Luigi Aloe

In 1999, the prevailing response-to-injury hypothesis of Russell Ross stated that atherosclerosis is an inflammatory disease, leading - through an inside-out road - to endothelial and smooth muscle dysfunction resulting in the formation of atherosclerotic plaques. Accordingly, intima-media thickness became an accepted measure of structural vascular remodeling and a strong predictor of atherosclerosis. However, it is unlikely that such a road may solely travel the whole multiplex network like that of atherogenesis. Recently things changed dramatically and the attention was moved from inside-out to outside-in road emphasizing the role for adventitial and adipose dysfunction in the processes of atherogenesis.

Diabesity is a new term which refers to type 2 diabetes mellitus and obesity found in one individual, hence Homo diabesus. Previously we presented our hypothesis of metabotrophic factors (MTF), also termed metabotrophins. Onward we described Homo obesus (man obese) as a metabotrophin-deficient species. Now - as a phenotypic variety of this species - we introduce H. diabesus. Endogenous MTF are in general signaling proteins able to improve cardiovascular and metabolic homeostasis including that of lipids, glucose, energy, inflammation, angiogenesis, and cognition. Hence pharmacological manipulations of the secretion and/or signaling of MTF might bring a therapeutic benefit for H. diabesus. Here we Dance Round the hypothesis that deficit and/or dysfunction of MTF may lead to diabesity. Arguably, an updated list of MTF including nerve growth factor, brain-derived neurotrophic factor, adiponectin, humanin, irisin and other adipose- and nonadipose-derived bioactive molecules is presented. Overall this may cultivate a novel pathogenic and therapeutic thinking for cardiometabolic disease. Adipobiology 2012; 5: 45-49.

BDNF is present in human serum and its level changes have been used as a marker of antidepressant efficacy in some psychiatric disorders. In addition, the positive effects of light therapy on major depression suggest that circadian-regulated factors should be taken into account in the management of mood disorders. The aim of the present study was to test ultradian fluctuations in serum and salivary BDNF levels and their interaction with light therapy in a sample of healthy women. The study included 16 young women. Psychopathological status and chronotype traits were assessed by SPAQ, BDI, STAI, TAS, and MEQ. Standard light treatment protocol was applied. Serum and saliva were collected at 8.00, 13.00 and 20.00 hrs on the same day and at the end of light therapy. BDNF levels declined over the course of the day both in serum and saliva, and a correlation between diurnal BDNF trend and personality traits and habits characterizing the morning and evening types in healthy women was found. The present study is one of the first to show measurable BDNF in human saliva and to demonstrate its daily fluctuations in both saliva and serum of healthy young women. The correlation between diurnal changes in BDNF and the personality traits associated with body rhythms corroborates the notion that salivary BDNF may be a useful biomarker for stress-related research and different clinical investigations.

VEGF and NGF are known to modulate corneal healing, neovascularisation and tear secretion. While a VEGF-NGF cross talk has been recently shown to modulate corneal healing in rats, it is not known whether it also plays a role in the regulation of lacrimal function. In this study we aim to investigate the effects of anti-VEGF eye drop treatment on lacrimal gland function and on the local expression of VEGF and NGF in rats. Tear function was measured in 3 months old rats by modified Schirmer test at baseline and after 3 weeks of topical anti-VEGF eye drop treatment. Whole lacrimal glands from rats were removed after treatment and analysed by ELISA for VEGF and NGF levels. To investigate if the effects of anti-VEGF were mediated by changes in the NGF-pathway, we repeated the experiments in RCS rats, a strain with NGF-pathway impairment associated with decreased tear flow. After topical treatment with anti-VEGF eye drops, an increase in tear secretion was observed in both wild-type and RCS rats. A significant decrease of VEGF levels was also observed in lacrimal glands of both RCS and SD rats, accompanied by a significant increase in NGF levels. Inhibition of VEGF at the ocular surface in rats results in changes of tear function and lacrimal gland levels of VEGF and NGF. Further studies on the VEGF/NGF cross-talk at the ocular surface may expand our knowledge on the pathogenesis of several diseases characterized by tear dysfunction.

Published on 1 December 1994 issue of Nature, the Jeffrey Friedman's discovery "gave leptin in the beginning" of the endocrine saga of adipose tissue. Onwards, studies on this tissue have enjoyed an explosive growth that conceptualized a novel field of research, adipobiology. Arguably, in the heart of adipobiology and adipopharmacology are studies focusing on the pathogenesis, prevention and therapy of cardiometabolic diseases (CMD) including atherosclerosis, hypertension, obesity, type 2 diabetes, metabolic syndrome (global cardiometabolic risk), and lipodystrophies. Adipobiology 2010; 2: 5-8.

Published on 1 December 1994 issue of Nature, the Jeffrey Friedman's discovery "gave leptin in the beginning" of the endocrine saga of adipose tissue. Onwards, studies on this tissue have enjoyed an explosive growth that conceptualized a novel field of research, adipobiology. Arguably, in the heart of adipobiology and adipopharmacology are studies focusing on the pathogenesis, prevention and therapy of cardiometabolic diseases (CMD) including atherosclerosis, hypertension, obesity, type 2 diabetes, metabolic syndrome (global cardiometabolic risk), and lipodystrophies. Biomedical Reviews 2009; 20: 1-5.

Rats exposed during prenatal life to methylazoxymethanol (MAM) display in postnatal age structural and behavioral deficits resembling those observed in schizophrenic patients. These deficits are associated with significant changes in brain nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF), particularly in the hippocampus and entorhinal cortex. In the present study, we used the MAM model to investigate in young rats the effect of antipsychotics, Clozapine and Haloperidol, on brain and blood NGF and BDNF presence. Young animals were used because administration of antipsychotics during adolescence is a common feature of intervention. The results showed that administration of Clozapine and Haloperidol causes significant changes in the concentration of NGF and BDNF in the brain and bloodstream of MAM-treated rats. These findings indicate that these drugs may affect the synthesis and release of neurotrophins in the central nervous system and in the blood circulation. In addition, the MAM model can be a useful tool to investigate the biochemical and molecular mechanisms regarding the effects of antipsychotics.