In recent years, the simple paradigm of adipose tissue as merely a fat store is rapidly evolving into a complex paradigm of this tissue as multipotential secretory organ, partitioned into a few large depots, including visceral and subcutaneous location, and many small depots, associated with a variety of organs in the human body. The major secretory compartment of adipose tissue consists of adipocytes, fibroblasts, and mast cells. These cells, using endocrine, paracrine and autocrine pathways, secrete multiple bioactive molecules, conceptualized as adipokines or adipocytokines. This review examines current information in adipobiology of various diseases besides obesity and related diseases such as type 2 diabetes, metabolic syndrome, and cardiovascular disease. Finally, we emphasize the possibilities for adipokine-targeted pharmacology in adiponectin (Acrp30, apM1, AdipoQ, GBP28), angiotensin II, estrogens, nerve growth factor, tumor necrosis factor-alpha, and also adipose mast cells.

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While multiple growth factor, cytokines, and immune cells are identified in atherosclerotic lesions, as well as an essential nonneuronal function of neurotrophins implicated in cardiovascular tissue development and in lipid and glucose metabolism, the role of the neurotrophins NGF and BDNF and also the adipokine leptin in human coronary atherosclerosis and related disorders, such as metabolic syndrome, remains unclear. Here we report that (i) both the amount and the immunoreactivity of NGF was reduced and the expression of p75NGF receptor and the number of mast cell increased in human atherosclerotic coronary arteries (n = 12) compared with control specimens (n = 9) obtained from autopsy cases, and (ii) NGF and BDNF plasma levels were reduced in patients with metabolic syndrome (n = 23) compared with control subjects (n = 10). Also, in metabolic syndrome patients, a positive correlation between the plasma leptin levels and the number of adipose tissue mast cells was found, suggesting that leptin may be a novel adipoimmune mediator. Altogether, the results provide the first correlative evidence for the potential involvement of NGF, BDNF, leptin, and mast cells in human coronary atherosclerosis and metabolic syndrome, implying neuroimmune and adipoimmune pathways in the pathobiology of these cardiovascular disorders.

The aim of this study was to investigate the effects of melatonin on burn-induced inflammatory responses and coagulation disorders in a rat model. Under ether anesthesia, shaved dorsa of rats were exposed to 90 degrees C for 10 s to induce burn injury. Melatonin (10 mg/kg) was administered immediately and after 12 h. Standard coagulation tests (prothrombin activity [PA] and activated partial thromboplastin time [aPTT]), platelet number and morphology; proinflammatory markers (C-reactive protein [CRP] and fibrinogen) and lipid peroxidation marker (malondialdehyde [MDA]) levels were assayed. Thermal injury increased the levels of MDA (by 76%, P < 0.0001), CRP (by 33%, P < 0.0001), fibrinogen (4.5-fold, P < 0.0001) and PA (by 37%; P < 0.01). Changes in aPTT and platelet numbers were nonsignificant. Melatonin diminished the elevated CRP and fibrinogen levels, normalized MDA levels, platelet morphology and decreased PA. A positive association of MDA with fibrinogen and MDA with PA were noted after melatonin treatment. To conclude, melatonin as an antioxidant and anti-inflammatory agent exerted a suppressive effect on burn-induced disorders in blood coagulation and might be useful in the prevention of disseminated intravascular microthrombosis.

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