contrast, the term "lipolysis" refers to the breakdown of "lipid stores for utilization by the body (10:385-392)." This break down is largely mediated by hormone-sensitive lipase. Once the enzyme metabolizes an adipocyte's triglycerides, the free fatty acids and glycerol are then able to move into the vascular system and provide energy to other parts of the body.
The control mechanisms for lipogenesis and lipolysis are complex. Many different hormones influence both pathways. For example, insulin inhibits lipolysis and facilitates lipogenesis. In contrast, the catecholamines--which may exert dual effects--primarily stimulate lipolysis. Other hormones that stimulate lipolysis include cortisol, glucagon, adrenocorticotropic hormone, thyroid-stimulating hormone, growth hormone, and vasopressin. These various modulators are thought to permit very precise control of fat metabolism (10:385-392).
In the past, obesity has been classified as either hyperplastic or hypertrophic. Hyperplastic obesity refers to an increase in fat cell number; whereas, hypertrophic obesity involves an increase in fat cell size. In the past, it was widely believed that childhood-onset obesity was hyperplastic, and adult-onset obesity was hypertrophic. More recent research, however, indicates that there are exceptions to this hypothesis (10:385-392).
The etiology of human obesity remains unknown. Many obesity theories have been proposed. For the most part, these different mechanisms involve either the hypothalamus or the adipocyte. The hypothalamic hypotheses generally imply that a central regulatory abnormality is responsible for obesity; whereas, the adipocyte hypotheses relate to fat cell abnormalities. It is highly likely, however, that obes
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