Adipose tissue was dissected completely from 14 polar bears (Ursus maritimus) killed in the southeastern Northwest Territories and northern Manitoba in November 1988. Mean adipocyte volume, collagen content, the activities of hexokinase and phosphofructokinase, and the fatty acid composition of the triacylglycerols were measured in samples of adipose tissue from several superficial, intra-abdominal, and inter-muscular depots homologous to those of other terrestrial mammals. The total adipocyte complement was calculated from the mass of each depot and its site-specific adipocyte volume. All the adipose depots found in other Carnivora and most other mammals are present in polar bears. The superficial layer of adipose tissue in polar bears arises from thickening and lateral expansion of depots that are discrete in most other mammals. All depots except the cardiac adipose tissue expand with increasing fatness, but the superficial depots expand faster than any of the internal depots, almost entirely by adipocyte proliferation. The gross anatomy of the superficial adipose tissue is determined mainly by the effect of body mass on the ratio of the surface area of the body to its volume. The superficial depots account for a greater proportion of the total adipose tissue in larger bears and in fatter specimens. The total adipocyte complement is about two to three times greater than that predicted from allometric equations relating adipocyte complement to body mass in non-arctic carnivores. The fatty acid composition of the triacylglycerols in the adipose tissue of polar bears is similar to that of the milk and the serum, but there were fewer long-chain polyunsaturated fatty acids than in their principal prey, ringed seals. There was no clearcut biochemical evidence for the existence of a thermal gradient between the inner and outer sides of the superficial adipose tissue. We conclude that in spite of their arctic habitat, neither the gross distribution of adipose tissue of polar bears nor its biochemical properties are adapted to thermal insulation. The enlarged superficial layer of adipose tissue is primarily an adaptation to increased energy storage.
In a sample of 31 sedentary, ad libitum-fed monkeys, most specimens had less than 5 % adipose tissue by weight. Total fatness correlated closely with the number of adipocytes per kilogram lean body mass, but not at all with mean adipocyte volume, except in specimens below 5 % fat. The total number of adipocytes per kilogram of lean body mass increased more than tenfold in the most obese specimens. These data suggest that, like humans but in contrast to laboratory rodents, adipocyte proliferation, not adipocyte enlargement, is the chief mechanism of adipose tissue expansion except in very lean monkeys. Adipose tissue was found in all the typical mammalian depots and in the superficial abdominal paunch, which enlarged disproportionately in obese specimens, forming an almost continuous layer over most of the body. Site-specific differences in the activities of some glycolytic enzymes were similar to those of other mammals. Adipocytes in the paunch depot showed biochemical properties in common with those in the groin depots. The distribution and cellularity of adipose tissue in normal humans were similar to those of exceptionally obese monkeys. Many of the interspecific and sex differences can be attributed to the much greater abundance of adipose tissue in humans, and may not be associated with hair reduction or aquatic habits. Some minor changes in the size or shape of certain adipose depots may have arisen recently under sexual selection. The relevance of laboratory rodents as animal models of human obesity is assessed from comparison of the cellular structure, anatomical distribution and enzyme profiles of adipose tissue in monkeys with those of human and other mammals.
Total dissection of a randomly collected sample of 202 adult and subadult eutherian mammals, combined with site-specific adipocyte volume determination, shows that the number of adipocytes in the body is proportional to (Body Mass) for predominantly carnivorous species and to (Body Mass) for mainly herbivorous, nonruminant mammals. Adipocyte expansion or shrinkage, not proliferation or depletion of adipocyte number, is the principal mechanism of adipose tissue enlargement and reduction. Therefore, the adipocytes of large mammals are larger than those of smaller specimens of similar dietary habits and fatness. We suggest that the presence of more numerous, smaller adipocytes in smaller mammals is related to their higher mass-specific metabolic rate. The adipose tissue of mammals with a predominantly carnivorous diet contains 4.6 times as many adipocytes as that of herbivorous nonruminants of similar body mass; but nonruminant herbivores are not necessarily fatter because the adipocytes of carnivorous mammals are proportionately smaller than those of nonruminant herbivores. We suggest that a carbohydrate-based energy metabolism is associated with fewer, relatively larger adipocytes and that when lipids and proteins form the major dietary energy source, adipose tissue consists of a greater number of smaller adipocytes.
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