It seems to be generally accepted that leptin may be an important signal that connects energy stores with the immune system (3,5,10). In fact, leptin has been considered an indicator of nutritional status. Thus, falling leptin levels in starvation may alert the organism to avoid energy wasting and to seek energy storing. Therefore, the lack or decrease of leptin levels may play a role in the immunosuppression of starvation. In this context, leptin may serve to signal the organism to conserve energy by shutting down nonessential systems. Moreover, leptin might be not only a signal for the adaptation of starvation, but in addition, leptin could have played a role in selection, helping the better nourished to survive under starving conditions, allowing the defense against infection to those better prepared.
The same immune deficiency observed in starvation has been found in human obesity syndromes caused by a deficiency of leptin production or leptin action (46). In addition, leptin administration in obesity caused by lack of leptin can restore immune function as observed in a similar way as that seen in starving conditions (6-8).
On the other hand, an excess of leptin in the circulation that occurs in obesity and overweight could have a role in pathological conditions mediated by an excess of immune response (73). This "proinflammatory state" may be relevant for cardiovascular disease and the risk for myocardial infarction that is increased in obese people. Moreover, leptin, together with other adipokines, could be a common link between obesity and cardiovascular risk in metabolic syndrome. Because obese people do not respond to leptin properly, central versus peripheral leptin resistance may underlie the pathophysiology of obesity, and therefore, the study of leptin signaling at central versus peripheral levels may improve our understanding of the mechanisms involved in the metabolic and immune alterations in the metabolic syndrome that lead to increased cardiovascular risk. These molecular defects may connect the thrifty phenotype with the proinflammatory phenotype in a common trait that turns out to be lethal in the Westernized way of life.
Recent data also suggest the possible role of leptin in the pathophysiology of some autoimmune diseases. This has already been demonstrated in some animal models, such as the experimental autoimmune encephalomyelitis, antigen-induced arthritis, models of type 1 diabetes, autoimmune colitis, and experimental hepatitis, as well as some clinical studies (15,17,72-74). However, this is the subject of other chapters in this book, and we are not reviewing the possible role of leptin in the pathophysiology of immune diseases.
Finally, leptin administration has been proposed as a possible treatment, not only for the immunodeficiency of obesity syndromes caused by a deficit of leptin (46), but also in some immunodeficiency syndromes, such as the common variable immunodeficiency, to improve both function of T-cells and the synthesis of immunoglobulins. In this line, recent data obtained using cells from patients in vitro support this hypothesis (75).
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