Autonomic Nervous System in Obesity and Insulin-Resistance-The Complex Interplay between Leptin and Central Nervous System.

The role of the autonomic nervous system in obesity and insulin-resistant conditions has been largely explored. However, the exact mechanisms involved in this relation have not been completely elucidated yet, since most of these mechanisms display a bi-directional effect. Insulin-resistance, for instance, can be caused by sympathetic activation, but, in turn, the associated hyperinsulinemia can activate the sympathetic branch of the autonomic nervous system. The picture is made even more complex by the implicated neural, hormonal and nutritional mechanisms. Among them, leptin plays a pivotal role, being involved not only in appetite regulation and glucose homeostasis but also in energy expenditure. The purpose of this review is to offer a comprehensive view of the complex interplay between leptin and the central nervous system, providing further insights on the impact of autonomic nervous system balance on adipose tissue and insulin-resistance. Furthermore, the link between the circadian clock and leptin and its effect on metabolism and energy balance will be evaluated.

The risk of carotid plaque instability in patients with metabolic syndrome is higher in women with hypertriglyceridemia.

BACKGROUND: Metabolic syndrome certainly favors growth of carotid plaque; however, it is uncertain if it determines plaque destabilization. Furthermore, it is likely that only some components of metabolic syndrome are associated with increased risk of plaque destabilization. Therefore, we evaluated the effect of different elements of metabolic syndrome, individually and in association, on carotid plaques destabilization. METHODS: A total of 186 carotid endarterectomies from symptomatic and asymptomatic patients were histologically analysed and correlated with major cardiovascular risk factors. RESULTS: Metabolic syndrome, regardless of the cluster of its components, is not associated with a significant increase in risk of plaque destabilization, rather with the presence of stable plaques. The incidence of unstable plaques in patients with metabolic syndrome is quite low (43.9 %), when compared with that seen in the presence of some risk factors, but significantly increases in the subgroup of female patients with hypertriglyceridemia, showing an odds ratio of 3.01 (95% CI, 0.25-36.30). CONCLUSIONS: Our data may help to identify patients with real increased risk of acute cerebrovascular diseases thus supporting the hypothesis that the control of hypertriglyceridemia should be a key point on prevention of carotid atherosclerotic plaque destabilization, especially in post-menopausal female patients.

Natural Bioactive Compounds Useful in Clinical Management of Metabolic Syndrome.

Metabolic syndrome (MetS) is a clinical manifestation characterized by a plethora of comorbidities, including hyperglycemia, abdominal obesity, arterial hypertension, and dyslipidemia. All MetS comorbidities participate to induce a low-grade inflammation state and oxidative stress, typical of this syndrome. MetS is related to an increased risk of cardiovascular diseases and early death, with an important impact on health-care costs. For its clinic management a poly-pharmaceutical therapy is often required, but this can cause side effects and reduce the patient's compliance. For this reason, finding a valid and alternative therapeutic strategy, natural and free of side effects, could represent a useful tool in the fight the MetS. In this context, the use of functional foods, and the assumption of natural bioactive compounds (NBCs), could exert beneficial effects on body weight, blood pressure and glucose metabolism control, on endothelial damage, on the improvement of lipid profile, on the inflammatory state, and on oxidative stress. This review focuses on the possible beneficial role of NBCs in the prevention and in the clinical management of MetS and its comorbidities.

Functional retinal impairment in type 1 diabetic patients without any signs of retinopathy.

PURPOSE: To investigate functional and morphological retinal changes in the long-term follow-up in subjects with type 1 diabetes mellitus (DM1) without any signs of retinal vasculopathy. METHODS: Functional testing included Humphrey Matrix perimetry (30-2 threshold program) and white-on-white Humphrey perimetry (HFA, 30-2 SITA standard), while retinal nerve fibre layer (RNFL) thickness was measured by scanning laser polarimetry with variable corneal birefringence compensator. RESULTS: Data from 20 eyes of 20 subjects with DM1 were analysed. No changes of HFA mean deviation (MD: -2.20 ± 3.44 vs. -1.63 ± 2.47; p = 0.14) and pattern standard deviation (PSD: 2.50 ± 1.71 vs. 2.28 ± 1.36; p = 0.31), and Matrix MD (-1.06 ± 3.62 vs. -1.24 ± 2.99; p = 0.65) were found after 5 years. A significant change was found for Matrix PSD between baseline and the end of follow-up (2.76 ± 0.59 vs. 3.1 ± 0.68; p = 0.0078). RNFL parameters were not changed. A significant relationship was found between HbA1c levels and changes from baseline of Matrix PSD (R(2) 0.29, p = 0.02). CONCLUSIONS: Progressive retinal functional impairment could be detected in DM1 subjects by frequency doubling perimetry before the onset of any overt retinal vasculopathy and functional impairment seems to be significantly related to glycaemic control.