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Although poor cardiorespiratory function is a powerful predictor of mortality in patients with obesity, functional evaluation has been given little attention after laparoscopic sleeve gastrectomy (LSG). The aim of this study was thus to investigate the impact of LSG on functional capacity analysing a shorter and longer post-surgical follow-up. In this observational study, 24 patients with severe obesity (BMI 44.04 ± 5.84 kg/m2, age 47.0 ± 9.0 years) performed cardiopulmonary exercise testing 7 months pre-, 6 and 16 months post-LSG. Exercise capacity, oxygen uptake and VO2 kinetics were analysed during treadmill exercise testing. Although patients showed an improved peak work capacity after LSG, parameters of maximal absolute aerobic capacity demonstrated a significant decrease, which was confirmed also in the follow-up analysis. Furthermore, the time constant Tau (τ) of the fundamental component of VO2 kinetics was altered by LSG, however, within the 16 months of follow-up it returned towards baseline values. It can thus be concluded that LSG improved peak work capacity along with a lower maximal absolute aerobic capacity, which might be due to a loss of muscle mass and potentially impaired peripheral oxidative muscle metabolism. However, VO2 kinetics might suggest an initial restoration of peripheral oxidative muscle capacity after a longer follow-up.

Although poor cardiorespiratory function is a powerful predictor of mortality in patients with obesity, functional evaluation has been given little attention after laparoscopic sleeve gastrectomy (LSG). The aim of this study was thus to investigate the impact of LSG on functional capacity analysing a shorter and longer post-surgical follow-up. In this observational study, 24 patients with severe obesity (BMI 44.04 ± 5.84 kg/m

Type 2 diabetis mellitus (T2DM) and obesity are global health care problems that are closely linked together. The precise mechanisms linking the two conditions remain unclear. Indeed, while the close relationship between T2DM and weight gain is well established, not all obese subjects are diabetic and this paradox is still unexplained. Impaired tissue perfusion has been proposed as one of the common metabolic defects, but little is known about adipose tissue (AT) microangiopathy and its possible role in T2DM. In animal models of obesity and diabetes, expanding AT microvasculature appears structurally altered and the angiogenetic potential of adipose derived stem cells impaired. Several studies, in humans, suggest that obesity leads to an impaired angiogenesis and AT hypoxia, inducing an inflammatory and a profibrotic response that plays a pivotal role in the pathogenesis of metabolic complications related to weight gain, first of all insulin resistance and diabetes. Moreover, from a pathophysiological point of view it is well established that dysfunctional visceral adipose tissue (VAT) is one of the major determinants of metabolic complications of obesity, while subcutaneous depots has been considered metabolically healthy. Nevertheless it could be hypothesized that in the progress of obesity through the metabolic impairment, SAT could become dysfunctional as VAT. On the basis of these data, we planned to study both subcutaneous and visceral adipose tissue in terms of adipocytes size, capillary density, adipose tissue stem cells (ASCs), endotelial precursor of AT and adipogenic potential, in obese subjects compared to lean subjects and in obese patients with a different glyceamic profile. We collected subcutaneous (SAT) and/or visceral (VAT) adipose tissue (AT) from 249 patients divided in 5 different groups: 18 lean normal weight and normoglycemic subjects (18.5 < BMI < 24,9 kg/m2) as control group, 68 normoglycemic obese subjects (ob N), 65 pre-diabetic obese subjects (ob pre-T2DM), 57 diabetic obese subjects (ob T2DM) and 41obese patients after underwent to a relevant weight loss (ob WL), corresponding to at least 10% of body weight. In different representative subgroups of these samples we performed: 1) immunohistochemical analysis to evaluate the morphometry of adipocyte and capillary density; 2) flow cytofluorimetric analysis of stromal vascular fraction (SVF) in order to quantify adipose tissue stem cells (ASCs), defined as CD45-CD34+CD31-, and endothelial precursors cells (EPs) defined as CD45-CD34+CD31+; 3) in vitro culture of ASCs obtained from SVF, in order to estimate the adipogenic potential in the different groups and different depot of AT; 4) gene expression profile by RT-Real Time PCR of PPRγ, Leptin, VEGFA, VEGF2, HIF1α to correlate their expression with previous findings. Our study confirm that obese AT is less vascularized than lean AT but T2DM does not represent an aggravating factor to the vascular reduction already present in obesity. On the contrary, T2DM and also prediabetic condition are able to further modify AT architecture, remodeling mature adipocyte size and adipogenic potential mediated by ASCs, importantly reducing AT hyperplastic growth capacity. Moreover our results allow us to assume that primum movens in development of T2DM must be searched in AT architecture and that both depots, SAT and VAT, play a pivotal role in the development of this disease. Furthermore, considering the continuous increase in bariatric procedures to treat both weigh gain and associated co-morbidities, we plan to evaluate the effects of laparoscopic sleeve gastrectomy (LSG) after one year. Indeed, whereas the beneficial effects of this bariatric procedure are well known, side effects are lesser known. In particular, postprandial hypoglycaemia is a well described side effect after RYGB, but few data are available for LSG.. We enrolled a total of 197 consecutive non-diabetic morbidly obese who underwent to LSG in our Center for the Study and the Integrated Treatment of Obesity (Ce.S.I.T.O.). All patients were studied 12 months before and after LSG and, anthropometrics parameters, medical history, clinical examination, complete blood count and complete metabolic panel including a 3- hour OGTT, were collected. One year after LSG, all patients had a significant reduction in weight and BMI, a significant improvement in glucose and insulin profile, and a significant decrease in inflammatory markers. We found an high incidence of severe hypoglycaemia (32,8%) after a provocative test (OGTT). Patients with hypoglycaemic events had a lower weight and BMI and a greater %EBML after LSG. compared to patients without hypoglycemic events. Hypoglycaemia was more frequent in patients having lower age, lower fasting blood glucose levels and higher triglycerides levels before LSG.

BACKGROUND: Mother-to-child transmission of hepatitis C virus (HCV) has been reported in around 5% of cases, and is much more likely to occur in case of coinfection with HIV. However, other cofactors influencing the vertical transmission are still debated. AIM: To assess the serum concentration of endogenous interferon (IFN) during pregnancy, and its eventual role on the vertical transmission of HCV. METHODS: Forty-seven HCV-infected pregnant women, and 3 control groups: (1) 75 HCV-negative pregnant women; (2) 29 HCV-positive nonpregnant women; (3) 29 HCV-negative nonpregnant women entered into the study. Endogenous IFN was assayed by enzyme-linked immunosorbent assay. The following parameters were also analyzed: viral load, HIV infection, risk factors for acquiring HCV, parity, gestational age, mode and course of delivery. RESULTS: Vertical transmission of HCV was observed in 2 cases (4.3%). Plasma levels of IFN were significantly higher in HCV-positive pregnant women compared with either HCV-positive and HCV-negative nonpregnant women. The 2 mothers who transmitted the infection had IFN levels within the same range as the women who did not transmit the infection. CONCLUSIONS: In HCV-positive pregnant women, there is an increased production of endogenous IFN-α. Further studies are warranted for clarifying the mechanisms of this cytokine in the prevention of HCV transmission. © 2008 Lippincott Williams & Wilkins, Inc.