ABSTRACT
Adipose tissue metabolism has been studied since the 1950s. Thousands of studies have established its metabolic pathways and high sensitivity to the hormones which regulate lipid synthesis and lipid mobilization. This biochemical approach, however, can lead to misinterpretation when comparisons are made between adipose tissues differing in weight due to age or pathological states. In these conditions fat cell size and number have to be taken into account. It is now well established that the metabolism of fat cells is related to fat cell size. 14 Adipose tissue metabolism in man and animals has been shown to be similar, when age is taken into account. For example, the levels of endogenous lipogenesis in human adipose tissue is known to be very low in normal and obese subjects; this is also the case in adult lean and obese mice and rats. 5-7 Also, as in human obesity, 89 fat cell lipoprotein lipase activity in animal experimental obesities of genetic 10 or dietary 6 origin is increased. The metabolic effects of hormones too, are quite similar in rat, mouse, and human fat cells and may or may not be related to fat cell size. Many attempts have been made to find a specific metabolic defect in obese fat cells, but these have been unsuccessful to date. This can be illustrated by the experiments of Hausberger 14 and of Liebelt 15 who grafted adipose tissue from lean and obese animals in obese and lean siblings. In recent studies Ashwell et al. 16 confirmed that no innate defect in the fat cell per se can explain obesity in the genetically obese mouse.
