). Litters of nine were considered as control groups. Overfeeding during the suckling period did not change the development and the number of IgA plasma cells of the small intestine. By contrast, the weanling protein-energy malnourished mice had shorter intestines, reduced weight of gut mucosal, muscular and serosal layers and reduced length of villi. However, protein-energy malnutrition, when limited to the suckling period, had no marked effect on the development of IgA plasma cells. A diminished number of these cells was observed only when a more severe and prolonged state of malnutrition was induced.

Adipose-tissue lipoprotein lipase activity and cellularity in the genetically obese Zucker rat (fa-fa).

The lipoprotein lipase activity per adipocyte was increased in the genetically obese rat (fa/fa). However, there was no difference between obese and lean animals when the enzyme activities were related to adipocyte surface area. The possible implications of the findings are discussed.