Neuroendocrine-Adipose-Immune Interactions: An integrative sight.

SPINEDI E; GIOVAMBATTISTA A

Buenos Aires

Simposio; XXII Congreso Latinoamericano y 1ro Ibero-Americano de Ciencias; 2006

IBERO-ALACF

Interactions between neuroendocrine, adipose and immune functions became, during the last decade, very attractive for a better understanding of integrative processes involved in maintaining organism’s homeostasis. It is known that a sex-hormone basis is a regulatory factor  for the activity of those systems. For instance hypothalamo-pituitary-adrenal axis and immune responses to an inflammatory noxa are greater in females than in males, and testosterone is able to enhance leptin metabolic clearance rate. Thus clearly indicating a clear sexual dimorphism characterizing either individual function. Additionally, changes in the energetic condition of an individual is recognized as another condition impacting many of these activities. Hypoleptinemia results as a consequence of, among others, fasting or decreased body fat mass. This diminished signal in the circulation allows the adrenal gland to spontaneously secrete more glucocorticoid than as it occurs during homeostasis. Conversely, the postprandial increase in circulating leptin concentrations decreases adrenal glucocorticoid release. Glucocorticoids play anti-inflammatory and immune-suppressor roles, but also directly stimulate adipocyte leptin production. Additionally, leptin is enhanced in the circulation during the acute phase response of inflammation. It has been suggested that this rapid increase in circulating leptin levels is responsible, at least partially, for the anorexigenic characteristic of the acute inflammatory process. But enhanced leptin secretion during inflammation will also impact the immune system. In fact, leptin exerts protective anti-inflammatory effect in models of acute inflammation and during activation of innate immune response. In contrast, leptin stimulates T lymphocyte response, thus having rather a pro-inflammatory role in models of autoimmune diseases. Thus, the inter-relationship between signals derived from these systems is a very complex one. More deep investigation is still needed for a better understanding of the mechanisms involved in the integrated response of the organism to an inflammatory noxa.