Endocrinology of Adipose Tissue

The last decade of obesity research was characterized by a dramatic change in our understanding of adipose tissue function. The traditional view was that adipose tissue is a rather inactive organ that serves mainly to store excess calories in the form of triglycerides which is the most efficient manner of energy storage in man. In case of increased demand or food shortage lipolytic agents such as catecholamines readily mobilize this energy reservoir.

Although this classical function is still valid, there is growing evidence that adipose tissue is a multifunctional organ that produces a variety of secretory factors that act either at the local level (autocrine/paracrine/intracrine) or the systemic level (endocrine). This list of secretory products is growing almost monthly. Thus, it seems more and more obvious that an intense cross-talk exists between fat cells and many other tissues such as endothelium, muscle, liver, pancreas, adrenal glands, and central nervous structures.

These new findings are of great clinical importance. An excess of body fat or a central distribution of adipose tissue is known to be associated with a variety of adverse consequences that may decrease not only quality-of-life but also life expectancy. There are now first hints that these disturbances may also be due to an impaired secretory function of fat cells. For example, adipose cells produce substantial amounts of interleukin-6 and PAI-1 and the circulating levels of both factors are markedly elevated in obesity. Likewise, adipose tissue is an important source of other inflammatory proteins. On the other hand, the anti-inflammatory fat cell product adiponectin is decreased in the obese state suggesting that an unfavorable pattern of pro- and anti-inflammatory proteins may favour the development of type 2 diabetes and atherosclerosis.

In this particular issue of Hormone and Metabolic Research the focus is on the endocrinology of adipose cells. This is the third special issue in the area of obesity research. The first special issue published in 1996 dealt with the newly discovered fat cell hormone leptin and contributed a variety of novel observations [1]. The second special issue already focused on secretory products of fat cells, their regulation as well as their possible clinical role [2].

The current issue presents many new data on the regulation and action of some of these factors that are evolving to be directly related to insulin resistance and the chronic inflammatory status of obesity, e.g. adiponectin, resistin, IL-6, leptin and angiotensin II, illustrating the impressive progress in the field. In the first part, the focus of the contributions is on more general aspects, i.e. the communication between the adipocyte and neurons in the control of energy homeostasis and on regional differences in gene expression and secretory function between subcutaneous and visceral fat cells. The final part covers steroid hormone metabolism in adipose tissue, thereby recognizing that this organ is an important production site of steroid hormones. The recent observations in a transgenic animal that over-expression of 11β-hydroxysteroid dehydrogenase in adipose tissue results in visceral obesity gives further support to the notion that adipose tissue produces glucocorticoids and may thereby promote the development of the metabolic syndrome [3].

The central message of this issue is that obesity represents a state of chronic inflammation which may act as common soil for the development of insulin resistance and cardiovascular dysfunction. The long-term consequences of this process are the appearance of the metabolic syndrome and cardiovascular complications that have become a tremendous burden for the healthcare systems. In this context, it is also promising that this issue contains data on the effects of dietary measures as well as of specific drugs that may be able to restore the dysregulated endocrine system of adipose tissue. This raises the hope that through prevention and intervention the deleterious sequelae of obesity and, in particular, of the visceral accumulation of body fat may be avoided.

References

• 1 Campfield L A, Smith F J, Burn P. The OB protein (leptin) pathway - a link between adipose tissue mass and central neural networks.  Horm Metab Res. 1996;  28 619-632
• 2 Hauner H, Després J P. Special issue on “adipose tissue: a multifunctional organ” (editorial).  Horm Metab Res. 2000;  32 441-442
• 3 Masuzaki H, Paterson J, Shinyama H, Morton N M, Mullins J J, Seckl J R, Flier J S. A transgenic model of visceral obesity and the metabolic syndrome.  Science. 2001;  294 2166-2170