Abstract
Obesity is the condition where the lipid store of the body, adipose tissue, is enlarged. The main, functional unit of adipose tissue is the adipocyte. Enlargement of adipose tissue is accomplished first by enlargement of adipocyte contents of storage fat, triglyceride. At some point after the plateau in cell size is reached, an increase in obesity must be accompanied by an increase in number of adipocytes. It should be emphasized, that adipocytes have a unique ability to change their capacity for triglyceride storage. The fatty acid composition of triglyceride in the adipose tissue is affected by that of fat in a meal. However, the fatty acid composition of the adipose tissue do not differ between obese and non-obese subjects.
In obesity, the excess depot fat is presumably accumulated in the available depots by principally the same regulatory mechanisms as in the physiological non-obese state. Triglyceride in adipocyte is synthesized from blood glucose and circulating fat in the form of chylomicron and very low density lipopretein, and hydrolyzed to glycerol and fatty acids by hormone-sensitive lipase. Recent work has demonstrated that lipid mobilization in the adipocyte were regurated by genetic, nervous, endocrine, and metabolic factors.
Now, the description and risk of excess adipose tissue in obesity are fairly well establised. Accumulation of triglyceride in adipocytes in the end result of the balance between triglyceride synthesis and degradation. Therefore, lipid mobilization is of importance for the obesity. Clearly, more studies are needed in the area.
